Regulation of mononuclear phagocyte proliferation by colony-stimulating factor-1.
Regulation of mononuclear phagocyte proliferation by colony-stimulating factor-1.
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集落刺激因子 1 对单核吞噬细胞增殖的调节。
DOI：
10.1002/stem.5530080706
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Sherr,CJ
中科院分区：
文献类型：
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作者：
Sherr,CJ
集落刺激因子-1（CSF-1或M-CSF）调节巨噬细胞及其定向骨髓祖细胞的多效性发育和功能反应，并支持单核吞噬细胞谱系细胞的活力。其作用是通过与细胞表面CSF-1受体（CSF-1 R）结合介导的，CSF-1 R表现出配体刺激的酪氨酸激酶活性。CSF-1 R诱导的细胞内蛋白底物磷酸化启动了一系列生化反应，将信号传递到细胞核，引发CSF-1应答基因的转录，并最终导致细胞分裂。CSF-1 R激酶的作用可通过某些单克隆抗体与受体胞外结构域的结合或通过激活蛋白激酶C并加速受体转换的药物中断。CSF-1 R由c-fms原癌基因编码，组成性激活受体激酶的特定遗传改变为细胞生长提供持续信号，从而导致细胞转化。因此，c-fms原癌基因的结构或表达的扰动可能导致白血病。
Colony‐stimulating factor‐1 (CSF‐1 or M‐CSF) regulates pleiotropic developmental and functional responses of macrophages and their committed bone marrow progenitors and supports the viability of cells of the mononuclear phagocyte lineage. Its actions are mediated through its binding to cell surface CSF‐1 receptors (CSF‐1R) that exhibit ligand‐stimulated tyrosine kinase activity. CSF‐1R‐induced phosphorylation of intracellular protein substrates initiates a cascade of biochemical reactions that relay signals to the cell nucleus, elicit transcription of CSF‐1‐responsive genes and culminate in cell division. The actions of the CSF‐1R kinase can be interrupted by binding of certain monoclonal antibodies to the extracellular domain of the receptor or by agents which activate protein kinase C and accelerate receptor turnover. CSF‐1R is encoded by the c‐fmsproto‐oncogene, and specific genetic alterations, which constitutively activate the receptor kinase, provide sustained signals for cell growth leading to cell transformation. Perturbations in the structure or expression of the c‐fmsproto‐oncogene might therefore contribute to leukemia.