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  • 标题:Ras is an indispensable coregulator of the class IB phosphoinositide 3-kinase p87/p110γ
  • 本地全文:下载
  • 作者:Barbara Kurig ; Aliaksei Shymanets ; Thomas Bohnacker
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:2009
  • 卷号:106
  • 期号:48
  • 页码:20312-20317
  • DOI:10.1073/pnas.0905506106
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:Class IB phosphoinositide 3-kinase {gamma} (PI3K{gamma}) elicits various immunologic and cardiovascular responses; however, the molecular basis for this signal heterogeneity is unclear. PI3K{gamma} consists of a catalytic p110{gamma} and a regulatory p87PIKAP (p87, also p84) or p101 subunit. Hitherto p87 and p101 are generally assumed to exhibit redundant functions in receptor-induced and G protein {beta}{gamma} (G{beta}{gamma})-mediated PI3K{gamma} regulation. Here we investigated the molecular mechanism for receptor-dependent p87/p110{gamma} activation. By analyzing GFP-tagged proteins expressed in HEK293 cells, PI3K{gamma}-complemented bone marrow-derived mast cells (BMMCs) from p110{gamma}-/- mice, and purified recombinant proteins reconstituted to lipid vesicles, we elucidated a novel pathway of p87-dependent, G protein-coupled receptor (GPCR)-induced PI3K{gamma} activation. Although p101 strongly interacted with G{beta}{gamma
  • 关键词:confocal life cell imaging ; G protein ; receptor signaling ; mast cells
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