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JAK2与c-kit原癌基因产物相关,并在干细胞因子的作用下发生磷酸化。

JAK2 is associated with the c-kit proto-oncogene product and is phosphorylated in response to stem cell factor.

作者信息

Weiler S R, Mou S, DeBerry C S, Keller J R, Ruscetti F W, Ferris D K, Longo D L, Linnekin D

机构信息

Division of Cancer Treatment, and Biological Carcinogenesis and Development Program, SAIC Frederick, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702, USA.

出版信息

Blood. 1996 May 1;87(9):3688-93.

PMID:8611693
Abstract

Stem cell factor (SCF) is a hematopoietic growth factor that interacts with the receptor tyrosine kinase, c-kit. We have found that SCF-stimulates rapid and transient tyrosine phosphorylation of JAK2 in human and murine cell lines, as well as in normal human progenitor cells. JAK2 and c-kit were associated in unstimulated cells with further recruitment of JAK2 to the c-kit receptor complex after SCF stimulation. Treatment of cells with JAK2 antisense oligonucleotides resulted in a 46% decrease in SCF-induced proliferation. These data demonstrate that SCF induces tyrosine phosphorylation of JAK2 and suggest that JAK2 is a component of the SCF signal transduction pathway.

摘要

干细胞因子(SCF)是一种造血生长因子,它与受体酪氨酸激酶c-kit相互作用。我们发现,SCF可刺激人源和鼠源细胞系以及正常人祖细胞中JAK2的快速和瞬时酪氨酸磷酸化。在未受刺激的细胞中,JAK2与c-kit相关联,SCF刺激后JAK2会进一步募集到c-kit受体复合物中。用JAK2反义寡核苷酸处理细胞会导致SCF诱导的增殖减少46%。这些数据表明,SCF可诱导JAK2的酪氨酸磷酸化,并提示JAK2是SCF信号转导途径的一个组成部分。

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1
JAK2 is associated with the c-kit proto-oncogene product and is phosphorylated in response to stem cell factor.JAK2与c-kit原癌基因产物相关,并在干细胞因子的作用下发生磷酸化。
Blood. 1996 May 1;87(9):3688-93.
2
JAK2 is constitutively associated with c-Kit and is phosphorylated in response to stem cell factor.JAK2 与 c-Kit 持续相关,并在干细胞因子的作用下发生磷酸化。
Acta Haematol. 1996;95(3-4):224-8. doi: 10.1159/000203882.
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Stat1 associates with c-kit and is activated in response to stem cell factor.信号转导和转录激活因子1(Stat1)与原癌基因c-kit相关联,并在对干细胞因子的反应中被激活。
Biochem J. 1997 Oct 1;327 ( Pt 1)(Pt 1):73-80. doi: 10.1042/bj3270073.
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Stem cell factor synergistically enhances thrombopoietin-induced STAT5 signaling in megakaryocyte progenitors through JAK2 and Src kinase.干细胞因子通过JAK2和Src激酶协同增强血小板生成素诱导的巨核细胞祖细胞中的STAT5信号传导。
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Co-stimulation with stem cell factor and erythropoietin enhances migration of c-Kit expressing cervical cancer cells through the sustained activation of ERK1/2.干细胞因子和促红细胞生成素共同刺激通过持续激活ERK1/2增强表达c-Kit的宫颈癌细胞的迁移。
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Lyn associates with the juxtamembrane region of c-Kit and is activated by stem cell factor in hematopoietic cell lines and normal progenitor cells.Lyn与c-Kit的近膜区域相关联,并在造血细胞系和正常祖细胞中被干细胞因子激活。
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Stem cell factor induces phosphorylation of a 200 kDa protein which associates with c-kit.干细胞因子诱导一种与c-kit相关的200 kDa蛋白质的磷酸化。
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JAK2 contributes to the intrinsic capacity of primary hematopoietic cells to respond to stem cell factor.
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Modulation of Kit/stem cell factor receptor-induced signaling by protein kinase C.蛋白激酶C对Kit/干细胞因子受体诱导信号传导的调节
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The receptor protein tyrosine phosphatase, PTP-RO, is upregulated during megakaryocyte differentiation and Is associated with the c-Kit receptor.受体蛋白酪氨酸磷酸酶PTP-RO在巨核细胞分化过程中上调,并与c-Kit受体相关。
Blood. 1999 Jul 15;94(2):539-49.

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