Smad-mediated spliceosome assembly and alternative splicing

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670168
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Pathological medical chemistry
• Research Institution: Showa Pharmaceutical University
• Principal Investigator: SAKATA Nobuo 昭和薬科大学, 薬学部, 講師 (00170598)
• Co-Investigator(Kenkyū-buntansha): ITOH Susumu 昭和薬科大学, 薬学部, 教授 (70223154)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: Alternative splicing / Smad / LUC7L3 / JMJD6

Outline of Final Research Achievements

We examined the possibility that Smads, TGF-β signal transducer, are involved in the alternative splicing events producing splice variants. Among Smad binding proteins identified in proteomic analysis, we analyzed the interaction of LUC7L3, spliceosome components, and Smads by the co-immunoprecipitation (Co-IP) method in detail. Otherwise, the binding of these molecules was not identified. Therefore, we tested the interaction of JMJD6 and Smads, because JMJD6 are involved in alternative splicing and interacted with LUC7L3. JMJD6 was successfully interacted with Smad2 and Smad3 by the analysis of Co-IP. Further study is needed, which will be shed light on a new scheme of Smads and alternative splicing.

Free Research Field

薬学