Molecular mechanism analysis of STAT activation in breast tumor cells regulated by adaptor protein

2016 Fiscal Year Final Research Report

• Project/Area Number: 26440016
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Structural biochemistry
• Research Institution: Hokkaido University
• Principal Investigator: OSE Toyoyuki 北海道大学, 薬学研究院, 准教授 (80380525)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 蛋白質

Outline of Final Research Achievements

The non-receptor tyrosine kinase breast tumor kinase (Brk), has been identified as a highly expressed Protein-tyrosine kinases in human melanocyte. Brk was reported to play key roles for cancer progression via overactivation of Signal Transducers and Activator of Transcription (STAT), especially STAT3 and STAT5. This activation is mediated by an adaptor protein STAP-2, which expresses ubiquitously and harobors many important functions for cell signal regulation. We successfully expressed recombinant Brk and STAP-2 including their mutants, checked kinase activity, monitored interactions, and structurally analyzed using small angle x-ray scattering (SAXS). The C-terminal phosphorylation site of Brk is, on the contrary to our expectation, didn’t produce open/close conformational change.

Free Research Field

構造生物化学