首页> 外文期刊>Molecular and Cellular Biology >P21 v-ras inhibits induction of c-myc and c-fos expression by platelet-derived growth factor.
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P21 v-ras inhibits induction of c-myc and c-fos expression by platelet-derived growth factor.

机译:P21 v-ras抑制血小板衍生生长因子诱导c-myc和c-fos表达。

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The viral oncogene v-ras inhibited the platelet-derived growth factor (PDGF)-induced upregulation of c-myc and c-fos proto-oncogene expression in fibroblast monolayers. These v-ras-containing cells proliferated in the absence of c-myc induction and no longer required PDGF to support growth. Fibroblasts expressing v-ras continued to express the same number of functional PDGF receptors on their surface as uninfected cells, yet the usual induction of transcription of the genes c-myc, c-fos, and JE in response to PDGF stimulation did not occur in the presence of newly introduced v-ras or chronic v-ras gene expression, and synthesis of c-myc protein did not occur. This inhibitory effect on growth factor-mediated induction of cellular proto-oncogenes was specific for PDGF in that induction of the c-myc and c-fos genes by certain other factors was not impaired.
机译:病毒癌基因v-ras抑制了血小板衍生生长因子(PDGF)诱导的成纤维细胞单层c-myc和c-fos原癌基因表达上调。这些不含v-ras的细胞在不存在c-myc诱导的情况下增殖,不再需要PDGF支持生长。表达v-ras的成纤维细胞继续在其表面上表达与未感染细胞相同数量的功能性PDGF受体,但是在2000年,并未发生响应于PDGF刺激而通常诱导的基因c-myc,c-fos和JE转录。新引入的v-ras或慢性v-ras基因表达的存在以及c-myc蛋白的合成均未发生。这种对生长因子介导的细胞原癌基因诱导的抑制作用对PDGF是特异性的,因为某些其他因子对c-myc和c-fos基因的诱导不会受到损害。

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