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    National Tsing Hua University Institutional Repository > 生命科學院  > 生命科學系 > 期刊論文 >  Adapter protein SH2-B beta undergoes nucleocytoplasmic shuttling: Implications for nerve growth factor induction of neuronal differentiation


    Please use this identifier to cite or link to this item: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/49058


    Title: Adapter protein SH2-B beta undergoes nucleocytoplasmic shuttling: Implications for nerve growth factor induction of neuronal differentiation
    Authors: Chen, LY;Carter-Su, C
    教師: 陳令儀
    Date: 2004
    Publisher: American Society for Microbiology
    Relation: MOLECULAR AND CELLULAR BIOLOGY,American Society for Microbiology,Volume 24,Issue 9,MAY 2004,Pages 3633-3647
    Keywords: INSULIN-RECEPTOR KINASE
    SIGNAL-REGULATED KINASE
    RHO-FAMILY GTPASES
    PC12 CELLS
    NUCLEAR TRANSLOCATION
    PHOSPHATIDYLINOSITOL 3-KINASE
    TRANSCRIPTION FACTOR
    NEURITE OUTGROWTH
    COMPLEX-FORMATION
    SCAFFOLD PROTEIN
    Abstract: The adapter protein SH2-B has been shown to bind to activated nerve growth factor (NGF) receptor TrkA and has been implicated in NGF-induced neuronal differentiation and the survival of sympathetic neurons. However, the mechanism by which SH2-B enhances and maintains neurite outgrowth is unclear. We examined the ability of truncation mutants to regulate neuronal differentiation and observed that certain truncation mutants localized in the nucleus rather than in the cytoplasm or at the plasma membrane as reported for wild-type SH2-Bbeta. Addition of the nuclear export inhibitor leptomycin B caused both overexpressed wild-type and endogenous SH2-Bbeta to accumulate in the nucleus of both PC12 cells and COS-7 cells as did deletion of a putative nuclear export sequence (amino acids 224 to 233) or mutation of two critical lysines in that sequence. Deleting or mutating the nuclear export signal caused SH2-Bbeta to lose its ability to enhance NGF-induced differentiation of PC12 cells. Neither the NGF-induced phosphorylation of ERKs 1 and 2 nor their subcellular distribution was altered in PC12 cells stably expressing the nuclear export-defective SH2-Bbeta(L231A, L233A). These data provide strong evidence that SH2-Bbeta shuttles constitutively between the nucleus and cytoplasm. However, SH2-Bbeta needs continuous access to the cytoplasm and/or plasma membrane to participate in NGF-induced neurite outgrowth. These data also suggest that the stimulatory effect of SH2-Bbeta on NGF-induced neurite outgrowth of PC12 cells is either downstream of ERKs or via some other pathway yet to be identified.
    URI: http://www.asm.org/
    http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/49058
    Appears in Collections:[生命科學系] 期刊論文

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