Protein tyrosine kinases in granulocyte colony stimulating factor receptor signal transduction, myeloid cell proliferation, and neutrophil activation.

Protein tyrosine kinases in granulocyte colony stimulating factor receptor signal transduction, myeloid cell proliferation, and neutrophil activation.
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粒细胞集落刺激因子受体信号转导、骨髓细胞增殖和中性粒细胞激活中的蛋白酪氨酸激酶。

DOI:
10.1016/s0024-3205(96)00697-2
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发表时间:
1997
期刊:
影响因子:
6.1
通讯作者:
Moore,MA
Moore,MA
中科院分区:
医学2区
文献类型:
--
作者:
Deshpande,RV;Peterson,RH;Moore,MA

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Granulocyte colony-stimulating factor (G-CSF) plays an important role in the growth and maturation of granulocytic precursor cells. Although the interaction between G-CSF and its receptor (G-CSF-R) is an obligatory event during proliferation and differentiation of myeloid cells, the signal transduction mechanisms leading to these effects are not completely known. We investigated the kinetics of protein tyrosine kinase (PTK) activation in G-CSF-R signal transduction in myeloid leukemic cell lines and peripheral blood neutrophils. G-CSF treatment of myeloid cell-lines (HL-60, KG-1, NFS-60) and neutrophils resulted in a rapid increase in PTK activity. This induction was inhibited by an anti-G-CSF monoclonal antibody and various PTK-specific inhibitors. PTK activity was important for proliferation of myeloid cells; its inhibition resulted in decreased proliferation and clonogenicity of these cells. PTK-induction was not involved in G-CSF-R expression, internalization or recycling, but was partially responsible for up-regulation of CD11b expression on neutrophils. In contrast to neutrophilic cell-lines, the myelo-monocytic cell lines (U-937, WEHI-3B) showed no change in PTK levels in response to G-CSF. The results indicate that the G-CSF-R-mediated PTK up-regulation may be a neutrophil-lineage-restricted signal, and that PTK may play an important role in the proliferation of neutrophil-precursors and functional activation of mature neutrophils.
Lavendustin-A及其类似物抑制表皮生长因子受体酪氨酸激酶的动力学分析。
DOI: 10.1016/s0021-9258(18)54826-2
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DOI: --
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