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由v-abl癌基因诱导的Jak-STAT信号传导。

Jak-STAT signaling induced by the v-abl oncogene.

作者信息

Danial N N, Pernis A, Rothman P B

机构信息

Integrated Program in Molecular, Cellular, and Biophysical Studies, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

出版信息

Science. 1995 Sep 29;269(5232):1875-7. doi: 10.1126/science.7569929.

Abstract

The effect of the v-abl oncogene of the Abelson murine leukemia virus (A-MuLV) on the Jak-STAT pathway of cytokine signal transduction was investigated. In murine pre-B lymphocytes transformed with A-MuLV, the Janus kinases (Jaks) Jak1 and Jak3 exhibited constitutive tyrosine kinase activity, and the STAT proteins (signal transducers and activators of transcription) normally activated by interleukin-4 and interleukin-7 were tyrosine-phosphorylated in the absence of these cytokines. Coimmunoprecipitation experiments revealed that in these cells v-Abl was physically associated with Jak1 and Jak3. Inactivation of v-Abl tyrosine kinase in a pre-B cell line transformed with a temperature-sensitive mutant of v-abl resulted in abrogation of constitutive Jak-STAT signaling. A direct link may exist between transformation by v-abl and cytokine signal transduction.

摘要

研究了阿贝尔森鼠白血病病毒(A-MuLV)的v-abl癌基因对细胞因子信号转导的Jak-STAT途径的影响。在用A-MuLV转化的小鼠前B淋巴细胞中,Janus激酶(Jaks)Jak1和Jak3表现出组成型酪氨酸激酶活性,并且通常由白细胞介素-4和白细胞介素-7激活的STAT蛋白(信号转导子和转录激活子)在没有这些细胞因子的情况下被酪氨酸磷酸化。免疫共沉淀实验表明,在这些细胞中v-Abl与Jak1和Jak3物理结合。在用v-abl的温度敏感突变体转化的前B细胞系中,v-Abl酪氨酸激酶的失活导致组成型Jak-STAT信号传导的废除。v-abl介导的转化与细胞因子信号转导之间可能存在直接联系。

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