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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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