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首页> 外文期刊>Molecular and Cellular Biology >Tyrosine kinase oncogenes abrogate interleukin-3 dependence of murine myeloid cells through signaling pathways involving c-myc: conditional regulation of c-myc transcription by temperature-sensitive v-abl.
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Tyrosine kinase oncogenes abrogate interleukin-3 dependence of murine myeloid cells through signaling pathways involving c-myc: conditional regulation of c-myc transcription by temperature-sensitive v-abl.

机译：酪氨酸激酶致癌基因通过涉及c-myc的信号传导途径消除了小鼠骨髓细胞的白介素3依赖性：温度敏感的v-abl对c-myc转录的条件调节。

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摘要

Retroviral expression vectors carrying the tyrosine kinase oncogenes abl, fms, src, and trk abrogate the requirements of murine myeloid FDC-P1 cells for interleukin-3 (IL-3). Factor-independent clones constitutively express c-myc in the absence of IL-3, whereas in parental cultures c-myc transcription requires the presence of the ligand. To directly test the effect of a tyrosine kinase oncogene on c-myc expression, retroviral constructs containing three different temperature-sensitive mutants of v-abl were introduced into myeloid IL-3-dependent FDC-P1 and 32D cells. At the permissive temperature, clones expressing temperature-sensitive abl behaved like wild-type abl-containing cells in their growth properties and expressed c-myc constitutively. Temperature shift experiments demonstrated that both IL-3 abrogation and the regulation of c-myc expression correlated with the presence of functional v-abl. Induction of c-myc expression by reactivation of temperature-sensitive v-abl mimicked c-myc induction by IL-3 in that it did not require protein synthesis and occurred at the level of transcription, with effects on both initiation and a transcription elongation block. However, v-abl-regulated FDC-P1 cell growth differed from IL-3-regulated growth in that c-fos and junB, which are normally induced by IL-3, were not induced by activation of v-abl.
机译：携带酪氨酸激酶癌基因abl，fms，src和trk的逆转录病毒表达载体消除了鼠髓样FDC-P1细胞对白介素3（IL-3）的需求。不依赖因子的克隆在没有IL-3的情况下组成性表达c-myc，而在亲代培养中，c-myc转录需要配体的存在。为了直接测试酪氨酸激酶致癌基因对c-myc表达的影响，将包含三种不同的v-abl温度敏感突变体的逆转录病毒构建体引入到依赖髓样IL-3的FDC-P1和32D细胞中。在允许的温度下，表达温度敏感性abl的克隆的生长特性类似于包含野生型abl的细胞，并组成性表达c-myc。温度变化实验表明，IL-3的废除和c-myc表达的调节均与功能性v-abl的存在有关。通过重新激活温度敏感的v-abl模拟IL- 3诱导的c-myc诱导来诱导c-myc表达，因为它不需要蛋白质合成，并且在转录水平上发生，对起始和转录延伸阻滞都有影响。但是，v-abl调节的FDC-P1细胞生长与IL-3调节的生长不同，因为通常由IL-3诱导的c-fos和junB不能通过v-abl的活化来诱导。

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