Faculty Profiles - Sawatsubashi Shun

写真a

Sawatsubashi Shun

Organization

Institute for Emerging Medical Innovation Special-Appointment Professor

Homepage

https://www.iams.tokushima-u.ac.jp/lab/sawatsubashi/

External link

Degree

農学博士 ( 東京大学 )

Research Interests

乾癬
エピゲノム
転写制御
脱毛
ビタミンD受容体
グルココルチコイド
転写
O-GlcNAc
核内受容体
毛周期
表皮
ステロイドホルモン
ビタミンD
クロマチン
エネルギー代謝
くる病
S100A8
内分泌学
エクダイソン受容体
グルココルチコイド受容体
ヒストンシャペロン
ゲノム編集
転写共役因子
液-液相分離

Education

The University of Tokyo 大学院農学生命科学研究科応用生命工学専攻

2002.4 - 2005.9

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Shizuoka University 大学院理工学研究科生物地球環境科学専攻

2000.4 - 2002.3

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Shizuoka University 理学部生物地球環境科学科

1996.4 - 2000.3

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Research History

Okayama University Advanced Research Fields, Institute for Emerging Medical Innovation, Translation Animal Model Innovation Core Professor

2026.6

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Country：Japan

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The University of Tokushima 先端酵素学研究所 Associate Professor

2022.9 - 2027.3

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株式会社セツロテック最高科学責任者（CSO）

2022.3 - 2022.8

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The University of Tokushima 先端酵素学研究所

2020.4 - 2022.2

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株式会社セツロテック取締役（兼務）

2017.2

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The University of Tokushima 先端酵素学研究所

2016.4 - 2020.3

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The University of Tokushima 藤井節郎記念医科学センター

2015.3 - 2016.3

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The University of Tokushima 藤井節郎記念医科学センター

2014.3 - 2015.2

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Gunma University Institute for Molecular and Cellular Regulation Assistant Professor

2010.3 - 2014.2

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Japan Science and Technology Agency 戦略的創造研究推進事業（ERATO） Researcher

2006.4 - 2010.2

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The University of Tokyo Institute of Molecular and Cellular Biosciences

2005.10 - 2006.3

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Professional Memberships

THE MOLECULAR BIOLOGY SOCIETY OF JAPAN

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THE JAPANESE BIOCHEMICAL SOCIETY

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JAPAN SOCIETY FOR BIOSCIENCE, BIOTECHNOLOGY, AND AGROCHEMISTRY

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日本骨代謝学会

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The Japan Endocrine Society

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Papers

MED26 facilitates Mediator-Pol II complex assembly and promotes nuclear stress body formation during heat stress. Reviewed International journal

Kexin Li, Kazuki Furugori, Hidefumi Suzuki, Ryota Abe, Shun Sawatsubashi, Nanami Yasui, Yoko Ike, Keiko Horiuchi, Hidehisa Takahashi

iScience 29 ( 10 ) 117557 - 117557 2026.10

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Language：English Publishing type：Research paper (scientific journal)

Cells adapt to environmental stress by reprogramming gene expression. During heat stress, the transcription factor heat shock factor 1 (HSF1) translocates into the nucleus and activates heat shock-responsive loci, including the long non-coding RNA HSATIII, promoting nuclear stress body (nSB) formation. We show that the Mediator complex subunit MED26 enhances HSATIII transcription and nSB formation through a mechanism distinct from its role at heat-shock response (HSR) genes. Under heat stress, MED26-containing Mediator is recruited to HSR genes and nSBs through interactions with HSF1 and MED15. Phosphorylation of the intrinsically disordered region of HSF1 appears to facilitate Mediator recruitment to nSBs. Acute loss of MED26 leads to the dissociation of the Mediator and RNA polymerase II (Pol II) from HSR gene promoters, whereas the Mediator remains bound to HSATIII despite Pol II dissociation. These results suggest that MED26 acts as molecular switch, thereby facilitating Mediator-Pol II complex assembly at nSBs and promoting nSB formation during heat stress.

DOI： 10.1016/j.isci.2026.117557

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Expanding the scope of precision editing in seaweeds through the application of a novel CRISPR-associated nuclease 12a-aligned CRISPR system in Ulva prolifera. Reviewed International journal

Zheng Qin, Whelver Surnido, Shunya Hozumi, Takamasa Hirano, Shun Sawatsubashi, Hiroyuki Mizuta, Toshiki Uji

Journal of experimental botany 77 ( 17 ) 5560 - 5565 2026.9

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Language：English Publishing type：Research paper (scientific journal)

Seaweeds, such as the fast-growing green alga Ulva prolifera, can be harnessed as valuable marine crops. The lack of scalable genome-editing tools hampers functional genomics to explore and elucidate algal molecular pathways with industrial importance. Here, we expanded precision genome modification in seaweeds by successfully demonstrating gene editing with a transgene-free AT-rich-targeting CRISPR-associated protein (Cas) system in U. prolifera. By evaluating various delivery buffers, comparing different Cas systems, and optimizing incubation temperatures, we determined suitable conditions for more widespread applicability of a novel Cas12a-aligned ST8 editor. We obtained >50 ST8-mediated knockout mutants of a toxin-based endogenous marker gene, UpAPT, at 28 °C post-delivery incubations. Our work diversified the applicable genome-editing tools in seaweeds, advancing algal functional genomics and providing more strategies to precisely target unexplored seaweed resources.

DOI： 10.1093/jxb/erag302

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Identification and characterization of a novel Plakoglobin-binding protein highly expressed in the testes Reviewed

Miyu Yamashita, Kotone Teshima, Mizuki Higuchi, Riko Yamada, Shun Sawatsubashi, Atsushi Yokoyama, Ikuo Tomioka, Kei-ichiro Ishiguro, Hiroaki Konishi

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 2026.6

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Language：English Publishing type：Research paper (scientific journal)

DOI： 10.1016/j.bbamcr.2026.120170

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β-Nicotinamide mononucleotide preserves muscle strength in septic male mice Reviewed

Mari Saida, Noritaka Saeki, Hiroshi Sakai, Jun Iwanami, Atsushi Yokoyama, Shun Sawatsubashi, Motoi Kanagawa, Norio Sato, Yuuki Imai

Scientific Reports 16 ( 1 ) 2026.3

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DOI： 10.1038/s41598-026-43172-w

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Other Link： https://www.nature.com/articles/s41598-026-43172-w.pdf
HER2 Interactome Profiling Reveals MARCKS as a Candidate Marker Associated with Aggressive Breast Cancer Reviewed

Atsushi Yokoyama, Shun Sawatsubashi, Akiko Ebata, Yasuhiro Miki, Yuri Otsubo, Takashi Suzuki

Cancers 2025.9

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Authorship：Corresponding author Publishing type：Research paper (scientific journal)

DOI： 10.3390/cancers17172882

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Familial cases with adult-onset FGF23-related hypophosphatemic osteomalacia -A PHEX 3'-UTR change as a possible cause. Reviewed

Sawatsubashi S, Takashi Y, Endo I, Kondo T, Abe M, Matsumoto T, Fukumoto S

Bone 2024.2

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Authorship：Lead author Publishing type：Research paper (scientific journal)

Excessive actions of FGF23 cause several kinds of hypophosphatemic rickets/osteomalacia. It is possible that there still remain unknown causes or mechanisms for FGF23-elated hypophosphatemic diseases. We report two male cousins who had been suffering form FGF23-related hypophosphatemic osteomalacia. Sequencing of exons and exon-intron junctions of known causative genes for FGF23-related hypophosphatemic diseases and whole genome sequencing were conducted. Luciferase assay was used to evaluate the effect of a detected nucleotide change on mRNA stability. Two cousins showed hypophosphatemia with impaired proximal tubular phosphate reabsorption and high FGF23. Serum phosphate of their mothers was within the reference range. Exome sequencing of the proband detected no mutations. Whole genome sequencing of the patients and their mothers identified a nucleotide change in the 3'-UTR of phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX) gene (c.*1280_*1287dupGTGTGTGT) which is heterozygous in the mothers and hemizygous in the patients. While sixteen is the most prevalent number of GT repeats, this family had twenty repeats. Luciferase assay indicated that mRNA with 3'-UTR of PHEX with 20 GT repeats was more unstable than that with 16 repeats. Sequencing of exons and exon-intron junctions of known causative genes for FGF23-related hypophosphatemic diseases cannot identify all the genetic causes. Our results strongly suggest that changes of PHEX expression by a nucleotide change in the 3'-UTR is a novel mechanism of FGF23-related hypophosphatemic osteomalacia.

DOI： 10.1016/j.bone.2024.117057

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Cas12a and MAD7, genome editing tools for breeding Reviewed

Shunya Hozumi, Yi-Chen Chen, Tatsuya Takemoto, Shun Sawatsubashi

Breeding Science 2024

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Authorship：Corresponding author Language：English Publishing type：Research paper (scientific journal)

DOI： 10.1270/jsbbs.23049

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VDR is an essential regulator of hair follicle regression through the progression of cell death. Reviewed International journal

Yudai Joko, Yoko Yamamoto, Shigeaki Kato, Tatsuya Takemoto, Masahiro Abe, Toshio Matsumoto, Seiji Fukumoto, Shun Sawatsubashi

Life science alliance 6 ( 11 ) 2023.11

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Vitamin D receptor (VDR) is essential for hair follicle homeostasis as its deficiency induces hair loss, although the mechanism involved remains unknown. Our research shows that, in Vdr-knockout mice, the hair cycle is halted during the catagen stage, preceding alopecia. In addition, in Vdr-knockout hair follicles, epithelial strands that normally regress during the catagen phase persist as "surviving epithelial strands." Single-cell RNA sequencing analysis suggests that these surviving epithelial strands are formed by cells in the lower part of the hair follicle. These findings emphasize the importance of the regression phase in hair follicle regeneration and establish VDR as a regulator of the catagen stage.

DOI： 10.26508/lsa.202302014

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Osteoblast/osteocyte-derived interleukin-11 regulates osteogenesis and systemic adipogenesis Reviewed International journal

Bingzi Dong, Masahiro Hiasa, Yoshiki Higa, Yukiyo Ohnishi, Itsuro Endo, Takeshi Kondo, Yuichi Takashi, Maria Tsoumpra, Risa Kainuma, Shun Sawatsubashi, Hiroshi Kiyonari, Go Shioi, Hiroshi Sakaue, Tomoki Nakashima, Shigeaki Kato, Masahiro Abe, Seiji Fukumoto, Toshio Matsumoto

Nature Communications 13 ( 1 ) 7194 - 7194 2022.11

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Exercise results in mechanical loading of the bone and stimulates energy expenditure in the adipose tissue. It is therefore likely that the bone secretes factors to communicate with adipose tissue in response to mechanical loading. Interleukin (IL)-11 is known to be expressed in the bone, it is upregulated by mechanical loading, enhances osteogenesis and suppresses adipogenesis. Here, we show that systemic IL-11 deletion (IL-11-/-) results in reduced bone mass, suppressed bone formation response to mechanical loading, enhanced expression of Wnt inhibitors, and suppressed Wnt signaling. At the same time, the enhancement of bone resorption by mechanical unloading was unaffected. Unexpectedly, IL-11-/- mice have increased systemic adiposity and glucose intolerance. Osteoblast/osteocyte-specific IL-11 deletion in osteocalcin-Cre;IL-11fl/fl mice have reduced serum IL-11 levels, blunted bone formation under mechanical loading, and increased systemic adiposity similar to IL-11-/- mice. Adipocyte-specific IL-11 deletion in adiponectin-Cre;IL-11fl/fl did not exhibit any abnormalities. We demonstrate that osteoblast/osteocyte-derived IL-11 controls both osteogenesis and systemic adiposity in response to mechanical loading, an important insight for our understanding of osteoporosis and metabolic syndromes.

DOI： 10.1038/s41467-022-34869-3

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Other Link： https://www.nature.com/articles/s41467-022-34869-3.pdf
IRF2BP2 is a novel HNF4α co-repressor: Its role in gluconeogenic gene regulation via biochemically labile interaction. Reviewed International journal

Takumi Kouketsu, Rina Monma, Yuri Miyairi, Shun Sawatsubashi, Hiroki Shima, Kazuhiko Igarashi, Akira Sugawara, Atsushi Yokoyama

Biochemical and biophysical research communications 615 81 - 87 2022.5

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Hepatocyte nuclear factor 4α (HNF4α) has essential roles in controlling the expression of a variety of genes involved in key metabolic pathways, including gluconeogenesis in the liver. The mechanistic and physiological significance of peroxisome proliferator-activated receptor gamma co-activator-1α (PGC-1α) for HNF4α-mediated transcriptional activation models for gluconeogenic genes is well characterized. However, the transcriptional repression of HNF4α for those genes remains to be examined. In this study, we applied novel proteomic techniques to evaluate the interactions of HNF4α, including those with biochemically labile binding proteins. Based upon our experiments, we identified interferon regulatory factor 2 binding protein 2 (IRF2BP2) as a novel HNF4α co-repressor. This interaction could not be detected by conventional immunoprecipitation. IRF2BP2 repressed the transcriptional activity of HNF4α dependent on its E3 ubiquitin ligase activity. Deficiency of the IRF2BP2 gene in HepG2 cells induced gluconeogenic genes comparable to that of forskolin-treated wild-type HepG2 cells. Together, these results suggest that IRF2BP2 represents a novel class of nuclear receptor co-regulator.

DOI： 10.1016/j.bbrc.2022.04.133

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Identification and Functional Characterization of a Novel Androgen Receptor Coregulator, EAP1. Reviewed International journal

Atsushi Yokoyama, Takumi Kouketsu, Yuri Otsubo, Erika Noro, Shun Sawatsubashi, Hiroki Shima, Ikuro Satoh, Sadafumi Kawamura, Takashi Suzuki, Kazuhiko Igarashi, Akira Sugawara

Journal of the Endocrine Society 5 ( 11 ) bvab150 2021.11

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Language：English Publishing type：Research paper (scientific journal) Publisher：The Endocrine Society

The androgen receptor (AR) plays an essential role in the development of prostate cancer, and androgen-deprivation therapy is used as a first-line treatment for prostate cancer. However, under androgen-deprivation therapy, castration-resistant prostate cancer inevitably arises, suggesting that the interacting transcriptional coregulators of AR are promising targets for developing novel therapeutics. In this study, we used novel proteomic techniques to evaluate the AR interactome, including biochemically labile binding proteins, which might go undetected by conventional purification methods. Using rapid immunoprecipitation mass spectrometry of endogenous proteins, we identified enhanced at puberty 1 (EAP1) as a novel AR coregulator, whereas its interaction with AR could not be detected under standard biochemical conditions. EAP1 enhanced the transcriptional activity of AR via the E3 ubiquitin ligase activity, and its ubiquitination substrate proteins included AR and HDAC1. Furthermore, in prostate cancer specimens, EAP1 expression was significantly correlated with AR expression as well as a poor prognosis of prostate cancer. Together, these results suggest that EAP1 is a novel AR coregulator that promotes AR activity and potentially plays a role in prostate cancer progression.

DOI： 10.1210/jendso/bvab150

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Other Link： http://academic.oup.com/jes/advance-article-pdf/doi/10.1210/jendso/bvab150/40352572/bvab150.pdf
Skeletal FGFR1 signaling is necessary for regulation of serum phosphate level by FGF23 and normal life span. Reviewed International journal

Yuichi Takashi, Shun Sawatsubashi, Itsuro Endo, Yukiyo Ohnishi, Masahiro Abe, Munehide Matsuhisa, Daiji Kawanami, Toshio Matsumoto, Seiji Fukumoto

Biochemistry and biophysics reports 27 101107 - 101107 2021.9

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Fibroblast growth factor (FGF) 23 produced by the bone is the principal hormone to regulate serum phosphate level. Serum FGF23 needs to be tightly regulated to maintain serum phosphate in a narrow range. Thus, we hypothesized that the bone has some phosphate-sensing mechanism to regulate the production of FGF23. Previously we showed that extracellular phosphate induces the phosphorylation of FGF receptor 1 (FGFR1) and FGFR1 signaling regulates the expression of Galnt3, whose product works to increase FGF23 production in vitro. In this study, we show the significance of FGFR1 in the regulated FGF23 production and serum phosphate level in vivo. We generated late-osteoblast/osteocyte-specific Fgfr1-knockout mice (Fgfr1 fl/fl ; Ocn Cre/+ ) by crossing the Ocn-Cre and the floxed Fgfr1 mouse lines. We evaluated serum phosphate and FGF23 levels, the expression of Galnt3 in the bone, the body weight and life span. A selective ablation of Fgfr1 aborted the increase of serum active full-length FGF23 and the enhanced expression of Galnt3 in the bone by a high phosphate diet. These mice showed more pronounced hyperphosphatemia compared with control mice. In addition, these mice fed with a control diet showed body weight loss after 23 weeks of age and shorter life span. These results reveal a novel significance of FGFR1 signaling in the phosphate metabolism and normal life span.

DOI： 10.1016/j.bbrep.2021.101107

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Other Link： https://repo.lib.tokushima-u.ac.jp/116283
Transcriptional Regulation of 25-Hydroxyvitamin D-24-Hydroxylase (CYP24A1) by Calcemic Factors in Keratinocytes. Reviewed

Yoshiaki Kanemoto, Akira Hayakawa, Takahiro Sawada, Rei Amano, Tomohiro Kurokawa, Shun Sawatsubashi, Seiji Fukumoto, Jinichi Mori, Shigeaki Kato

Journal of nutritional science and vitaminology 67 ( 6 ) 424 - 428 2021

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CYP24A1 regulates serum vitamin D (VD) levels by inactivating 25(OH)2D3, which is the precursor of the active form of VD [1α,25(OH)2D3], and CYP24A1 expression is controlled by multiple calcemic factors such as 1α,25(OH)2D3, calcium, and phosphate. A major phosphaturic factor, FGF23, has also been identified as a regulator of serum VD levels by affecting renal CYP24A1 gene expression; however, its effect on CYP24A1 in extrarenal cells remains largely unstudied. Therefore, the direct effect of FGF23 on CYP24A1 was examined in a human keratinocyte cell line (HaCaT). In this cell line, significant induction of CYP24A1 gene expression by 1α,25(OH)2D3 was seen within 4 h by qRT-PCR, and this was mediated by the VD receptor, as shown in a mutant cell line genetically deficient in this receptor. However, FGF23 treatment up to 12 h did not induce CYP24A1 expression, although the expected activation of the downstream MAPK signaling pathway was seen. High calcium and phosphate treatments were also ineffective in inducing CYP24A1 gene expression. Furthermore, a luciferase assay showed no activation of a VD-sensitive proximal CYP24A1 promoter in response to the calcium and phosphate treatments, suggesting that the effect of FGF23 on dermal CYP24A1 gene expression is indirect. From these findings, we speculate that CYP24A1 gene regulation by FGF23 occurs mainly in renal cells, but not in extrarenal cells, at least not in keratinocytes.

DOI： 10.3177/jnsv.67.424

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Mechanisms of osteoprotective actions of estrogens

Shigeaki Kato, Shun Sawatsubashi, Atsushi Yokoyama, Takashi Nakamura, Alexander Kouzmenko

Encyclopedia of Bone Biology 503 - 523 2020.6

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Language：English Publishing type：Part of collection (book) Publisher：Elsevier

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Dystrobrevin alpha gene is a direct target of the vitamin D receptor in muscle. Reviewed International journal

Tsoumpra MK, Sawatsubashi S, Imamura M, Fukumoto S, Takeda S, Matsumoto T, Aoki Y

Journal of molecular endocrinology 64 ( 3 ) 195 - 208 2020.1

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The biologically active metabolite of vitamin D, 1,25-dihydroxyvitamin D3 (VD3), exerts its tissue-specific actions through binding to its intracellular vitamin D receptor (VDR) which functions as a heterodimer with retinoid X receptor (RXR) to recognize vitamin D response elements (VDRE) and activate target genes. Upregulation of VDR in murine skeletal muscle cells occurs concomitantly with transcriptional regulation of key myogenic factors upon VD3 administration, reinforcing the notion that VD3 exerts beneficial effects on muscle. Herein we elucidated the regulatory role of VD3/VDR axis on the expression of dystrobrevin alpha (DTNA), a member of dystrophin-associated protein complex (DAPC). In C2C12 cells, Dtna and VDR gene and protein expression were upregulated by 1-50 nM of VD3 during all stages of myogenic differentiation. In the dystrophic-derived H2K-mdx52 cells, upregulation of DTNA by VD3 occurred upon co-transfection of VDR and RXR expression vectors. Silencing of MyoD1, an E-box binding myogenic transcription factor, did not alter the VD3-mediated Dtna induction, but Vdr silencing abolished this effect. We also demonstrated that VD3 administration enhanced the muscle-specific Dtna promoter activity in presence of VDR/RXR only. Through site-directed mutagenesis and chromatin immunoprecipitation assays, we have validated a VDRE site in Dtna promoter in myogenic cells. We have thus proved that the positive regulation of Dtna by VD3 observed during in vitro murine myogenic differentiation is VDR mediated and specific. The current study reveals a novel mechanism of VDR-mediated regulation for Dtna, which may be positively explored in treatments aiming to stabilize the DAPC in musculoskeletal diseases.

DOI： 10.1530/jme-19-0229

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How do we sense phosphate to regulate serum phosphate level?

Seiji Fukumoto, Yuichi Takashi, Maria K Tsoumpra, Shun Sawatsubashi, Toshio Matsumoto

Journal of bone and mineral metabolism 38 ( 1 ) 1 - 6 2020.1

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Abnormal phosphate levels result in several pathological conditions such as rickets/osteomalacia and ectopic calcification indicating that there must be a system that regulates phosphate level within a narrow range. FGF23 has been shown to be an essential hormone regulating serum phosphate level. FGF23 binds to Klotho-FGF receptor complex to reduce serum phosphate level. Several reports suggested that FGF receptor is involved in the regulation of FGF23 production. It has been also shown that high extracellular phosphate can activate several intracellular signaling pathways. However, it has been unclear whether and how phosphate regulates FGF23 production in vivo. Our recent results indicate that high extracellular phosphate directly activates FGF receptor 1 and the downstream intracellular signaling enhances FGF23 production. Thus, there is a negative feedback system for the regulation of serum phosphate level involving FGF receptor and FGF23. We propose that FGF receptor works at least as one of phosphate sensors in the maintenance of serum phosphate level.

DOI： 10.1007/s00774-019-01066-0

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Activation of unliganded FGF receptor by extracellular phosphate potentiates proteolytic protection of FGF23 by its O-glycosylation. Reviewed International journal

Takashi Y, Kosako H, Sawatsubashi S, Kinoshita Y, Ito N, Tsoumpra MK, Nangaku M, Abe M, Matsuhisa M, Kato S, Matsumoto T, Fukumoto S

Proceedings of the National Academy of Sciences of the United States of America 116 ( 23 ) 11418 - 11427 2019.6

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Language：English Publishing type：Research paper (scientific journal) Publisher：Proceedings of the National Academy of Sciences

Fibroblast growth factor (FGF) 23 produced by bone is a hormone that decreases serum phosphate (Pi). Reflecting its central role in Pi control, serum FGF23 is tightly regulated by serum Pi alterations. FGF23 levels are regulated by the transcriptional event and posttranslational cleavage into inactive fragments before its secretion. For the latter, O-glycosylation of FGF23 by <italic>GALNT3</italic> gene product prevents the cleavage, leading to an increase in serum FGF23. However, the molecular basis of Pi sensing in the regulation of serum FGF23 remains elusive. In this study, we showed that high Pi diet enhanced the skeletal expression of <italic>Galnt3</italic>, but not <italic>Fgf23</italic>, with expected increases in serum FGF23 and Pi in mice. <italic>Galnt3</italic> induction by high Pi was further observed in osteoblastic UMR 106 cells, and this was mediated by activation of the extracellular signal-regulated kinase (ERK) pathway. Through proteomic searches for the upstream sensor for high Pi, we identified one subtype of the FGF receptor (FGFR1c), which was phosphorylated by high Pi in the absence of FGFs. The mode of unliganded FGFR activation by high Pi appeared different from that of FGFR bound to a canonical FGFR ligand (FGF2) when phosphorylation of the FGFR substrate 2α and ERK was monitored. Finally, we showed that an FGFR inhibitor and conditional deletion of <italic>Fgfr1</italic> in osteoblasts/osteocytes abrogated high Pi diet-induced increases in serum FGF23 and femoral <italic>Galnt3</italic> expression in mice. Thus, these findings uncover an unrecognized facet of unliganded FGFR function and illustrate a Pi-sensing pathway involved in regulation of FGF23 production.

DOI： 10.1073/pnas.1815166116

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Other Link： https://syndication.highwire.org/content/doi/10.1073/pnas.1815166116
The Function of the Vitamin D Receptor and a Possible Role of Enhancer RNA in Epigenomic Regulation of Target Genes: Implications for Bone Metabolism. Reviewed International journal

Sawatsubashi S, Nishimura K, Mori J, Kouzmenko A, Kato S

Journal of bone metabolism 26 ( 1 ) 3 - 12 2019.2

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Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

Vitamin D (VD) is essential for bone health, and VD or its analogues are widely used in clinics to ameliorate bone loss. The targets and mode of VD anti-osteoporotic actions appear to be different from those of other classes of drugs modulating bone remodeling. VD exerts its biological activities through the nuclear VD receptor (VDR)-mediated transcriptional regulation of target mRNA and non-coding RNA genes. VD-induced gene regulation involves epigenetic modifications of chromatin conformation at the target loci as well as reconfiguration of higher-order chromosomal organization through VDR-mediated recruitment of various regulatory factors. Enhancer RNAs (eRNA), a class of non-coding enhancer-derived RNAs, have recently emerged as VDR target gene candidates that act through reorganization of chromatin looping to induce enhancer-promoter interaction in activation of mRNA-encoding genes. This review outlines the molecular mechanisms of VD actions mediated by the VDR and suggests novel function of eRNAs in VDR transactivation.

DOI： 10.11005/jbm.2019.26.1.3

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Development of versatile non-homologous end joining-based knock-in module for genome editing Reviewed International journal

Shun Sawatsubashi, Yudai Joko, Seiji Fukumoto, Toshio Matsumoto, Shigeo S. Sugano

Scientific Reports 8 ( 1 ) 593 - 593 2018.12

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Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Nature Publishing Group

DOI： 10.1038/s41598-017-18911-9

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FGF Receptor 1c Works as a Phosphate-Sensor to Regulate FGF23 Production

Shun Sawatsubashi

JOURNAL OF BONE AND MINERAL RESEARCH 2018

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Corepressive Action of CBP on Androgen Receptor Transactivation in Pericentric Heterochromatin in a Drosophila Experimental Model System (vol 29, pg 1017, 2009)

Shun Sawatsubashi

MOLECULAR AND CELLULAR BIOLOGY 2017

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DOI： 10.1128/MCB.00355-17

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[Update on recent progress in vitamin D research. Vitamin D in the treatment of psoriasis.]

Sawatsubashi S

Clinical calcium 27 ( 11 ) 1629 - 1635 2017

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Language：Japanese Publishing type：Research paper (scientific journal)

Active vitamin D and analogs exert immunomodulatory effects and potent effects on cellular differentiation and proliferation in the skin. In the last few decades, it has convincingly been shown that these analogs are effective and safe in the topical treatment of psoriasis, where they nowadays represent a standard therapy. However, the mechanism of vitamin D action in the treatment of psoriasis remains largely unknown. Here, we reviewed and discussed the recent findings of molecular action of vitamin D in psoriasis.

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[Hair follicle stem cells.]

Sawatsubashi S

Clinical calcium 27 ( 6 ) 803 - 808 2017

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Language：Japanese Publishing type：Research paper (scientific journal)

The hair follicle is a complex miniorgan of the skin and undergoes cycles of growth(anagen), apoptosis-mediated regression(catagen)and rest(telogen). Regeneration of the new hair shaft dependent on the activation of hair follicle stem cells(HFSCs), harboured in the bulge region. Using a hair follicle model, some molecular players that control the balance between HFSC maintenance and ageing-associated HFSC dysfunction have been identified. Here, we reviewed and discussed the recent findings of molecular characterization of HFSCs biology and pathology.

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[Bone and Nutrition. The vitamin D functions in osteoblasts and osteocytes].

Sawatsubashi S

Clinical calcium 25 ( 7 ) 991 - 997 2015.7

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[Current Topics on Vitamin D. The vitamin D functions in keratinocytes and its therapeutic applications].

Sawatsubashi S

Clinical calcium 25 ( 3 ) 367 - 371 2015.3

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Coactivation of Estrogen Receptor β by Gonadotropin-Induced Cofactor GIOT-4 (Retraction of vol 29, pg 83, 2009)

Shun Sawatsubashi

MOLECULAR AND CELLULAR BIOLOGY 2014

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DOI： 10.1128/MCB.00021-14

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Activation of facultatively silenced Drosophila loci associates with increased acetylation of histone H2AvD (Retraction of vol 13, pg 1279, 2008)

Shun Sawatsubashi

GENES TO CELLS 2013

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DOI： 10.1111/GTC.12113

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In vivo potentiation of human oestrogen receptor α by Cdk7-mediated phosphorylation (Retraction of vol 9, pg 983, 2004)

Shun Sawatsubashi

GENES TO CELLS 2013

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DOI： 10.1111/GTC.12110

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CDP/Cut Is an Osteoblastic Coactivator of the Vitamin D Receptor (VDR) (Retraction of vol 25, pg 1157, 2010)

Shun Sawatsubashi

JOURNAL OF BONE AND MINERAL RESEARCH 2013

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DOI： 10.1002/JBMR.1832

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Epigenetic Silencing of Core Histone Genes by HERS in Drosophila Reviewed International journal

Saya Ito, Sally Fujiyama-Nakamura, Shuhei Kimura, Jinseon Lim, Yuki Kamoshida, Yumi Shiozaki-Sato, Shun Sawatsubashi, Eriko Suzuki, Masahiko Tanabe, Takashi Ueda, Takuya Murata, Hiromi Kato, Fumiaki Ohtake, Ryoji Fujiki, Tsuneharu Miki, Alexander Kouzmenko, Ken-ichi Takeyama, Shigeaki Kato

MOLECULAR CELL 45 ( 4 ) 494 - 504 2012.2

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DOI： 10.1016/j.molcel.2011.12.029

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Anti-IL-7 receptor-α reverses established type 1 diabetes in nonobese diabetic mice by modulating effector T-cell function (vol 109, pg 12674, 2012)

Shun Sawatsubashi

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2012

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DOI： 10.1073/PNAS.1214896109

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A histone chaperone, DEK, transcriptionally coactivates a nuclear receptor (vol 24, pg 159, 2010)

Shun Sawatsubashi

GENES & DEVELOPMENT 2012

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A histone chaperone, DEK, transcriptionally coactivates a nuclear receptor Reviewed International journal

Shun Sawatsubashi, Takuya Murata, Jinseon Lim, Ryoji Fujiki, Saya Ito, Eriko Suzuki, Masahiko Tanabe, Yue Zhao, Shuhei Kimura, Sally Fujiyama, Takashi Ueda, Daiki Umetsu, Takashi Ito, Ken-ichi Takeyama, Shigeaki Kato

GENES & DEVELOPMENT 24 ( 2 ) 159 - 170 2010.1

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Identification and characterization of a D12 mega size complex

Shun Sawatsubashi

ENDOCRINE JOURNAL 2010

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A novel transcriptional corepressor, SNASH regulates maintenance of neuronal stem cell differentiation

Shun Sawatsubashi

ENDOCRINE JOURNAL 2010

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BTB protein, dKLHL18/CG3571, serves as an adaptor subunit for a dCul3 ubiquitin ligase complex Reviewed International journal

Sally Fujiyama-Nakamura, Saya Ito, Shun Sawatsubashi, Yoshio Yamauchi, Eriko Suzuki, Masahiko Tanabe, Shuhei Kimura, Takuya Murata, Toshiaki Isobe, Ken-ichi Takeyama, Shigeaki Kato

GENES TO CELLS 14 ( 8 ) 965 - 973 2009.8

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DOI： 10.1111/j.1365-2443.2009.01323.x

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Aberrant E2F activation by polyglutamine expansion of androgen receptor in SBMA neurotoxicity Reviewed International journal

Eriko Suzuki, Yue Zhao, Saya Ito, Shun Sawatsubashi, Takuya Murata, Takashi Furutani, Yuko Shirode, Kaoru Yamagata, Masahiko Tanabe, Shuhei Kimura, Takashi Ueda, Sally Fujiyama, Jinseon Lim, Hiroyuki Matsukawa, Alexander P. Kouzmenko, Toshiro Aigaki, Tetsuya Tabata, Ken-ichi Takeyama, Shigeaki Kato

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 106 ( 10 ) 3818 - 3822 2009.3

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DOI： 10.1073/pnas.0809819106

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Corepressive Action of CBP on Androgen Receptor Transactivation in Pericentric Heterochromatin in a Drosophila Experimental Model System Reviewed International journal

Yue Zhao, Ken-ichi Takeyama, Shun Sawatsubashi, Saya Ito, Eriko Suzuki, Kaoru Yamagata, Masahiko Tanabe, Shuhei Kimura, Sally Fujiyama, Takashi Ueda, Takuya Murata, Hiroyuki Matsukawa, Yuko Shirode, Alexander P. Kouzmenko, Feng Li, Testuya Tabata, Shigeaki Kato

MOLECULAR AND CELLULAR BIOLOGY 29 ( 4 ) 1017 - 1034 2009.2

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DOI： 10.1128/MCB.02123-07

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RNA-binding protein hoip accelerates polyQ-induced neurodegeneration in Drosophila Reviewed International journal

Takuya Murata, Eriko Suzuki, Saya Ito, Shun Sawatsubashi, Yue Zhao, Kaoru Yamagata, Masahiko Tanabe, Sally Fujiyama, Shuhei Kimura, Takashi Ueda, Hiroyuki Matsukawa, Alexander Kouzmenko, Takashi Furutani, Erina Kuranaga, Masayuki Miura, Ken-ichi Takeyama, Shigeaki Kato

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY 72 ( 9 ) 2255 - 2261 2008.9

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DOI： 10.1271/bbb.70829

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Drosophila arginine methyltransferase 1 (DART1) is an ecdysone receptor co-repressor Reviewed International journal

Shuhei Kimura, Shun Sawatsubashi, Saya Ito, Alexander Kouzmenko, Eriko Suzuki, Yue Zhao, Kaoru Yamagata, Masahiko Tanabe, Takashi Ueda, Sari Fujiyama, Takuya Murata, Hiroyuki Matsukawa, Ken-ichi Takeyama, Nobuo Yaegashi, Shigeaki Kato

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 371 ( 4 ) 889 - 893 2008.7

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DOI： 10.1016/j.bbrc.2008.05.003

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A TFTC/STAGA module mediates histone H2A and H2B deubiquitination, coactivates nuclear receptors, and counteracts heterochromatin silencing Reviewed International journal

Yue Zhao, Guillaume Lang, Saya Ito, Jacques Bonnet, Eric Metzger, Shun Sawatsubashi, Eriko Suzuki, Xavier Le Guezennec, Hendrilk G. Stunnenberg, Aleksey Krasnov, Sofia G. Georgieva, Roland Schuele, Ken-Ichi Takeyama, Shigeaki Kato, Laszlo Tora, Didier Devys

MOLECULAR CELL 29 ( 1 ) 92 - 101 2008.1

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DOI： 10.1016/j.moicel.2007.12.011

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The novel functions of the TFTC/STAGA HAT complex in histone deubiquitination dependent chromatin remodelling and transcription activation

Shun Sawatsubashi

FEBS JOURNAL 2008

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Identification of osteoblast-specific co-regulator complex for vitamin D receptor (VDR)

Shun Sawatsubashi

JOURNAL OF BONE AND MINERAL RESEARCH 2007

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Identification of osteoblast-specific co-regulator complex for vitamin D receptor (VDR).

Shun Sawatsubashi

JOURNAL OF BONE AND MINERAL RESEARCH 2006

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Wnt/beta-catenin and estrogen signaling converge in vivo Reviewed International journal

AP Kouzmenko, K Takeyama, S Ito, T Furutani, S Sawatsubashi, A Maki, E Suzuki, Y Kawasaki, T Akiyama, T Tabata, S Kato

JOURNAL OF BIOLOGICAL CHEMISTRY 279 ( 39 ) 40255 - 40258 2004.9

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DOI： 10.1074/jbc.C400331200

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Ecdysone receptor-dependent gene regulation mediates histone poly(ADP-ribosyl)ation Reviewed International journal

S Sawatsubashi, A Maki, S Ito, Y Shirode, E Suzuki, Y Zhao, K Yamagata, A Kouzmenko, K Takeyama, S Kato

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 320 ( 1 ) 268 - 272 2004.7

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DOI： 10.1016/j.bbrc.2004.05.157

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Juvenile hormones antagonize ecdysone actions through co-repressor recruitment to EcR/USP heterodimers Reviewed International journal

A Maki, S Sawatsubashi, S Ito, Y Shirode, E Suzuki, Y Zhao, K Yamagata, A Kouzmenko, K Takeyama, S Kato

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 320 ( 1 ) 262 - 267 2004.7

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DOI： 10.1016/j.bbrc.2004.05.156

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A novel genetic system for analysis of co-activators for the N-terminal transactivation function domain of the human androgen receptor Reviewed International journal

K Takeyama, S Ito, S Sawatsubashi, Y Shirode, A Yamamoto, E Suzuki, A Maki, K Yamagata, Y Zhao, A Kouzmenko, T Tabata, S Kato

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY 68 ( 6 ) 1209 - 1215 2004.6

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DOI： 10.1271/bbb.68.1209

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Endocrine disrupting chemicals: interference of thyroid hormone binding to transthyretins and to thyroid hormone receptors Reviewed International journal

A Ishihara, S Sawatsubashi, K Yamauchi

MOLECULAR AND CELLULAR ENDOCRINOLOGY 199 ( 1-2 ) 105 - 117 2003.1

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DOI： 10.1016/s0303-7207(02)00302-7

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Organization and expression of the Paramecium caudatum gene encoding nucleosome assembly protein 1 Reviewed

N Nishiyama, S Sawatsubashi, M Ishida, K Yamauchi

GENE 280 ( 1-2 ) 107 - 114 2001.12

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DOI： 10.1016/s0378-1119(01)00778-8

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臨床基礎研究につながる分子生物学

加藤, 茂明

クリニコ出版 2024.4 （ ISBN:9784910396408 ）

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Total pages：366p Language：Japanese

CiNii Books

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ビタミン・バイオファクター総合事典

日本ビタミン学会, 竹谷, 豊, 生城, 浩子, 池田, 彩子, 石川, 孝博, 太田, 好次, 小暮, 健太朗, 瀧谷, 公隆, 田中, 清, 津川, 尚子, 内藤, 裕二, 野坂, 和人, 福渡, 努

朝倉書店 2021.7 （ ISBN:9784254102925 ）

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MISC

おらが町の酵母はどんな味? 徳島発アザレアエールの挑戦

2026

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DOI： 10.34565/seibutsukogaku.104.3_1

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Mediator Bodyによる遺伝子発現制御機構の解明

鈴木秀文, 阿部竜太, 沢津橋俊, 池陽子, 古郡華月, 安井七海, 小川真太郎, 豊田敦, 鈴木穣, 井野洋子, 木村弥生, 堀内恵子, 秋山智彦, 廣瀬智威, 高橋秀尚

日本分子生物学会年会プログラム・要旨集(Web) 47th 2024

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PHEX遺伝子3’-UTR変異による家族性成人発症FGF23関連低リン血症性骨軟化症

沢津橋俊, 高士祐一, 遠藤逸朗, 近藤剛史, 安倍正博, 松本俊夫, 福本誠二

日本骨代謝学会学術集会プログラム抄録集(CD-ROM) 42nd 2024

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Development of genome editing technology in industrial Yeast using genome editing factor ST8

沢津橋俊, 中島俊雄, 藤田(竹下)結衣, 穂積俊矢

日本農芸化学会大会講演要旨集(Web) 2024 2024

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転写共役因子の天然変性領域(IDR)を介した光誘導性相互作用解析法の確立

沢津橋俊, 西村耕一

日本生化学会大会プログラム・講演要旨集 96回 [1T12a - 415)] 2023.10

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VDRは細胞死を介した毛周期の進行に不可欠な制御因子である

沢津橋俊, 上甲裕大, 松本俊夫, 福本誠二

日本内分泌学会雑誌 99 ( 3 ) 720 - 720 2023.7

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カルシウム代謝調整因子群によるCYP24A1転写制御

加藤茂明, 金本義明, 早川哲, 澤田崇広, 沢津橋俊, 福本誠二, 森甚一

ビタミン 96 ( 8 ) 376 - 377 2022.8

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2022&ichushi_jid=J01262&link_issn=&doc_id=20220825160009&doc_link_id=10.20632%2Fvso.96.8_376&url=https%3A%2F%2Fdoi.org%2F10.20632%2Fvso.96.8_376&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif
カルシウム代謝調整因子群によるCYP24A1転写制御

加藤茂明, 金本義明, 早川哲, 澤田崇広, 沢津橋俊, 福本誠二, 森甚一

ビタミン 96 ( 8 ) 376 - 377 2022.8

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新規ヒトビタミンD標的non-coding RNA遺伝子群の同定

金本義明, 西村耕一, 澤田崇広, 早川哲, 黒川友博, 沢津橋俊, 森甚一, 加藤茂明

日本骨代謝学会学術集会プログラム抄録集 40回 152 - 152 2022.7

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ヒト疾患型点変異を導入したビタミンD依存性くる病/骨軟化症モデルマウスの機能解析

沢津橋俊, 池戸葵, 松本俊夫, 今井祐記, 福本誠二

日本骨代謝学会学術集会プログラム抄録集 40回 119 - 119 2022.7

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カルシウム代謝調整因子群によるCYP24A1転写制御

金本義明, 沢津橋俊, 福本誠二, 加藤茂明

日本骨代謝学会学術集会プログラム抄録集 40回 119 - 119 2022.7

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骨のリンセンサー分子FGFR1による高リン血症発症防御は生存率を向上させる

高士祐一, 沢津橋俊, 小迫英尊, 大西幸代, 遠藤逸朗, 田邉真紀人, 安倍正博, 松久宗英, 松本俊夫, 福本誠二, 川浪大治

日本体質医学会雑誌 84 ( 2 ) 134 - 135 2022.6

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新規ヒトビタミンD標的non-coding RNA遺伝子群の同定

金本義明, 西村耕一, 澤田崇広, 早川哲, 黒川友博, 沢津橋俊, 森甚一, 加藤茂明

日本栄養・食糧学会大会講演要旨集 76回 251 - 251 2022.5

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カルシウム代謝調整因子群によるCYP24A1転写制御

金本義明, 早川哲, 澤田崇広, 沢津橋俊, 福本誠二, 森甚一, 加藤茂明

日本栄養・食糧学会大会講演要旨集 76回 251 - 251 2022.5

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アンドロゲン受容体新規転写共役因子の探索

横山敦, 纐纈拓海, 尾坪優李, 沢津橋俊, 島弘季, 佐藤郁郎, 川村貞文, 鈴木貴, 五十嵐和彦, 菅原明

日本アンドロロジー学会総会記事 41st 2022

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核内受容体新規転写共役因子の探索

横山敦, 纐纈拓海, 尾坪優李, 沢津橋俊, 島弘季, 佐藤郁郎, 川村貞文, 鈴木貴, 五十嵐和彦, 菅原明

日本アンドロロジー学会総会記事 41st 2022

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疾患モデル動物の多品種生産・大量生産のための自動装置の開発

平岡忠志, 森本巌, 平野研, 竹本龍也, 竹澤慎一郎, 沢津橋俊

徳島県立工業技術センター業務報告 2020 2022

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ヒストンシャペロンDEKによる核内構造体形成メカニズムの解明

沢津橋俊, 西村耕一, 松本俊夫, 福本誠二

日本生化学会大会プログラム・講演要旨集 94回 [P - 554] 2021.11

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骨のFGFR1によるリン濃度感知、高リン血症発症防御は生存率を向上させる

高士祐一, 大西幸代, 遠藤逸朗, 沢津橋俊, 田邉真紀人, 安倍正博, 川浪大治, 松本俊夫, 福本誠二

日本骨代謝学会学術集会プログラム抄録集 39回 154 - 154 2021.10

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骨のリンセンサー分子FGFR1による高リン血症発症防御は生存率を向上させる

高士祐一, 沢津橋俊, 小迫英尊, 大西幸代, 遠藤逸朗, 田邉真紀人, 安倍正博, 松久宗英, 松本俊夫, 福本誠二, 川浪大治

日本体質医学会雑誌 83 ( 3 ) 175 - 175 2021.8

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新規ビタミンD標的non-coding RNA遺伝子群の同定

金本義明, 西村耕一, 澤田崇広, 早川哲, 黒川友博, 沢津橋俊, 森甚一, 加藤茂明

日本栄養・食糧学会大会講演要旨集 75回 ( 4 ) 94 - 94 2021.7

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新規ビタミンD標的non-coding RNA遺伝子群の同定

金本義明, 西村耕一, 澤田崇広, 早川哲, 黒川友博, 沢津橋俊, 森甚一, 加藤茂明

日本栄養・食糧学会大会講演要旨集 75回 ( 4 ) 94 - 94 2021.7

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核内ビタミンD受容体による転写制御に関与するスーパーエンハンサー領域の役割と機能解析

早川哲, 金本義明, 森甚一, 澤田崇広, 馬場泰輔, 古谷駿治, 天野伶, 沢津橋俊, 加藤茂明

ビタミン 95 ( 4 ) 211 - 211 2021.4

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栄養代謝状態が調節するグルココルチコイド受容体の転写制御機構の解明

沢津橋俊, 貝沼梨沙, 松本俊夫, 福本誠二

日本内分泌学会雑誌 97 ( 1 ) 271 - 271 2021.4

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SWI/SNF複合体のIDRによる相分離を介した核内受容体AF-1領域との相互作用解析

西村耕一, 西村耕一, 沢津橋俊, 松本俊夫, 福本誠二

日本生化学会大会(Web) 94th 2021

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骨特異的FGFR1欠失マウスを用いたリン感知分子としてのFGFR1の解析

高士祐一, 沢津橋俊, 遠藤逸朗, 安倍正博, 松久宗英, 田邉真紀人, 川浪大治, 松本俊夫, 福本誠二

日本骨代謝学会学術集会プログラム抄録集 38回 152 - 152 2020.10

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表皮・毛包の恒常性におけるビタミンD受容体の機能解析

沢津橋俊, 松本俊夫, 福本誠二

日本骨代謝学会学術集会プログラム抄録集 38回 140 - 140 2020.10

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栄養情報が調節するグルココルチコイド受容体の転写制御機構の解析

沢津橋俊, 松本俊夫, 福本誠二

日本内分泌学会雑誌 96 ( 1 ) 238 - 238 2020.8

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核内ビタミンD受容体による転写制御における新規enhancer RNAの同定と機能解析

早川哲, 西村耕一, 森甚一, 沢津橋俊, 山形薫, 田中良哉, 松本俊夫, 加藤茂明

日本栄養・食糧学会大会講演要旨集 74回 251 - 251 2020.4

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ゲノム編集を利用したくる病型点変異導入ビタミンD受容体の機能解析

沢津橋俊, 横山敦, 上甲裕大, 松本俊夫, 福本誠二

日本生化学会大会プログラム・講演要旨集 92回 [2T07a - 04] 2019.9

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FGFR1は血中FGF23濃度を制御するリン感知受容体である

高士祐一, 沢津橋俊, 遠藤逸朗, 安倍正博, 松久宗英, 松本俊夫, 福本誠二

日本骨代謝学会学術集会プログラム抄録集 37回 207 - 207 2019.9

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クローズアップ実験法(series 312) 培養細胞における簡便なノックインを可能とするゲノム編集法 VIKING法

沢津橋俊, 上甲裕大, 菅野茂夫

実験医学 37 ( 11 ) 1825 - 1831 2019.7

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皮膚における非リガンド結合型VDRの機能

加藤茂明, 上甲裕大, 福本誠二, 松本俊夫, 沢津橋俊

ビタミン 93 ( 5-6 ) 264 - 264 2019.6

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FGFR1はFGF23濃度調節を媒介するリン感知受容体である

高士祐一, 小迫英尊, 沢津橋俊, 木下祐加, 伊東伸朗, 安倍正博, 松久宗英, 加藤茂明, 松本俊夫, 福本誠二

日本内分泌学会雑誌 95 ( 1 ) 333 - 333 2019.4

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核内ビタミンD受容体による転写制御における新規enhancer RNAの同定と機能解析

西村耕一, 森甚一, 沢津橋俊, 山形薫, 田中良哉, 松本俊夫, 加藤茂明

ビタミン 93 ( 4 ) 206 - 206 2019.4

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FGFR1はFGF23濃度を制御する骨におけるリン感知分子である

高士祐一, 木下祐加, 伊東伸朗, 沢津橋俊, 小迫英尊, 松久宗英, 松本俊夫, 福本誠二

日本骨代謝学会学術集会プログラム抄録集 36回 153 - 153 2018.7

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核内ビタミンD受容体による転写制御における新規enhancer RNAの同定と機能解析

西村耕一, 森甚一, 沢津橋俊, 山形薫, 田中良哉, 松本俊夫, 加藤茂明

ビタミン 92 ( 7 ) 327 - 328 2018.7

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核内ビタミンD受容体による転写制御における新規enhancer RNAの同定と機能解析

西村耕一, 森甚一, 沢津橋俊, 山形薫, 田中良哉, 松本俊夫, 加藤茂明

ビタミン 92 ( 7 ) 327 - 328 2018.7

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ビタミンD受容体による毛周期制御機構の解明

沢津橋俊, 上甲裕大, 松本俊夫, 福本誠二

日本内分泌学会雑誌 94 ( 1 ) 395 - 395 2018.4

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骨の血中リン濃度感知によるリン代謝恒常性維持機構の解明

高士祐一, 木下祐加, 伊東伸朗, Tsoumpra Maria, 沢津橋俊, 松久宗英, 松本俊夫, 福本誠二

日本内分泌学会雑誌 94 ( 1 ) 291 - 291 2018.4

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核内ビタミンD受容体による転写制御における新規enhancer RNAの同定と機能解析

西村耕一, 森甚一, 沢津橋俊, 山形薫, 田中良哉, 松本俊夫, 加藤茂明

ビタミン 92 ( 4 ) 224 - 224 2018.4

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骨の血中リン濃度感知によるリン代謝恒常性維持機構の解明

高士祐一, 木下祐加, 伊東伸朗, Tsoumpra Maria, 沢津橋俊, 松久宗英, 松本俊夫, 福本誠二

日本内分泌学会雑誌 94 ( 1 ) 291 - 291 2018.4

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ビタミンD受容体による毛周期制御機構の解明

沢津橋俊, 上甲裕大, 松本俊夫, 福本誠二

日本内分泌学会雑誌 94 ( 1 ) 395 - 395 2018.4

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ビタミンD受容体は表皮と毛包の恒常性に必須である

上甲裕大, 沢津橋俊, 山本陽子, 竹本龍也, 福本誠二, 松本俊夫

日本分子生物学会年会プログラム・要旨集(Web) 41st 2018

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VIKING法によるノックアウト/ノックイン細胞を用いた比較プロテオーム解析によるビタミンD受容体複合体の探索

沢津橋俊, 横山敦, 上甲裕大, 菅野茂夫, 菅野茂夫, 松本俊夫, 福本誠二

日本分子生物学会年会プログラム・要旨集(Web) 41st 2018

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ビタミンD受容体は毛周期の成長期から退縮期への移行を制御する

上甲裕大, 沢津橋俊, 山本陽子, 福本誠二, 松本俊夫

生命科学系学会合同年次大会 2017年度 [2P - 0621] 2017.12

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ビタミンD受容体は毛周期の成長期から退縮期への移行を制御する

上甲裕大, 沢津橋俊, 山本陽子, 福本誠二, 松本俊夫

生命科学系学会合同年次大会 2017年度 [2P - 0621] 2017.12

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核内受容体が制御する多彩な生命現象表皮特異的ビタミンD受容体ノックアウトマウスから理解する正常な表皮・毛包維持機構の解明

沢津橋俊, 上甲裕大, 山本陽子, 福本誠二, 松本俊夫

生命科学系学会合同年次大会 2017年度 [2AW03 - 1] 2017.12

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Muscle-Specific Vitamin D Receptor (VDR) Ablation Results in Reduced Grip Power and Altered Gene Expression Pattern in Mice. Reviewed

Maria Tsoumpra, Itsuro Endo, Shun Sawatsubashi, Yuichi Takashi, Seiji Fukumoto, Toshio Matsumoto

JOURNAL OF BONE AND MINERAL RESEARCH 32 S216 - S216 2017.12

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【ビタミンD Update】ビタミンDによる皮膚疾患治療

沢津橋俊

Clinical Calcium 27 ( 11 ) 1629 - 1635 2017.10

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骨におけるリンのシグナル伝達経路とFGF23の活性調節機構

高士祐一, 木下祐加, 伊東伸朗, ツンプラ・マリア, 沢津橋俊, 松本俊夫, 福本誠二

日本骨代謝学会学術集会プログラム抄録集 35回 185 - 185 2017.7

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骨格筋の代謝と全身性代謝の関わり筋特異的ビタミンD受容体除去はマウスにおけるビグリカン発現に変化をもたらす(Muscle-Specific Vitamin D Receptor(VDR) Ablation Results in Altered Biglycan Expression in Mice)

ツオウムプラ・マリア, 遠藤逸朗, 沢津橋俊, 高士祐一, 福本誠二, 松本俊夫

日本筋学会学術集会プログラム・抄録集 3回 60 - 60 2017.7

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骨格筋の代謝と全身性代謝の関わり筋特異的ビタミンD受容体除去はマウスにおけるビグリカン発現に変化をもたらす(Muscle-Specific Vitamin D Receptor(VDR) Ablation Results in Altered Biglycan Expression in Mice)

ツオウムプラ・マリア, 遠藤逸朗, 沢津橋俊, 高士祐一, 福本誠二, 松本俊夫

日本筋学会学術集会プログラム・抄録集 3回 60 - 60 2017.7

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【幹細胞システム】毛包幹細胞システム

沢津橋俊

Clinical Calcium 27 ( 6 ) 803 - 808 2017.5

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FGF23活性調節を担うGALNT3遺伝子の転写因子

高士祐一, 木下祐加, 伊東伸朗, Tsoumpra Maria K, 沢津橋俊, 松本俊夫, 福本誠二

日本内分泌学会雑誌 93 ( 1 ) 294 - 294 2017.4

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FGF23はERK-Egr-1経路を介したKlotho依存性経路によりCYP24A1転写を増強する(FGF23 enhances CYP24A1 transcription in Klotho-dependent way via ERK-Egr-1 pathway)

ツオウムプラ・マリア, 沢津橋俊, 高士祐一, 松本俊夫, 福本誠二

日本内分泌学会雑誌 93 ( 1 ) 295 - 295 2017.4

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リンによるFGF23の活性調節機構

高士祐一, 木下祐加, 伊東伸朗, ツォウムプラ・マリア, 沢津橋俊, 松本俊夫, 福本誠二

日本骨代謝学会学術集会プログラム抄録集 34回 181 - 181 2016.7

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GALNT3を介した翻訳後修飾によるリンに対するFGF23活性調節機構

高士祐一, 木下祐加, 堀倫子, 伊東伸朗, 田口学, 沢津橋俊, 松本俊夫, 福本誠二

日本内分泌学会雑誌 92 ( 1 ) 247 - 247 2016.4

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皮膚におけるビタミンD受容体の高次機能解析

沢津橋俊, 山本陽子, 福本誠二, 松本俊夫

日本内分泌学会雑誌 92 ( 1 ) 224 - 224 2016.4

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表皮特異的ビタミンD受容体ノックアウトマウスから理解する正常な表皮・毛包維持機構に関する研究

沢津橋俊, 上甲裕大, 福本誠二, 松本俊夫

日本分子生物学会年会プログラム・要旨集(Web) 39th 2016

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「FGF23の活性調節機構の検討」

高士祐一, 木下祐加, 堀倫子, 伊東伸朗, 田口学, 沢津橋俊, 松本俊夫, 福本誠二

日本腎性骨症研究会プログラム抄録集 2016 2016

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【骨と栄養】ビタミンD代謝と骨

沢津橋俊

Clinical Calcium 25 ( 7 ) 991 - 997 2015.6

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【ビタミンDをめぐる最近の話題】ビタミンDの皮膚細胞への作用と治療への応用

沢津橋俊

Clinical Calcium 25 ( 3 ) 367 - 371 2015.2

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DOI： 10.20837/4201503367

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O-GlcNAc転移酵素(OGT)によるグルココルチコイドレセプター(GR)の転写制御機構の解析

沢津橋俊, 松本俊夫

日本生化学会大会プログラム・講演要旨集 87回 [3T14p - 01] 2014.10

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多糸染色体から理解するクロマチン構造調節を介したゲノムデコード-新規ヒストンシャペロンDrosophila DEKによるエクダイソン受容体転写機構の解明-

沢津橋俊, 武山健一, 加藤茂明

日本農芸化学会大会講演要旨集(Web) 2012 2012

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クロマチン構造調節を担う新規メゾスケール複合体の解析

藤山(中村)沙理, 沢津橋俊, 伊藤(上田)紗弥, 鈴木(松浦)絵里子, 木村周平, 武山健一, 加藤茂明

日本農芸化学会大会講演要旨集(Web) 2012 2012

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活性型クロマチン構造調節に関わる新規クロマチン構造調節因子の探索及び機能解析

林珍仙, 沢津橋俊, 伊藤紗弥, 藤山沙理, 鈴木絵里子, 田辺真彦, 木村周平, 上田崇, 村田拓哉, 加藤裕美, 汐崎裕美, 武山健一, 加藤茂明

日本生化学会大会プログラム・講演要旨集 84回 4P - 0401 2011.9

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核内巨大分子量複合体を介したクロマチン構造調節機構の解明

中村(藤山)沙理, 伊藤紗弥, 沢津橋俊, 鈴木絵里子, 田辺真彦, 木村周平, 村田拓哉, 上田崇, 林珍仙, 加藤裕美, 武山健一, 加藤茂明

日本農芸化学会大会講演要旨集 2011 2011

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HOTALを介した細胞周期依存的なヒストン遺伝子発現抑制機構の解明

伊藤紗弥, 藤山沙理, 沢津橋俊, 鈴木絵里子, 田辺真彦, 木村周平, 上田崇, 村田拓哉, 林珍仙, 汐崎裕美, 加藤裕美, 武山健一, 加藤茂明

日本農芸化学会大会講演要旨集 2011 2011

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核内受容体研究の最先端クロマチン構造調節を介した核内受容体の転写制御機構の解析

武山健一, 沢津橋俊, 林珍仙, 伊藤紗弥, 田辺真彦, 村田拓哉, 木村周平, 上田崇, 加藤裕美, 汐崎裕美, 藤山沙理, 伊藤敬, 加藤茂明

日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 83回・33回 3W9 - 1 2010.12

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新規ヒストンシャペロンDEKによる核内受容体転写共役機能の解明(A Histone chaperone, DEK, transcriptionally coactivating a nuclear receptor: a functional link to leukemia)

沢津橋俊, 村田拓哉, 林珍仙, 藤木亮次, 伊藤紗弥, 鈴木絵里子, 田辺真彦, 木村周平, 藤山沙理, 上田崇, 伊藤敬, 武山健一, 加藤茂明

日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 83回・33回 2P - 0602 2010.12

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Identification of a novel factor required for spermatogenesis by an in vivo tesits luciferase assay (t-Luc) screen Reviewed

Shuhei Kimura, Saya Ito, Shun Sawatsubashi, Eriko Suzuki, Masahiko Tanabe, Takashi Ueda, Takuya Murata, Sally Fujiyama, Hiroyuki Matsukawa, Jinseon Lim, Ken-ichi Takeyama, Shigeaki Kato

ENDOCRINE JOURNAL 57 S614 - S614 2010.3

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Web of Science

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dBAHD1を介した細胞周期依存的なヒストン遺伝子発現制御機構の解明

伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, 鈴木絵里子, 田辺真彦, 田辺真彦, 木村周平, 上田崇, 藤山沙理, 藤山沙理, 村田拓哉, 松川紘之, 林珍仙, 武山健一, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2010 2010

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DEKはヒストンシャペロンとして機能する新規転写活性化共役因子である

沢津橋俊, 沢津橋俊, 村田拓哉, 林珍仙, 伊藤紗弥, 伊藤紗弥, 鈴木絵里子, 鈴木絵里子, 藤山沙理, 藤山沙理, 田辺真彦, 田辺真彦, 木村周平, 上田崇, 武山健一, 伊藤敬, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2010 2010

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遺伝学的アプローチとプロテオミクスを連携した新規活性化クロマチン構造調節因子D12の複合体解析

中村沙理, 中村沙理, 伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, 鈴木絵里子, 田辺真彦, 田辺真彦, 木村周平, 上田崇, 村田拓哉, 松川紘之, 林珍仙, 武山健一, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2010 2010

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新規クロマチンバウンダリー調節因子の遺伝学的探索

鈴木絵里子, 鈴木絵里子, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 伊藤紗弥, 藤山沙里, 藤山沙里, 田辺真彦, 田辺真彦, 木村周平, 上田崇, 村田拓哉, 林珍仙, 武山健一, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2010 2010

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Chromatin modification of Ecdyson dependent puff formation in Drosophila

LIM Jinseon, 沢津橋俊, 伊藤紗弥, 鈴木絵里子, 木村周平, 田辺真彦, 上田崇, 藤山沙里, 村田拓哉, 加藤裕美, 汐崎裕美, 武山健一, 加藤茂明

生化学 2010

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活性型クロマチン構造調節に関わるエクダイソンレセプターの転写共役因子の探索及び機能解析

林珍仙, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 伊藤紗弥, 鈴木絵里子, 鈴木絵里子, 田辺真彦, 田辺真彦, 木村周平, 上田崇, 藤山沙里, 藤山沙里, 村田拓哉, 松川紘之, 加藤裕美, 汐崎裕美, 武山健一, 加藤茂明

日本農芸化学会大会講演要旨集 2010 2010

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Notchシグナルを調節する細胞分化制御機構の解析

武山健一, 伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, 鈴木絵里子, 田辺真彦, 田辺真彦, 木村周平, 上田崇, 村田拓哉, 松川紘之, 林珍仙, 藤山沙理, 藤山沙理, 大竹史明, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2010 2010

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アンドロゲン受容体新規転写共役抑制因子を介したアンドロゲン依存性癌の分子機構の解析

上田崇, 伊藤紗弥, 沢津橋俊, 鈴木絵里子, 山形薫, 藤山沙理, 田辺真彦, 木村周平, 林珍仙, 村田拓哉, 松川紘之, 武山健一, 加藤茂明

日本内分泌学会雑誌 85 ( 1 ) 320 - 320 2009.4

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カイコ・ホルモンレセプターに対するBmHSP90コシャペロンの機能解析

山下隼, 門宏明, 光延仁志, 沢津橋俊, 加藤茂明, LEE J.Man, 河口豊, 日下部宣宏

日本分子生物学会年会講演要旨集 32nd ( Vol.3 ) 2009

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活性型クロマチン構造調節に関わる新規転写共役因子の探索の試み

林珍仙, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 伊藤紗弥, 山形薫, 山形薫, 鈴木絵里子, 鈴木絵里子, 田辺真彦, 木村周平, 上田崇, 藤山沙里, 藤山沙里, 村田拓哉, 松川紘之, 武山健一, 加藤茂明

日本農芸化学会大会講演要旨集 2009 2009

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新規クロマチンバウンダリー調節因子の探索とその解析

鈴木絵里子, 鈴木絵里子, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 伊藤紗弥, 山形薫, 山形薫, 田辺真彦, 木村周平, 藤山沙理, 藤山沙理, 上田崇, 村田拓哉, 松川紘之, 林珍仙, 武山健一, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2009 2009

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新規クロマチン構造調節因子BAHD1を介した転写抑制機構の解析

伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, 鈴木絵里子, 山形薫, 山形薫, 田辺真彦, 木村周平, 上田崇, 藤山沙理, 藤山沙理, 村田拓哉, 松川紘之, 林珍仙, 武山健一, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2009 2009

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BTBタンパク質dKLHL18/CG3571はE3ユビキチンリガーゼCul-3複合体のアダプターとして機能する

中村沙理, 中村沙理, 伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, 鈴木絵里子, 田辺真彦, 村田拓哉, 武山健一, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2009 2009

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核輸送制御とクロマチン構造調節の相互作用を担う新規因子の探索

村田拓哉, 伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, 鈴木絵里子, 田辺真彦, 田辺真彦, 藤山沙理, 藤山沙理, 木村周平, 上田崇, 松川紘之, LIM Jinseon, 武山健一, 加藤茂明, 加藤茂明

日本分子生物学会年会講演要旨集 32nd ( Vol.3 ) 2009

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新規クロマチン構造調節因子を介した転写抑制機構の解析

伊藤紗弥, 沢津橋俊, 山形薫, 鈴木絵里子, 趙越, 田辺真彦, 木村周平, 上田崇, 藤山沙理, 村田拓哉, 松川紘之, 武山健一, 加藤茂明

日本農芸化学会大会講演要旨集 2008 2008

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分子遺伝学とプロテオミクスのアプローチによる新規BTB/POZタンパク質群の網羅的機能解析

藤山沙理, 藤山沙理, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 伊藤紗弥, 木村周平, 村田拓哉, 鈴木絵里子, 田辺真彦, 趙越, 上田崇, 松川紘之, 山形薫, 山形薫, 武山健一, 加藤茂明

日本農芸化学会大会講演要旨集 2008 2008

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新規クロマチン構造調節因子BAHD1を介した転写抑制機構の解明

伊藤紗弥, 沢津橋俊, 鈴木絵里子, 伊藤紗弥, 沢津橋俊, 鈴木絵里子, ZHAO Yue, 山形薫, 山形薫, 田辺真彦, 木村周平, 上田崇, 藤山沙理, 藤山沙理, 村田拓哉, 松川紘之, LIM Jinseon, 武山健一, 加藤茂明, 加藤茂明

生化学 2008

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ショウジョウバエ分子遺伝学とプロテオミクス解析による新規転写共役抑制因子Z4の解析

村田拓哉, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 伊藤紗弥, 鈴木絵里子, 山形薫, 山形薫, 趙越, 田辺真彦, 藤山沙理, 藤山沙理, 木村周平, 上田崇, 松川紘之, 武山健一, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2008 2008

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カイコシャペロン過剰発現のもたらすターゲットタンパク質への影響

山下隼, 山下隼, 宮川世志幸, 門宏明, 光延仁志, 光延仁志, 久保雄二, 沢津橋俊, 加藤茂明, LEE Jaeman, 河口豊, 日下部宜宏

生化学 2008

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アンドロゲン受容体新規転写共役抑制因子を介したアンドロゲン依存性癌の分子機構の解析

上田崇, 伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, 趙越, 趙越, 山形薫, 山形薫, 藤山沙理, 藤山沙理, 田辺真彦, 木村周平, 村田拓哉, 松川紘之, 武山健一, 加藤茂明, 加藤茂明

日本アンドロロジー学会総会記事 27th 2008

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ショウジョウバエzinc-fingerタンパクZ4の新規クロマチン凝集化機能の解析

村田拓哉, 沢津橋俊, 伊藤紗弥, 鈴木絵里子, 山形薫, 沢津橋俊, 伊藤紗弥, 鈴木絵里子, 山形薫, ZHAO Yue, 田辺真彦, 藤山沙理, 藤山沙理, 木村周平, 上田崇, 松川紘之, LIM Jinseon, 武山健一, 加藤茂明, 加藤茂明

生化学 2008

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女性ホルモン・エストロゲンによるmiRNA産生抑制機構の解析

山形薫, 鈴木絵里子, 沢津橋俊, 伊藤紗弥, 藤山沙理, 田辺真彦, 上田崇, 村田拓哉, ZHAO Yue, 松川紘之, LIM Jinseon, 汐崎裕美, 武山健一, 加藤茂明

生化学 2008

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分子遺伝学的手法による新規転写共役因子の網羅的探索法の構築と機能解析

武山健一, 伊藤紗弥, 沢津橋俊, 鈴木絵里子, 趙越, 山形薫, 田辺真彦, 木村周平, 上田崇, 藤山沙理, 村田拓哉, 松川紘之, KOUZMENKO Alexander, 加藤茂明

日本農芸化学会大会講演要旨集 2008 2008

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新規ヒストンシャペロンDrosophila DEKはクロマチン構造変換を介してエクダイソンレセプターの転写反応を正に制御する転写共役因子である

沢津橋俊, 武山健一, 伊藤紗弥, 鈴木絵里子, 田辺真彦, ZHAO Yue, 山形薫, 木村周平, 村田拓哉, 藤山沙理, 上田崇, 松川紘之, LIM Jinseon, 多羽田哲也, 伊藤敬, 加藤茂明, 加藤茂明

生化学 2008

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骨芽細胞における新規ビタミンD受容体(VDR)転写共役因子複合体の同定

落合鋭士, 北川浩史, 高田伊知郎, 對馬佑, 藤山沙理, 沢津橋俊, 金美善, 目崎喜弘, 高木健一郎, 武山健一, 山岡一良, 加藤茂明, 上村孝

日本骨代謝学会学術集会プログラム抄録集 25回 192 - 192 2007.6

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エストロゲン応答miRNA発現のプロファイリング

山形薫, 鈴木絵里子, 沢津橋俊, 伊藤紗弥, 藤山沙理, 田辺真彦, 上田崇, 村田拓哉, ZHAO Yue, 松川紘之, 武山健一, 加藤茂明

生化学 2007

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ショウジョウバエの胚発生における特異的ヒストン化学修飾酵素の機能解析

木村周平, 伊藤紗弥, 沢津橋俊, 鈴木絵里子, ZHAO Yue, 山形薫, 田辺真彦, 上田崇, 藤山沙理, 村田拓哉, 松川紘之, 武山健一, 加藤茂明, 加藤茂明

生化学 2007

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アンドロゲン受容体新規転写共役抑制因子を介したアンドロゲン依存性癌の分子機構の解析

上田崇, 伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, ZHAO Yue, ZHAO Yue, 山形薫, 山形薫, 藤山沙理, 藤山沙理, 田辺真彦, 木村周平, 村田拓哉, 松川紘之, 武山健一, 加藤茂明, 加藤茂明

生化学 2007

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転写依存的ヒストンバリアントH2Av置換可視化モデルショウジョウバエの構築

田辺真彦, 伊藤紗弥, 沢津橋俊, 鈴木絵里子, ZHAO Yue, 山形薫, 藤山沙理, 村田拓哉, 木村周平, 上田崇, 松川紘之, 武山健一, 加藤茂明, 加藤茂明

生化学 2007

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Notchシグナル伝達依存的な新規転写抑制因子の同定と機能解析

武山健一, 伊藤紗弥, 沢津橋俊, 沢津橋俊, KOUZMENKO Alexander, KOUZMENKO Alexander, 鈴木絵里子, 山形薫, 山形薫, 趙越, 田辺真彦, 木村周平, 上田崇, 村田拓哉, 藤山沙理, 藤山沙理, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2007 2007

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染色体構造変換を介した新規転写共役抑制因子の探索と機能解析

伊藤紗弥, 沢津橋俊, 沢津橋俊, 鈴木絵里子, ZHAO Yue, 山形薫, 山形薫, 田辺真彦, 木村周平, 上田崇, 藤山沙理, 藤山沙理, 村田拓哉, 松川紘之, 武山健一, 加藤茂明, 加藤茂明

生化学 2007

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未知クロマチンバウンダリー制御因子の新たな探索法確立の試み

鈴木絵里子, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 伊藤紗弥, ZHAO Yue, 山形薫, 山形薫, 田辺真彦, 木村周平, 藤山沙理, 藤山沙理, 上田崇, 村田拓哉, 松川紘之, KOUZMENKO Alexander, KOUZMENKO Alexander, 武山健一, 加藤茂明, 加藤茂明

生化学 2007

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遺伝学的アプローチとプロテオミクスを連携した新規活性化クロマチン構造調節因子の網羅的探索と機能解析

藤山沙理, 藤山沙理, 沢津橋俊, 沢津橋俊, 鈴木絵里子, 伊藤紗弥, 伊藤紗弥, 田辺真彦, ZHAO Yue, 木村周平, 上田崇, 山形薫, 山形薫, 村田拓哉, 松川紘之, 武山健一, 加藤茂明, 加藤茂明

生化学 2007

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ショウジョウバエ分子遺伝学とプロテオミクス解析による新たな神経変性誘導機構の解析

村田拓哉, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 伊藤紗弥, ZHAO Yue, 山形薫, 山形薫, 鈴木絵里子, 田辺真彦, 藤山沙理, 藤山沙理, 木村周平, 上田崇, 松川紘之, KOUZMENKO Alexander, KOUZMENKO Alexander, 武山健一, 加藤茂明, 加藤茂明

生化学 2007

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未知クロマチンバウンダリー制御因子の新たな探索法確立の試み

鈴木絵里子, 沢津橋俊, 沢津橋俊, 伊藤紗弥, 田辺真彦, 木村周平, 趙越, 山形薫, 山形薫, 上田崇, 村田拓也, KOUZMENKO Alexander, KOUZMENKO Alexander, 武山健一, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2007 2007

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新規転写共役抑制因子p170はNotchシグナル転写抑制を介して神経細胞分化誘導を制御する

武山健一, 伊藤紗弥, 伊藤紗弥, 沢津橋俊, 沢津橋俊, KOUZMENKO Alexander, KOUZMENKO Alexander, 鈴木絵里子, 山形薫, 山形薫, ZHAO Yue, 田辺真彦, 木村周平, 上田崇, 村田拓也, 松川紘之, 藤山沙理, 藤山沙理, 平林祐介, 後藤由季子, 加藤茂明

生化学 2007

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分子遺伝学的アプローチによるヒト核内レセプター新規転写共役因子BAHD1の機能解析

伊藤紗弥, 武山健一, 沢津橋俊, 鈴木絵里子, 趙越, 山形薫, 田辺真彦, KOUZMENKO Alexander, KOUZMENKO Alexander, 城出裕子, 城出裕子, 多羽田哲也, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2006 2006

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クロマチン構造を介したエクダイソンレセプター転写制御機構の解明に関する研究

沢津橋俊, 武山健一, 伊藤紗弥, 鈴木絵里子, 田辺真彦, 趙越, 山形薫, 城出裕子, 多羽田哲也, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2006 2006

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男性ホルモンレセプター(AR)変異により発症する球脊髄性筋萎縮症(SBMA)における転写破綻機構の解析

山形薫, 武山健一, 鈴木絵里子, 沢津橋俊, 伊藤紗弥, 城出裕子, 趙越, 加藤茂明

日本内分泌学会雑誌 81 ( 1 ) 167 - 167 2005.4

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ショウジョウバエトランスジェニックを用いる修正位置効果の多様化(PEV)システムの解析(Analysis of the Modified Position Effect Variegation (PEV) System using Drosophila Transgenics)

趙越, 武山健一, 伊藤紗弥, 鈴木絵里子, 沢津橋俊, 城出裕子, 真木彰郎, 多羽田哲也, 加藤茂明

日本内分泌学会雑誌 81 ( 1 ) 118 - 118 2005.4

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網膜芽腫蛋白/E2F-1転写抑圧はヒトアンドロゲン受容体におけるポリグルタミン反復の拡大による神経変性を緩和する(Retinoblastoma protein/E2F-1 transcriptional repression reduces neurodegeneration by expansion of polyglutamine repeat in human androgen receptor)

鈴木絵里子, 武山健一, 伊藤紗弥, 沢津橋俊, 城出裕子, 真木彰郎, 山形薫, 趙越, Kouzmenko Alexander, 相垣敏郎, 多羽田哲也, 加藤茂明

日本内分泌学会雑誌 81 ( 1 ) 176 - 176 2005.4

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分子遺伝子学的アプローチによるヒト核内レセプター転写共役因子の探索と機能解析

武山健一, 伊藤紗弥, 沢津橋俊, 城出裕子, 城出裕子, 鈴木絵里子, 真木彰郎, ちょう越, 山形薫, 山形薫, KOUZMENKO Alexander, KOUZMENKO Alexander, 田辺真彦, 多羽田哲也, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2005 2005

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新規アンドロゲンレセプター転写共役因子の網羅的探索と機能解析

武山健一, 伊藤紗弥, 沢津橋俊, 城出裕子, 鈴木絵里子, 真木彰郎, ちょう越, 山形薫, KOUZMENKO Alexander

日本内分泌学会雑誌 81 ( 1 ) 2005

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クロマチン構造を介したエクダイソンレセプター転写制御機構の解明に関する研究

沢津橋俊, 武山健一, 伊藤紗弥, 鈴木絵里子, 田辺真彦, ZHAO Yue, 山形薫, 城出裕子, 赤松康宏, 多羽田哲也, 加藤茂明, 加藤茂明

日本分子生物学会年会講演要旨集 28th 2005

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ポリグルタミン鎖伸長異常アンドロゲンレセプターによって引き起こされる神経変性はRb/E2F-1転写調節機能の抑制化により回復する

鈴木絵里子, 武山健一, 伊藤紗弥, 沢津橋俊, 城出裕子, 城出裕子, 真木彰郎, 山形薫, 山形薫, ちょう越, KOUZMENKO Alexander, KOUZMENKO Alexander, 相垣敏郎, 多羽田哲也, 加藤茂明, 加藤茂明

日本農芸化学会大会講演要旨集 2005 2005

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網膜芽腫蛋白質/E2F-1転写レプレッサはヒトアンドロゲン受容体に存在するポリグルタミン鎖伸長による神経変性疾患を抑制する(原標題は英語)

鈴木絵里子, 武山健一, 伊藤紗弥, 沢津橋俊, 城出裕子, 真木彰郎, 山形薫, ちょう越, 相垣敏郎

日本内分泌学会雑誌 81 ( 1 ) 2005

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ショウジョウバエにおけるエクダイソン/幼若ホルモンによるエクダイソンレセプター転写制御メカニズムの解明

真木彰郎, 沢津橋俊, 伊藤紗弥, 鈴木絵里子, 城出裕子, ちょう越, 山形薫, KOUZMENKO A, 武山健一

日本農芸化学会大会講演要旨集 2004 2004

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ショウジョウバエエクダイソンレセプター転写制御を介したエクダイソン/幼若ホルモンきっ抗的作用メカニズムの解明

真木彰郎, 沢津橋俊, 伊藤紗弥, 鈴木絵里子, 城出裕子, ZHAO Y, 山形薫, KOUZMENKO A, 武山健一

日本分子生物学会年会プログラム・講演要旨集 27th 2004

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アンドロゲンレセプターを介したE2F-1/Rb転写制御機構の解析

鈴木絵里子, 武山健一, 伊藤沙弥, 沢津橋俊, 城出裕子, 真木彰郎, 山形薫, ZHAO Y, KOUZMENKO A

日本分子生物学会年会プログラム・講演要旨集 27th 2004

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分子遺伝学的アプローチによるヒト性ステロイドホルモンレセプター新規転写制御因子の網羅的Screening系の構築

伊藤紗弥, 武山健一, 沢津橋俊, KOUZMENKO A, 城出裕子, 鈴木絵里子, 真木彰郎, ZHAO Y, 相垣敏郎

日本分子生物学会年会プログラム・講演要旨集 27th 2004

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アンドロゲンレセプター転写制御機構におけるmediator TRAP240の機能解析

武山健一, 伊藤紗弥, 沢津橋俊, KOUZMENKO A P, 加藤茂明

日本農芸化学会大会講演要旨集 2003 2003

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アンドロゲンレセプター転写制御機構におけるmediator TRAP240の機能解析

武山健一, 伊藤紗弥, 沢津橋俊, 城出裕子, 鈴木絵里子, 真木彰郎, 山形薫, ZHAO Y, KOUZMENKO A

日本分子生物学会年会プログラム・講演要旨集 26th 2003

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ショジョウバエを用いたヒトエストロゲンレセプター転写制御機構の解明

伊藤紗弥, 武山健一, 沢津橋俊, ALEXANDER K, 加藤茂明

日本農芸化学会大会講演要旨集 2003 2003

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Presentations

栄養情報が調節するグルココルチコイド受容体の転写制御機構の解析

沢津橋俊, 松本俊夫, 福本誠二

第93回日本内分泌学会学術総会 2020.7.28

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Event date： 2020.7.20 - 2020.8.31

Presentation type：Oral presentation (general)

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OptoCap-MS Enables Biochemical Profiling of IDR-Driven Condensates in Living Cells.

Shun Sawatsubashi, Koichi Nishimura

2025.11.5

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VDR is an essential regulator of hair follicle regression through the progression of cell death

Shun Sawatsubashi

2024.11.6

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Development of methods for analyzing light-inducible interactions among the transcriptional co-regulators through intrinsic disordered regions (IDRs).

Shun Sawatsubashi, Koichi Nishimura

2023.10.31

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VDR is an essential regulator of hair follicle regression through the progression of cell death.

Shun Sawatsubashi

The 18th International Symposium of the Institute Network for Biomedical Sciences 2023.10.6

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Functional analysis of vitamin D-dependent rickets type II model mouse introducing the human disease-related point mutations. Invited

Shun Sawatsubashi

2022.10.15

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Functional analysis of vitamin D-dependent rickets type II model mouse introducing the human disease-related point mutations.

2022.7.22

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栄養代謝状態が調節するグルココルチコイド受容体の転写制御機構の解明

沢津橋俊, 貝沼梨沙, 松本俊夫, 福本誠二

第94回日本内分泌学会学術総会 2021.4.24

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Functional analysis of vitamin D receptor in hair follicle and epidermal homeostasis.

2020.10.10

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ゲノム編集を利用したくる病型点変異導入ビタミン D 受容体の機能解析

沢津橋俊, 横山敦, 上甲裕大, 松本俊夫, 福本誠二

第92回日本生化学会大会 2019.9.19

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栄養情報が調節するグルココルチコイド受容体の転写制御機構の解明

沢津橋俊

第37回内分泌代謝学サマーセミナー 2019.7.6

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核内受容体が制御する多彩な生命現象表皮特異的ビタミンD受容体ノックアウトマウスから理解する正常な表皮・毛包維持機構の解明

沢津橋俊, 上甲裕大, 山本陽子, 福本誠二, 松本俊夫

生命科学系学会合同年次大会 2017.12

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皮膚におけるビタミンD受容体の高次機能解析

沢津橋俊, 山本陽子, 福本誠二, 松本俊夫

日本内分泌学会雑誌 2016.4

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Industrial property rights

タンパク質、ポリヌクレオチド、ベクター、ベクター系、組成物、キット、細胞、標的DNAの修飾方法、および製造方法

穂積俊矢, 平野孝昌, 沢津橋俊

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Applicant：株式会社セツロテック

Application no：特願2024-195971 Date applied：2024.11.8

Patent/Registration no：特許第7662138号 Date registered：2025.4.7

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遺伝子改変動物由来の動物繊維

沢津橋俊, 稲谷結花, 渡邉忠由, 長尾勇佑, 上利尚大, 貝沼梨沙, 長尾朋子, 西村耕一, 穂積俊矢, 小野晃寛

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Applicant：株式会社セツロテック

Application no：特願2022-090657 Date applied：2022.6.3

Patent/Registration no：特許第7201190号 Date registered：2022.12.26

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遺伝子改変動物由来の動物繊維

沢津橋俊, 稲谷結花, 渡邉忠由, 長尾勇佑, 上利尚大, 貝沼梨沙, 長尾朋子, 西村耕一, 穂積俊矢, 小野晃寛

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Application no：特願2022-090657 Date applied：2022.6.3

Announcement no：特開2023-177792 Date announced：2023.12.14

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変異型MAD7タンパク質

穂積俊矢, 西村耕一, 増田憶良, 高寺悟, 貝沼梨沙, 山下裕紀子, 沢津橋俊

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Applicant：株式会社セツロテック

Application no：特願2022-011914 Date applied：2022.1.28

Patent/Registration no：特許第7113415号 Date registered：2022.7.28

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変異型MAD7タンパク質

穂積俊矢, 西村耕一, 増田憶良, 高寺悟, 貝沼梨沙, 山下裕紀子, 沢津橋俊

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Application no：特願2022-011914 Date applied：2022.1.28

Announcement no：特開2023-110449 Date announced：2023.8.9

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ゲノム編集方法

沢津橋俊, 菅野茂夫

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Applicant：国立大学法人徳島大学

Application no：特願2017-027384 Date applied：2017.2.16

Announcement no：特開2018-126122 Date announced：2018.8.16

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ゲノム編集方法

沢津橋俊, 菅野茂夫

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Applicant：国立大学法人徳島大学

Application no：特願2017-027384 Date applied：2017.2.16

Announcement no：特開2018-126122 Date announced：2018.8.16

Patent/Registration no：特許第6956995号 Date registered：2021.10.8

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Awards

科学技術大賞・科学技術振興部門

2020 徳島県

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第37回内分泌代謝学サマーセミナー・ポスター賞

2018 一般社団法人日本内分泌学会栄養情報が調節するグルココルチコイド受容体の転写制御機構の解明

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B.B.B.論文賞

2008 公益社団法人日本農芸化学会 RNA-Binding Protein Hoip Accelerates PolyQ-Induced Neurodegeneration in Drosophila

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B.B.B.論文賞

2004 公益社団法人日本農芸化学会 A Novel Genetic System for Analysis of Co-activators for the N-Terminal Transactivation Function Domain of the Human Androgen Receptor

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Research Projects

ステロイド骨粗鬆症へのSema3A, IL-11の関与と新規治療への応用

Grant number：25K11823 2025.04 - 2028.03

日本学術振興会科学研究費助成事業基盤研究(C)

遠藤逸朗, 沢津橋俊, 原倫世, 日浅雅博, 金井麻衣

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Grant amount：\4680000 （ Direct expense: \3600000 、 Indirect expense：\1080000 ）

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毛包をモデルとした臓器・器官の恒常性維持機構とその破綻による病態の解明

Grant number：24K10533 2024.04 - 2027.03

日本学術振興会科学研究費助成事業基盤研究(C)

沢津橋俊

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Grant amount：\4550000 （ Direct expense: \3500000 、 Indirect expense：\1050000 ）

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糖質応答転写因子ChREBPの新規阻害薬を用いた糖尿病性腎臓病の病態解明・制御

Grant number：24K02875 2024.04 - 2027.03

日本学術振興会科学研究費助成事業基盤研究(B)

菅原明, 岩渕好治, 広川貴次, 横山敦, 沢津橋俊, 岡本好司

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Grant amount：\10010000 （ Direct expense: \7700000 、 Indirect expense：\2310000 ）

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ゲノム多型に起因する疾患の発症プロセスの解明

Grant number：23K24081 2022.04 - 2025.03

日本学術振興会科学研究費助成事業基盤研究(B)

沖真弥, 竹本龍也, 沢津橋俊

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Grant amount：\17030000 （ Direct expense: \13100000 、 Indirect expense：\3930000 ）

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Study on the actions of phosphate as a first messenger

Grant number：19H03676 2019.04 - 2022.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

FUKUMOTO Seiji

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Grant amount：\16900000 （ Direct expense: \13000000 、 Indirect expense：\3900000 ）

Fibroblast growth factor 23 (FGF23) is a hormone that is produced by bone and essential for the regulation of serum phosphate level. Excessive and deficient actions of FGF23 result in hypophosphatemia rickets/osteomalacia and hyperphosphatemic tumoral calcinosis, respectively, indicating that there must be a regulatory system to maintain serum phosphate and FGF23 levels in our body. We have revealed that FGF receptor 1 in bone works as a phosphate-sensing mechanism to regulate FGF23 production by analyzing the controlling system of FGF23 production. In addition, this phosphate-sensing by FGF receptor 1 in bone was essential for maintaining normal life span.

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Identification and functional analysis of noncoding SNPs causative for genetic disorders

Grant number：18KT0024 2018.07 - 2021.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

OKi Shinya

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Grant amount：\18590000 （ Direct expense: \14300000 、 Indirect expense：\4290000 ）

GWAS and other case-control studies have identified many disease-associated single nucleotide polymorphisms (marker SNPs). However, since about 90% of disease-associated marker SNPs are located in non-coding regions, it is very difficult to understand the causal relationship between SNPs, which genes they affect, and why they lead to diseases. In this study, we focused on SNPs in non-coding regions that are associated with diseases, and aimed to elucidate the disease process caused by them. As a result, we identified a region where multiple transcription factors involved in immunity and inflammation bind within the linkage disequilibrium region of disease-related SNPs in the non-coding region.

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Mechanistic insights of the pathogenesis of alopecia using a novel vitamin D-dependent richets mouse model

Grant number：18K19518 2018.06 - 2021.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory)

SAWATSUBASHI Shun

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Grant amount：\6370000 （ Direct expense: \4900000 、 Indirect expense：\1470000 ）

The hair follicle is a dynamically regenerating organ, and the hair cycle is an important model for regeneration research. In this study, we focused on the pathogenesis of hair loss in a vitamin D-dependent rickets model mouse, and aimed to clarify the regulatory mechanism of the catagen, which has not yet been elucidated.
As a result, we established a novel mouse model of rickets that mimics point mutations in human disease. Furthermore, we succeeded in establishing 10 strains of the VDR mutations using genome editing, and investigated the pathophisiology. Interestingly, each point-mutated VDR showed differences in the interacting proteins that reduced their binding ability. This is an important result to reconsider the conventional disease mechanism, in which the loss of interaction with RXR, a heterodimer of VDR, has been considered as the main cause.

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Role and mechanism of action of IL-11 on the regulation of bone and adipose tissue interaction

Grant number：16H05327 2016.04 - 2019.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

MATSUMOTO Toshio

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Grant amount：\17420000 （ Direct expense: \13400000 、 Indirect expense：\4020000 ）

Interleukin (IL)-11 enhances osteogenesis and suppresses adipogenesis from bone marrow stromal cells, by enhancing Wnt signaling via suppression of Wnt inhibitors. To clarify the role of IL-11 in bone remodeling, IL-11 knockout (IL-11-/-) mice were created. IL-11-/- mice exhibited reduced bone formation with suppressed Wnt signaling via enhanced expression of Wnt inhibitors. These mice showed not only reduced bone mass but also increased white adipose tissue with glucose intolerance. Osteoblast-specific IL-11 deletion in osteocalcin-Cre;IL-11fl/fl mice showed reduced serum IL-11 level and almost the same phenotype as IL-11-/- mice. Adipocyte-specific IL-11 deletion in adiponectin-Cre; IL-11fl/fl mice exhibited no abnormality. Thus, osteoblast-derived IL-11 controls not only osteogenesis but also systemic adipogenesis and energy metabolism. Receptors and intracellular signaling mediating these effects of IL-11 are currently under investigation.

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Innovation of novel therapeutics against diabetic nephropathy targeting ChREBP

Grant number：16K15492 2016.04 - 2018.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

Sugawara Akira, SAWATUBASHI Shun, TAKEMOTO Tatsuya, YAMAMOTO Yasuhiko, TAKAGI Kiyoshi, Sato Horoshi, Yokoyama Atsushi, ITO Ryo, DOI Takayuki

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Grant amount：\3120000 （ Direct expense: \2400000 、 Indirect expense：\720000 ）

1) Generation of ChREBP KO mice. We have succeeded in generating ChREBP KO mice (C57BL/6J) using CRISPR/Cas9 system. 2) Generation of high throughput screening (HTS) system using MES13 ChoRE-Luc cells. We have succeeded in generating HTS system using the cell line by obtaining Z score above 0.5. 3) HTS of Tohoku University chemical library: We obtained 13 hit chemicals among 5,861 compounds. Among them, we selected 1 compound (X) for the further investigation. 4) Administration of chemical compounds to Ins-iNOS-transgenic mice: We are now administrating the compound X to the mice.

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Role of vitamin D receptor target genes in the epidermal function and hair follicle homeostasis.

Grant number：16K19556 2016.04 - 2018.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)

SAWATSUBASHI Shun

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Grant amount：\3900000 （ Direct expense: \3000000 、 Indirect expense：\900000 ）

The in vivo function of vitamin D receptor (VDR) in skin is still unknown. To elucidate VDR function in epidermal development and homeostasis, we generated epidermis-specific VDR KO mice (VDR epiKO). The VDR epiKO mice shows epidermal thickness and hair loss phenotypes. As a result of microarray analysis, it was revealed that S100A8 gene expression was upregulated in VDR epiKO mice. In particular, S100A8 gene promoter was induced by inflammation-related transcription factor NF-kB p65 in cultured human keratinocytes. In contrast, VDR was repressed the NF-kB-meditated S100A8 promoter activation. Furthermore, we established the systemic and epidermis-specific S100 A8 KO mice. Analyses of these mouse lines suggests that S100A8 might be involved in epidermal defects of VDR epiKO mice.

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漢方米由来成分を素材とする次世代スキンケア製品開発のための評価系の構築

2016

科学技術振興機構産学が連携した研究開発成果の展開研究成果展開事業マッチングプランナープログラム

沢津橋俊

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Glucose regulates the function of glucocorticoid receptor via O-GlcNAc modification.

Grant number：24591357 2012.04 - 2015.03

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

SAWATSUBASHI Shun, KITAGAWA Hirochika, SATO Takashi

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Grant amount：\5460000 （ Direct expense: \4200000 、 Indirect expense：\1260000 ）

Glucocorticoids are widely used as anti-inflammatory drugs, the molecular mechanisms involved in this anti-inflammatory effect and associated with serious side effects remain unknown. In this study, we performed the proteomic analysis of post-translational modification on glucocorticoid receptor (GR) and identified a novel O-linked beta-N-acetylglucosamine (O-GlcNAc) modified sites. Moreover, this O-GlcNAcylation was regulated under conditions of glucose concentration in culture medium and detected in nucleus of mouse liver and cerebrum. Based on these results, we propose that this O-GlcNAcylation regulates the tissue-specific transcriptional activity of GR.

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慢性炎症病態を制御するシグナル依存性エピゲノム制御メカニズムの解析

Grant number：23117505 2011.04 - 2013.03

日本学術振興会科学研究費助成事業新学術領域研究(研究領域提案型)

沢津橋俊

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Grant amount：\7020000 （ Direct expense: \5400000 、 Indirect expense：\1620000 ）

グルココルチコイド(GC)はホルモンであると同時に、抗炎症薬として用いられるが副作用の問題は未解決である。一般にGCは核内受容体グルココルチコイドレセプター(GR)を介し、各標的組織における多様な生理作用を発揮するが、その組織特異性の機序は不明なままである。本研究では生化学的手法によるGRタンパク質精製とLC-MS解析系を用い、栄養情報を担うエピゲノム制御因子複合体の翻訳後修飾に着目し、探索を試みた。その結果、栄養情報を反映するGRの翻訳後修飾のひとつとしてO-結合型N-アセチルグルコサミン(O-GlcNAc)修飾の同定に成功した。また、この糖付加を担うO-GlcNAc転移酵素(OGT)はGR転写活性を負に制御した。さらに、高グルコース条件下ではGR転写活性が低下することを見出し、過剰発現及びノックダウン実験から、この機能低下の一部をOGTが担うことが示唆された。これとは逆に炎症系転写因子AP-1は高グルコースで転写活性が増強された。in vitroアッセイの結果、GRのO-GlcNAc修飾はGCに依存しないO-GlcNAc修飾と、GC依存性でかつアセチル化修飾酵素p300/CBPを必要とする新規O-GlcNAc修飾との2ステップに制御されており、後者はGR転写活性のグルコース感受性を担う可能性が示唆された。また、この修飾を特異的に認識する抗体を作出し、この新規修飾が細胞内に存在することを確認することで、エピゲノム制御因子によるアセチル化修飾とO-GlcNAc修飾間の新たなクロストークの重要性が示された。本研究で見出したエピゲノム制御因子p300/CBP-OGT間のクロストークはGRがグルコース感受能を発揮する上での重要な役割を担っており、GRの翻訳後修飾がGCの組織特異的作用とグルココルチコイド感受性を調節する分子メカニズムの一つであると考えられる。

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A genetical screening of a protein trap library for active chromatin-binding factors on polytene chromosome in Drosophila

Grant number：22770166 2010 - 2011

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)

SAWATSUBASHI Shun, LIM Jinseon

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Grant amount：\4290000 （ Direct expense: \3300000 、 Indirect expense：\990000 ）

It is evident that gene regulation is coupled with chromatin reorganaization, but factors and molecular basis involving in this process remain to be identified. In the present study, factors responsible for ecdysone-induced puff formation were genetically screened in Drosophila fly by establishing an EGFP protein-trap approach. Among the candidates, Drosophila CG11138/Ringfect was found as a co-activator for ecdysone receptor (EcR). Through biochemical characterization, Ringfect could be shown to serve as a histone chaperon. We describe the identification of novel puff-localized factors by screening the protein trap transgenic fly library. Drosophila CG11138/Ringfect and enolase were genetically identified as a puff-localized factor and a co-activator, and interacted with EcR in S2 cell. Thus, the present study suggests that Ringfect and enolase are categorized as a novel class of nuclear receptor co-activators.

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