Rchr
J-GLOBAL ID:201601008661079880   Update date: Jan. 31, 2024

Yamashita Takayuki

Yamashita Takayuki
Affiliation and department:
Research field  (1): Pathobiochemistry
Research keywords  (19): Stress signal, cell senescence, oncogenesis, DNA damage, DNA repair, genomic stability, mutagenesis, aging, molecular chaperone ,  molecular chaperone ,  aging ,  mutagenesis ,  genomic stability ,  DNA repair ,  DNA damage ,  oncogenesis ,  cell senescence ,  Stress signal ,  分子シャペロン ,  加齢 ,  変異発生 ,  ゲノム安定性 ,  DNA修復 ,  DNA損傷 ,  発がん ,  細胞老化 ,  ストレスシグナル
Research theme for competitive and other funds  (35):
  • 2019 - 2021 発がんシグナル誘導性複製ストレスへの応答機構を標的とする治療開発
  • 2015 - 2018 Molecular basis for the development of anti-tumor therapy by targeting HSF1.
  • 2015 - 2018 The role of Y-family polymerase in aberrant DNA replication and genomic instability
  • 2015 - 2018 Analysis of oncogene-induced replication stress response patyways
  • 2013 - 2015 がん遺伝子が誘導する複製ストレス応答におけるY-familyポリメラーゼの役割
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Papers (60):
  • Tsukasa Oda, Ruri Nakamura, Tetsuhiro Kasamatsu, Nanami Gotoh, Keiko Okuda, Takayuki Saitoh, Hiroshi Handa, Hirokazu Murakami, Takayuki Yamashita. DNA-double strand breaks enhance the expression of major histocompatibility complex class II through the ATM-NF-κΒ-IRF1-CIITA pathway. Cancer Gene Therapy. 2021
  • Kiminori Kurashima, Takayuki Sekimoto, Tsukasa Oda, Tsuyoshi Kawabata, Fumio Hanaoka, Takayuki Yamashita. Polη, a Y-family translesion synthesis polymerase, promotes cellular tolerance of Myc-induced replication stress. Journal of cell science. 2018. 131. 12
  • Tsukasa Oda, Takayuki Sekimoto, Kiminori Kurashima, Mitsuaki Fujimoto, Akira Nakai, Takayuki Yamashita. Acute HSF1 depletion induces cellular senescence through the MDM2-p53-p21 pathway in human diploid fibroblasts. Journal of Cell Science. 2018. 131. 9
  • 山下孝之. Fanconi貧血の疾患概念・病因・病態. 日本臨床(増刊号)「貧血学」. 2017. 75. 増刊1
  • 山下 孝之. 血液今昔物語-Fanconi貧血. 血液フロンティア. 2015. 25. 12
more...
MISC (111):
  • Tsukasa Oda, Takayuki Sekimoto, Kiminori Kurashima, Mitsuaki Fujimoto, Akira Nakai, Takayuki Yamashita. Acute HSF1 depletion induces cellular senescence through the MDM2-p53-p21 pathway in human diploid fibroblasts. Journal of Cell Science. 2018. 131. 9. UNSP jcs210724
  • Kurashima, Kiminori, Sekimoto, Takayuki, Oda, Tsukasa, Kawabata, Tsuyoshi, Hanaoka, Fumio, Yamashita, Takayuki. Polη, a Y-family translesion synthesis polymerase, promotes cellular tolerance of Myc-induced replication stress. JOURNAL OF CELL SCIENCE. 2018. 131. 12. UNSP jcs.212183
  • Oda, Tsukasa, Sekimoto, Takayuki, Kurashima, Kiminori, Fujimoto, Mitsuaki, Nakai. Akira, Yamashita, Takayuki. Acute HSF1 depletion induces cellular senescence through the MDM2-p53-p21 pathway in human diploid fibroblasts. JOURNAL OF CELL SCIENCE. 2018. 131. 9. UNSP jcs210724
  • Kurashima, Kiminori, Sekimoto, Takayuki, Oda, Tsukasa, Kawabata, Tsuyoshi, Hanaoka, Fumio, Yamashita, Takayuki. Polη, a Y-family translesion synthesis polymerase, promotes cellular tolerance of Myc-induced replication stress. JOURNAL OF CELL SCIENCE. 2018. 131. 12. UNSP jcs.212183
  • 山下孝之. Fanconi貧血の疾患概念・病因・病態. 日本臨床(増刊号)「貧血学」. 2017. 75. 増刊1. 409-413
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Books (18):
  • 血液病学
    3013
  • 「白血病学」Fanconi貧血
    2016
  • 特発性造血障害の疾患診療ガイド
    2013
  • 鉄代謝・骨髄機能不全 Fanconi貧血の分子病態 最近の進歩(解説)
    臨床血液 2009
  • Diamond-Blackfan貧血とリボソーム(解説)
    血液・腫瘍科 2009
more...
Lectures and oral presentations  (62):
  • がん遺伝子誘導性Replication Stress (RS) への応答におけるRAD51を介するフォーク保護機構の役割
    (2018)
  • メルファランはATM-NFkB-IRF1-CIITA経路を介して多発性骨髄腫細胞株に主要組織適合クラスIIの発現を誘導する
    (第41回日本分子生物学会年会 2018)
  • Pol-eta a member of Y-family DNA polymerases prevents generation of DNA double strand breaks induced by c-myc expression
    (2015)
  • Heat shock factor 1 (HSF1) 抑制による老化誘導機構は細胞種により異なり、またHSPs非依存的である
    (2015)
  • Y-family損傷乗り越えDNAポリメラーゼの一員Pol-etaはMYCがん遺伝子の誘導する複製ストレスを軽減する
    (2015)
more...
Education (2):
  • - 1980 University of Tokyo Faculty of Medicine
  • - 1980 The University of Tokyo Faculty of Medicine School of Medicine
Professional career (1):
  • Ph. D. (Kobe University)
Work history (1):
  • Gunma University
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