JAK-STAT SIGNALING INDUCED BY THE V-ABL ONCOGENE
JAK-STAT SIGNALING INDUCED BY THE V-ABL ONCOGENE
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DOI：
10.1126/science.7569929
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发表时间：
1995-09-29
期刊：
影响因子：
56.9
通讯作者：
ROTHMAN, PB
中科院分区：
文献类型：
--
作者：
DANIAL, NN;PERNIS, A;ROTHMAN, PB
研究了Abelson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）Jak 1和Jak 3表现出组成性酪氨酸激酶活性，通常由白细胞介素-4激活的STAT蛋白（信号转导和转录激活因子）酸化，并且在不存在这些细胞因子的情况下，白细胞介素-7被酪氨酸磷酸化。免疫共沉淀实验显示，在这些细胞中，V-Abl与Jak 1和Jak 3物理相关。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性Jak-STAT信号传导的消除。v-abl转化与细胞因子信号转导之间可能存在直接联系。
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, acid 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.