Special Feature

User Panel

My Panel

My Panel

Bookmark Science Articles

Recent News
Bookmark / Share This Science Site

Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses.

Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

  • Abstract Text of This Paper
  • Journal Published
  • MeSH Keywords of This Abstract
  • Chemicals and Substances Used in this Paper
  • Grants and Granting Agency of this Research
  • Database Accession Numbers Used in this Paper
  • Related Papers
  • Related Research Tags
  • Rate this Research Paper
  • Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses. Abstract Text:

    manchao zhangManchao Zhang,youping dengYouping Deng,ruchi tandonRuchi Tandon,cheng baiCheng Bai,heimo riedelHeimo Riedel,manchao zhangManchao Zhang,youping dengYouping Deng,ruchi tandonRuchi Tandon,cheng baiCheng Bai,heimo riedelHeimo Riedel,

    The positive regulatory role of PSM/SH2-B downstream of various mitogenic receptor tyrosine kinases or gene disruption experiments in mice support a role of PSM in the regulation of insulin action. Here, four alternative PSM splice variants and individual functional domains were compared for their role in the regulation of specific metabolic insulin responses. We found that individual PSM variants in 3T3-L1 adipocytes potentiated insulin-mediated glucose and amino acid transport, glycogenesis, lipogenesis, and key components in the metabolic insulin response including p70 S6 kinase, glycogen synthase, glycogen synthase kinase 3 (GSK3), Akt, Cbl, and IRS-1. Highest activity was consistently observed for PSM alpha, followed by beta, delta, and gamma with decreasing activity. In contrast, dominant-negative peptide mimetics of the PSM Pro-rich, pleckstrin homology (PH), or src homology 2 (SH2) domains inhibited any tested insulin response. Potentiation of the insulin response originated at the insulin receptor (IR) kinase level by PSM variant-specific regulation of the K(m) (ATP) whereas the V(max) remained unaffected. IR catalytic activation was inhibited by peptide mimetics of the PSM SH2 or dimerization domain (DD). Either peptide should disrupt the complex of a PSM dimer linked to IR via SH2 domains as proposed for PSM activation of tyrosine kinase JAK2. Either peptide abolished downstream insulin responses indistinguishable from PSM siRNA knockdown. Our results implicate an essential role of the PSM variants in the activation of the IR kinase and the resulting metabolic insulin response. PSM variants act as internal IR ligands that in addition to potentiating the insulin response stimulate IR catalytic activation even in the absence of insulin. J. Cell. Biochem. 103: 162-181, 2008. (c) 2007 Wiley-Liss, Inc.

    Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses. Publishing Authors By Initials

    m zhangM Zhang,y dengY Deng,r tandonR Tandon,c baiC Bai,h riedelH Riedel,m zhangM Zhang,y dengY Deng,r tandonR Tandon,c baiC Bai,h riedelH Riedel,

    For similar abstracts research abstracts see: abstracts research

    PUBMED ID PMID:

    MEDLINE DATE:

    Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Journal of cellular biochemistry

    VOLUME: 103

    Page Numbers: 162-81

    Journal Abbreviation: J. Cell. Biochem.

    ISSN: 0730-2312

    DAY: 1

    MONTH: Jan

    YEAR: 2008

    Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8205768

    Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses. Keywords Mesh Terms:

    KEYWORDS:

    MESH TERMS:

    Chemical & Substance for Abstract: Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses. Information

    Substance Name:

    Registry Number:

    Grant and Affiliation Information for Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses.

    AFFILIATION: Department of Biochemistry, West Virginia University, School of Medicine, Morgantown, West Virginia 26506-9142.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY:

    GRANT:

    ACRONYM:

    MEDLINETA: J Cell Biochem

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

    Essential role of PSM/SH2-B variants in insulin receptor catalytic activation and the resulting cellular responses Related Publications

     

    Molecular Station USER Menu

    Welcome to Molecular Station!

    You have to register before you can post on our forums or use our advanced features. Register Now! Its Free and Fast!

    Already registered? Login now below.

    User Name:

    Password:

    Already registered and Forgot your password? Click below to recover it.

    Recover Lost Password

    Join now - it's fast and free!

    Molecular Station is THE largest network of researchers, scientists and science lovers anywhere!

    Research Terms of Usage and Disclaimer
    Home
    Features

    Protocols

    DNA Forum

    Science Forum

    DNA Forum
    Biology Forum

    Science News


    [CaRP] XML error: Invalid document end at line 2

    For more click here:Science News