福井大学　研究者総覧
工学系部門
工学領域
生物応用化学講座
English
更新日：2025/05/22
教授
オキ　マサヤ
沖　昌也

福井大学 工学系部門 工学領域 生物応用化学講座　教授
工学部　基幹教員（教育課程の編成等への参画状況：教授会，主要授業科目担当） 　

学歴

  1. 1996/03修了富山大学工学研究科化学生物工学修士
  2. 1999/03修了九州大学その他分子生命科学系専攻博士

学位

  1. 理学博士

経歴

  1. 1999/04-2002/03日本学術振興会特別研究員 (PD)
  2. 2002/04-2003/02米国立衛生研究所研究員
  3. 2003/03-2005/02日本学術振興会海外特別研究員
  4. 2005/03-2005/06米国立衛生研究所研究員
  5. 2005/07-2006/07長崎大学助手
  6. 2006/07-2006/10理化学研究所研究員
  7. 2006/11福井大学助教授
  8. 2007/04福井大学准教授
  9. 2018/01/01福井大学学術研究院工学系部門教授

所属学協会

  1. 2021/04/01-2025/03/31日本遺伝学会
  2. 2019/06/01-2026/03/31日本エピジェネティクス 研究会
  3. 2017/10/01-2019/09/30日本生化学会北陸支部
  4. 2017/01/01-2020/03/31日本遺伝学会
  5. 2016/04/01-2017/03/31日本遺伝学会
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研究分野

  1. ライフサイエンス分子生物学

研究キーワード

  1. クロマチン、境界、ヒストン
  2. エピジェネティクス、遺伝

研究テーマ

  1. 染色体境界形成機構の解析
  2. エピジェネティックな遺伝子発現調節機構の解析

論文

  1. The HAT Inhibitor ISOX-DUAL Diminishes Ischemic Areas in a Mouse Model of Oxygen-Induced Retinopathy.2025/03Nakanishi Kengo,Takamura Yoshihiro,Nakano Yusei,Inatani Masaru,Oki MasayaGenes to cells : devoted to molecular & cellular mechanisms30/ 2, e1319610.1111/gtc.131961365-2443Retinal ischemic disease results in significant visual impairment due to the development of fragile and disorganized, pathologically running blood vessels in the eye. Currently, the mainstay treatment for this disease is the intravitreal administration of anti-VEGF drugs targeting vascular endothelial growth factor (VEGF), which induces angiogenesis. However, current anti-VEGF drugs do not diminish the ischemic areas that lead to angiogenesis, making fundamental treatment challenging. Since retinopathy is an acquired disease caused by hypoxic stimulation from ischemia, we paid particular attention to histone acetylases. We conducted a drug screening experiment using a mouse model of oxygen-induced retinopathy (OIR), which replicates retinal ischemic disease, through the intraperitoneal administration of 17 distinct inhibitors targeting histone acetyltransferases (HAT). The results indicated that, among the 17 inhibitors, only ISOX-DUAL decreased neovascularization and ischemic regions. Furthermore, microarray analysis was conducted on the drug-treated samples to refine genes altered by the administration of ISOX-DUAL. There were 21 genes associated with angiogenesis, including Angpt2, Hmox1, Edn1, and Serpine1, exhibited upregulation in OIR mice and downregulation following treatment with ISOX-DUAL. Furthermore, STRING analysis confirmed that the aforementioned four genes are downstream factors of hypoxia-inducible factors and are assumed to be important factors in retinal ischemic diseases.
  2. Identification of genes contributing to attenuation of rat model of galactose-induced cataract by pyruvate.2024/09/01Masuda Fuuga,Inami Mayumi,Takamura Yoshihiro,Inatani Masaru,Oki MasayaGenes to cells : devoted to molecular & cellular mechanisms10.1111/gtc.131501365-2443Cataracts are a disease that reduces vision due to opacity formation of the lens. Diabetic cataracts occur at young age and progress relatively quickly, so the development of effective treatment has been awaited. Several studies have shown that pyruvate inhibits oxidative stress and glycation of lens proteins, which contribute to onset of diabetic cataracts. However, detailed molecular mechanisms have not been revealed. In this study, we attempted to reduce galactose-induced opacity by pyruvate with rat ex vivo model. Rat lenses were extracted and cultured in galactose-containing medium to induce lens opacity. After opacity had developed, continued culturing with pyruvate in the medium resulted in a reduction of lens opacity. Subsequently, we conducted microarray analysis to investigate the genes that contribute to the therapeutic effect. We performed quantitative expression measurements using RT-qPCR for extracted genes that were upregulated in cataract-induced lenses and downregulated in pyruvate-treated lenses, resulting in the identification of 34 candidate genes. Functional analysis using the STRING database suggests that metallothionein-related factors (Mt1a, Mt1m, and Mt2A) and epithelial-mesenchymal transition-related factors (Acta2, Anxa1, Cd81, Mki67, Timp1, and Tyms) contribute to the therapeutic effect of cataracts.
  3. GTP-dependent regulation of heterochromatin fluctuations at subtelomeric regions in Saccharomyces cerevisiae.2024/03Ayano Takahito,Yokosawa Takuma,Oki MasayaGenes to cells : devoted to molecular & cellular mechanisms29/ 3, 217-23010.1111/gtc.130941365-2443In eukaryotes, single cells in a population display different transcriptional profiles. One of the factors regulating this heterogeneity is the chromatin state in each cell. However, the mechanisms of epigenetic chromatin regulation of specific chromosomal regions remain unclear. Therefore, we used single-cell tracking system to analyze IMD2. IMD2 is located at the subtelomeric region of budding yeast, and its expression is epigenetically regulated by heterochromatin fluctuations. Treatment with mycophenolic acid, an inhibitor of de novo GTP biosynthesis, triggered a decrease in GTP, which caused heterochromatin fluctuations at the IMD2 locus. Interestingly, within individually tracked cells, IMD2 expression state underwent repeated switches even though IMD2 is positioned within the heterochromatin region. We also found that 30% of the cells in a population always expressed IMD2. Furthermore, the addition of nicotinamide, a histone deacetylase inhibitor, or guanine, the GTP biosynthesis factor in salvage pathway of GTP biosynthesis, regulated heterogeneity, resulting in IMD2 expression being uniformly induced or suppressed in the population. These results suggest that gene expression heterogeneity in the IMD2 region is regulated by changes in chromatin structure triggered by slight decreases in GTP.
  4. IMD2, located near the boundary of heterochromatin regions, is regulated by multiple HAT-related factors.2024/03/26Ayano Takahito,Oki MasayaGenes & genetic systems9910.1266/ggs.23-002841880-5779In Saccharomyces cerevisiae, boundaries formed by DNA sequence-dependent or -independent histone modifications stop the spread of the heterochromatin region formed via the Sir complex. However, it is unclear whether the histone modifiers that control DNA sequence-independent boundaries function in a chromosome-specific or -nonspecific manner. In this study, we evaluated the effects of the SAGA complex, a histone acetyltransferase (HAT) complex, and its relationship with other histone-modifying enzymes to clarify the mechanism underlying boundary regulation of the IMD2 gene on the right subtelomere of chromosome VIII. We found that Spt8, a component of the SAGA complex, is important for boundary formation in this region and that the inclusion of Spt8 in the SAGA complex is more important than its interaction with TATA-binding protein and TFIIS. In addition to SAGA, various HAT-related factors, such as NuA4 and Rtt109, also functioned in this region. In particular, the SAGA complex induced weak IMD2 expression throughout the cell, whereas NuA4 induced strong expression. These results indicate that multiple HATs contribute to the regulation of boundary formation and IMD2 expression on the right subtelomere of chromosome VIII and that IMD2 expression is determined by the balance between these factors.
  5. A novel tracking and analysis system for time-lapse cellular imaging of Schizosaccharomyces pombe.2024/03/26Taniguchi Kei,Kajitani Takuya,Ayano Takahito,Yoshida Toshiyuki,Oki MasayaGenes & genetic systems9910.1266/ggs.23-002391880-5779The importance of the parent-progeny relationship tracking technique in single-cell analysis has grown with the passage of time. In this study, fundamental image-processing techniques were combined to develop software capable of inferring cell cycle alterations in fission yeast cells, which exhibit equipartition during division. These methods, exclusively relying on bright-field images as input, could track parent-progeny relationships after cell division by assessing the temporal morphological transformation of these cells. In the application of this technique, the software was employed for calculating intracellular fluorescent dots during every stage of the cell cycle, using a yeast strain expressing EGFP-fused Swi6, which binds to chromatin. The results obtained with this software were consistent with those of previous studies. This software facilitated single-cell-level tracking of parent-progeny relationships in cells exhibiting equipartition during division and enabled the monitoring of spatial fluctuations in a cell cycle-dependent protein. This method, expediting the analysis of extensive datasets, may also empower large-scale screening experiments that cannot be conducted manually.
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著書

  1. 遺伝学の百科事典公益財団法人　遺伝学普及会　日本遺伝学会 編10章　エピジェネティクス丸善出版2022/01/28
  2. 動物の事典沖昌也（第3章　動物の遺伝と遺伝子）第3章　動物の遺伝と遺伝子朝倉書店2020/11/19
  3. 比較内分泌学会誌沖　昌也単一細胞の世代を越えたエピジェネティックな発現状態変化比較内分泌学会2014/01
  4. 細胞工学沖　昌也単一細胞のエピジェネティクス秀潤社2013/02
  5. 日本エピジェネティクス研究会ニュース沖　昌也学会報告「Message from yeast to Epigenetics~Yeast clarifies the frontiers of life science~」日本エピジェネティクス研究会2013/01
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講演・口頭発表・ポスター等

  1. Analysis of biochemical reaction in liposomes after terahertz wave irradiationThe 9th International Workshop on Far-Infrared Technologies (IW-FIRT2024) and Symposium on Frontier of Terahertz Science (S-FTS2024)2024/10/16
  2. エピジェネティックな発現を制御することによる眼疾患治療薬の開発第97回日本薬理学会2023/12/15
  3. 酵母を用いたエピジェネティクスの基礎研究から創薬を目指した応用研究まで信州大学部局推進プロジェクト2023/11/30
  4. 白内障発症にエピジェネティックな発現制御はどのように関わってくるのか？第62回日本白内障学会総会・第49回水晶体研究会2023/07/23
  5. 酵母エピジェネティクス研究から創薬研究まで金沢大学異分野融合セミナー2023/01/26
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産業財産権

  1. 特許権白内障の予防剤および治療剤、並びに、これらを製造するための、ＰＰＡＲ活性化剤の使用特願2017-2546142017/12/28
  2. 特許権酢酸中のギ酸の定量方法2012-0298392012/02/14
  3. 特許権遺伝子発現状態追跡装置2010-2462592010/11/02
  4. 特許権細胞画像解析装置及び方法2010-1835032010/08/18
  5. 特許権ホルムアルデヒドの分解方法、及び、新規微生物2007-2203982007/08/27
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受賞

  1. 2015/01The teacher of the year
  2. 2014/03学長奨励賞「研究」
  3. 2014/01The teacher of the year
  4. 2013/06生化学会北陸支部奨励賞世代を越えたエピジェネティックな発現は一定の規則性をもとに制御されている
  5. 2013/01The teacher of the year
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科学研究費補助金・厚生科研補助金

  1. 2007文部科学省科学研究費補助金４次クロマチン構造による染色体機能ドメイン構築機構の解明特定領域研究高次クロマチン領域の協会決定機構の解析
  2. 2024日本学術振興会科学研究費助成事業クロマチン上に1度経験した記憶が残るメカニズムの解明挑戦的研究（萌芽）
  3. 2024日本学術振興会科学研究費助成事業特定のヘテロクロマチン領域を認識し遺伝子発現を制御するメカニズムの解明基盤研究(B)
  4. 2022日本学術振興会科学研究費助成事業特定のヘテロクロマチン領域を認識し遺伝子発現を制御するメカニズムの解明基盤研究(B)（一般）
  5. 2009文部科学省科学研究費補助金ヘテロクロマチン領域伸張停止メカニズムの解明若手研究(A)
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共同研究

  1. 2012エピジェネティックな遺伝子発現調節機構におけるrDNAの関与
  2. 2012MEMS 技術による水圧駆動マイクロピラーの開発
  3. 2012統計処理からのエピジェネティクスの機能解明
  4. 2011ChIP on chip 技術を用いたゲノムワイドな Sir3 タンパク質の機能解析
  5. 2011高次クロマチン構造による染色体機能ドメイン構築機構の解明
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