Differences in sequences encoding the carboxyl-terminal domain of the epidermal growth factor receptor correlate with differences in the disease potential of viral erbB genes.
Differences in sequences encoding the carboxyl-terminal domain of the epidermal growth factor receptor correlate with differences in the disease potential of viral erbB genes.
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编码表皮生长因子受体羧基末端结构域的序列差异与病毒 erbB 基因疾病潜力的差异相关。
DOI：
10.1073/pnas.83.16.6053
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发表时间：
1986
影响因子：
11.1
通讯作者：
Robinson,HL
中科院分区：
文献类型：
--
作者：
Gamett,DC;Tracy,SE;Robinson,HL
最近分离出的11种erbB转导病毒以及禽成红细胞增多症病毒（AEV）-R（ES 4）和AEV-H已被表征为它们引起的疾病类型、它们转化培养物中成纤维细胞的能力、它们在不同的鸡谱系中引起疾病的能力。对erbB诱导的成红细胞增多症的易感性及其erbB基因的结构。每个生物学参数的差异与编码表皮生长因子受体（EGFR）C-末端结构域的erbB序列的差异相关。7种病毒在诱导成红细胞增多症的能力方面受到菌株限制，并且不转化成纤维细胞。这7种病毒含有编码EGFR完整C末端的v-erbB基因。AEV-R和AEV-H诱导成红细胞增多症的能力没有家系限制，并能转化成纤维细胞。这些病毒含有v-erbB基因，该基因缺少EGFR C末端的密码子。三种病毒引起血管肉瘤，一种引起纤维肉瘤。血管肉瘤和纤维肉瘤诱导病毒没有菌株限制，不会引起成红细胞增多症。这些病毒中的每一种的v-erbB基因在编码EGFR的C-末端结构域的序列中含有广泛的内部缺失或3'截短。
Eleven recently isolated erbB-transducing viruses as well as avian erythroblastosis virus (AEV)-R (ES4) and AEV-H have been characterized for the type of disease they cause, their ability to transform fibroblasts in culture, their ability to cause disease in pedigrees of chicken that differ in susceptibility to erbB-induced erythroblastosis, and the structure of their erbB genes. Differences in each of the biological parameters correlated with differences in erbB sequences encoding the C-terminal domain of the epidermal growth factor receptor (EGFR). Seven viruses were strain restricted in their ability to induce erythroblastosis and did not transform fibroblasts. These seven viruses contained v-erbB genes encoding the complete C terminus of the EGFR. AEV-R and AEV-H were not pedigree restricted in their ability to induce erythroblastosis and could transform fibroblasts. These viruses contain v-erbB genes that lack codons for the immediate C terminus of the EGFR. Three viruses caused angiosarcoma and one caused fibrosarcoma. The angiosarcoma and fibrosarcoma-inducing viruses were not strain restricted and did not cause erythroblastosis. The v-erbB genes of each of these viruses contained extensive internal deletions or 3' truncations in sequences encoding the C-terminal domain of the EGFR.