Danial N N, Pernis A, Rothman P B
Integrated Program in Molecular, Cellular, and Biophysical Studies, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Science. 1995 Sep 29;269(5232):1875-7. doi: 10.1126/science.7569929.
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.
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。
