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KAKEN_25460073seika.pdf
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定量的リン酸化プロテオーム解析による慢性骨髄増殖性腫瘍の発症機序の解析
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テイリョウテキ リンサンカ プロテオーム カイセキ ニ ヨル マンセイ コツズイ ゾウショクセイ シュヨウ ノ ハツショウ キジョ ノ カイセキ
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Teiryoteki rinsanka puroteomu kaiseki ni yoru mansei kotsuzui zoshokusei shuyo no hatsusho kijo no kaiseki
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Analysis of the onset mechanism of myeloproliferative neoplasms by the quantitative phosphorylation proteome analysis
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多胡, めぐみ
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タゴ, メグミ
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Tago, Megumi
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慶應義塾大学・薬学部・准教授
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Research team head
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科研費研究者番号 : 30445192
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杉山, 直幸
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スギヤマ, ナオユキ
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Sugiyama, Naoyuki
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京都大学・薬学部・准教授
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Research team member
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科研費研究者番号 : 50545704
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上田, 史仁
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ウエダ, フミヒト
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Ueda, Fumihito
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Research team member
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2016
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科学研究費補助金研究成果報告書
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2015
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チロシンキナーゼJAK2の点変異体(V617F)は, 慢性骨髄増殖性腫瘍の原因遺伝子である。JAK2V617F変異体は恒常的な活性化型であり, 異常な細胞増殖や腫瘍形成を誘導することが知られているが, JAK2V617F変異体が誘導する発がんシグナルの分子機構は不明である。JAK2V617F変異体が誘導する発がんシグナルを理解するには, JAK2V617F変異体の下流における全てのシグナル分子の状態変化を同時に網羅的に解析する必要がある。本研究では, 定量的リン酸化プロテオーム解析を行い, JAK2V617F変異体の下流でリン酸化される分子を同定し, それらの発がんシグナルにおける役割を解析した。
A somatic mutation (V617F) in tyrosine kinase JAK2 was found in the majority of myeloproliferative neoplasm (MPN) patients. It has been shown that the JAK2 V617F mutant was constitutively active and induced the cytokine-independent cell proliferation and tumorigenesis, suggesting that it behaves as a potent oncogene product. However, the molecular mechanism how JAK2 V617F mutant induces cellular transformation has not been elucidated. To clarify the molecular mechanism of JAK2 V617F mutant-induced transformation, it is necessary to analyze the states of all signal molecules at the downstream of JAK2 V617F mutant at the same time. Therefore, we performed quantitative phosphoproteome analysis to identify the phosphorylated proteins at downstream of JAK2 V617F mutant and analyze the roles of these molecules.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2013～2015
課題番号 : 25460073
研究分野 : シグナル伝達
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