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摘要:
The Ca 2+-binding protein of the EF-hand type,S100B,exerts both intracellular and extracellular regulatory activities.As an intracellular regulator,S100B is involved in the regulation of energy metabolism,transcription,protein phosphorylation,cell proliferation,survival,differentiation and motility,and Ca 2+ homeostasis,by interacting with a wide array of proteins(i.e.,enzymes,enzyme substrates,cytoskeletal subunits,scaffold/adaptor proteins,transcription factors,ubiquitin E3 ligases,ion channels) in a restricted number of cell types.As an extracellular signal,S100B engages the pattern recognition receptor,receptor for advanced glycation end-products(RAGE),on immune cells as well as on neuronal,astrocytic and microglial cells,vascular smooth muscle cells,skeletal myoblasts and cardiomyocytes.However,RAGE may not be the sole receptor activated by S100B,the protein being able to enhance bFGF-FGFR1 signaling by interacting with FGFR1-bound bFGF in particular cell types.Moreover,extracellular effects of S100B vary depending on its local concentration.Increasing evidence suggests that at the concentration found in extracellular fluids in normal physiological conditions and locally upon acute tissue injury,which is up to a few nM levels,S100B exerts trophic effects in the central and peripheral nervous system and in skeletal muscle tissue thus participating in tissue homeostasis.The present commentary summarizes results implicating intracellular and extracellular S100B in tissue development,repair and regeneration.
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篇名 S100B protein in tissue development,repair and regeneration
来源期刊 世界生物化学杂志:英文版(电子版) 学科 医学
关键词 S100B CELL proliferation CELL differentiation CELL survival CELL MOTILITY DEVELOPMENT TISSUE homeostasis TISSUE REPAIR TISSUE REGENERATION
年,卷(期) 2013,(1) 所属期刊栏目
研究方向 页码范围 1-12
页数 12页 分类号 R341
字数 语种
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S100B
CELL
proliferation
CELL
differentiation
CELL
survival
CELL
MOTILITY
DEVELOPMENT
TISSUE
homeostasis
TISSUE
REPAIR
TISSUE
REGENERATION
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研究分支
研究去脉
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相关学者/机构
期刊影响力
世界生物化学杂志:英文版(电子版)
季刊
1949-8454
北京市朝阳区东四环中路62号楼远洋国际中
出版文献量(篇)
391
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0
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0
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