Analysis of the onset mechanism of myeloproliferative neoplasms by the quantitative phosphorylation proteome analysis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460073
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Keio University
• Principal Investigator: TAGO MEGUMI 慶應義塾大学, 薬学部, 准教授 (30445192)
• Co-Investigator(Renkei-kenkyūsha): SUGIYAMA NAOYUKI 京都大学, 薬学部, 准教授 (50545704)
• Research Collaborator: Ueda Fumihito
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: JAK2V617F変異体 / 定量的リン酸化プロテオーム解析 / 慢性骨髄増殖性腫瘍

Outline of Final Research Achievements

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.

Free Research Field

シグナル伝達