医科学専攻

  • Master's Courses 
    修士課程
  • Doctoral Courses 
    博士課程

Modomics Biology and Medicineモドミクス医学

  • RNA修飾
  • 代謝
  • 質量分析
  • ミトコンドリア
  • 加齢・老化
  • 液性因子
  • 緑内障

STAFF

Professor

  • Wei Fan YanProfessor. 魏 范研 教授

Other Faculty / Staff

  • Ogawa, Akiko
    Assistant Prof. 小川 亜希子 助教
  • Matsuda, Shigeru
    Assistant Prof. 松田 盛 助教

CONTACT

TEL:+81-22-717-8569
E-MAIL:fanayan.wei.d3*tohoku.ac.jp
(「*」を「@」に変換してください)

OUTLINE

More than 150 types of post-transcriptional modifications have been identified in various RNA species, including messenger RNA (mRNA), ribosomal RNA (rRNA), and transfer RNA (tRNA), from all three domains of life. These modifications are vital for RNA stability, intracellular localization, and decoding fidelity. Dysregulated modification of RNA has been associated with various human diseases, such as diabetes, mitochondrial disease, and intellecutual disability. In addition to regulating intracellular post-transcriptional gene expression, RNA modifications can greatly impact extracellular signaling because modified RNAs are catabolized into modified nucleosides that are released into extracellular fluids. These extracellular modified nucleosides are not only utilized as potential biomarkers of diseases, but also can act as ligands of selective receptors and trigger pathophysiological responses. Our labolatory investigates the molecular mechanism of regulatory roles of RNA modification both intracellularly and extracellulary.

外界からの化学的・物理的・生物学的なストレス、あるいは疾患や加齢などの内的要因によって、我々の体の中では様々な生体分子がダイナミックに「化学修飾」を受けることで新たな機能を獲得し、細胞や臓器機能に影響を及ぼしています。
これらの修飾の網羅的な解析を「モドミクス(Modification + Omics)」と名付け、私たちは中でも特にRNA修飾に注目し、RNAモドミクスと代謝・免疫・老化などの生理機能やヒト疾患病態との関わりについて先進的な研究を行っています。

  • Mass Spec
    質量分析装置

  • Cell culture
    細胞培養

  • Microscope
    顕微鏡

ARTICLE

N6-methyladenosine (m6A) is an endogenous A3 adenosine receptor ligand.
Ogawa A, Nagiri C, Shihoya W, Inoue A, Kawakami K, Hiratsuka S, Aoki J, Ito Y, Suzuki T, Suzuki T, Inoue T, Nureki O, Tanihara H, Tomizawa K, Wei FY.
Mol Cell. 81(4):659-674.e7. 2021.
URL:https://pubmed.ncbi.nlm.nih.gov/33472058/

Loss of Ftsj1 perturbs codon-specific translation efficiency in the brain and is associated with X-linked intellectual disability.
Nagayoshi Y, Chujo T, Hirata S, Nakatsuka H, Chen CW, Takakura M, Miyauchi K, Ikeuchi Y, Carlyle BC, Kitchen RR, Suzuki T, Katsuoka F, Yamamoto M, Goto Y, Tanaka M, Natsume K, Nairn AC, Suzuki T, Tomizawa K, Wei FY.
Sci Adv. 7(13):eabf3072. 2021
URL:https://pubmed.ncbi.nlm.nih.gov/33771871/

Ogawa A and Wei FY.
Protocol for preparation and measurement of intracellular and extracellular modified RNA using liquid chromatography-mass spectrometry.
STAR Protoc. in press. 2021

Cdk5rap1-mediated 2-methylthio modification of mitochondrial tRNAs governs protein translation and contributes to myopathy in mice and humans.
Wei FY, Zhou B, Suzuki T, Miyata K, Ujihara Y, Horiguchi H, Takahashi N, Xie P, Michiue H, Fujimura A, Kaitsuka T, Matsui H, Koga Y, Mohri S, Suzuki T, Oike Y, Tomizawa K.
Cell Metab. 21(3):428-42. 2015
URL:https://pubmed.ncbi.nlm.nih.gov/25738458/

Deficit of tRNA(Lys) modification by Cdkal1 causes the development of type 2 diabetes in mice.
Wei FY, Suzuki T, Watanabe S, Kimura S, Kaitsuka T, Fujimura A, Matsui H, Atta M, Michiue H, Fontecave M, Yamagata K, Suzuki T, Tomizawa K.
J Clin Invest. 121(9):3598-608. 2011
URL:https://pubmed.ncbi.nlm.nih.gov/21841312/

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