C-erbB and the epidermal growth-factor receptor: a molecule with dual identity.
C-erbB and the epidermal growth-factor receptor: a molecule with dual identity.
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C-erbB 和表皮生长因子受体：具有双重身份的分子。
DOI：
10.1016/0304-419x(89)90003-6
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Kung,HJ
中科院分区：
文献类型：
--
作者：
Maihle,NJ;Kung,HJ
在20世纪70年代末和80年代初，很明显，负责细胞转化的急剧转化的逆转录病毒(病毒癌基因，v-onc)的基因序列实际上是通过一种称为转导的过程盗取的正常细胞序列[1，2]。这一概念的演变迅速引起了相当大量的细胞“原癌”序列的鉴定，即与急性转化病毒的癌基因同源的细胞序列(参见。裁判。因此，c-erbB最初被确定为逆转录病毒转化基因o-erbB的细胞同源物[5]。两种急性转化的逆转录病毒，AEV-ES4和AEV-R，自本世纪初以来一直被研究，是病毒erbB序列的原始来源[6-8]。这两种禽类红细胞增生症病毒可能代表了一个几乎相同的病毒株的独立分离株。这两种病毒都表达两种病毒癌基因：v-erba和v-erbB。这两个癌基因显然是在独立的重组事件中捕获的，v-erba与v-erbB没有(结构上连锁或)相关，当独立表达时也不是致癌的，尽管它可以增强v-erbB介导的转化事件[9-13]。尽管o-erba产物对转化表型的贡献目前还不清楚，但很明显，该癌基因的细胞同源基因是类固醇激素受体家族的成员，而禽类c-erba产物似乎在功能上与人类T3受体等同[14，15]。相反，v-erbB产物的表达足以在体外转化红细胞和成纤维细胞，并在体内诱导红白血病和纤维肉瘤[9，16，17]。对v-erbB的细胞同源物的鉴定揭示了一个跨越20kb以上的基因组序列的大基因[18]。在鉴定正常的细胞erbB同源物之后，很快观察到病毒erbB产物与部分人表皮生长因子受体之间的结构同源性[19]。进一步的结构分析表明，正常的禽类c-erbB产物与人表皮生长因子受体在结构上是同源的。20-22；和未发表的数据)，而禽类c-erbB产物可能代表这种生长因子受体的功能等价物。在这项研究中，我们比较了致癌产物的结构和功能特性与正常受体的特性。由于人类EGF受体的特性已被广泛回顾[23-25]，在本报告中，我们重点介绍禽类致癌产物的特性。我们还严格地研究了激活这种生长因子受体致癌潜能的分子机制，最后，考虑了这些分子传递的正常和异常有丝分裂信号所涉及的可能的作用模式。
During the late 1970s and early 1980s, it became apparent that'the genetic sequences of acutely transforming retroviruses responsible for cellular transformation (viral oncogenes, v-onc) were actually normal cellular sequences pirated via a process known as transduction [1, 2]. The evolution of this concept quickly gave rise to the identification of a fairly large number of cellular'proto-oncogenic'sequences, ie, cellular sequences homologous to the oncogenes of the acutely transforming viruses (cf. Refs. 3 and 4 for reviews), c-erbB was, therefore, originally identified as the cellular homolog of the retroviral transforming gene, o-erbB [5]. Two acutely transforming retroviruses, AEV-ES4 and AEV-R, which have been studied since the early part of this century, were the original source of viral erbB sequences [6-8]. These two avian erythroblastosis viruses probably represent independent isolates of a virtually identical viral strain. Both of these viruses express two viral oncogenes: v-erbA and v-erbB. These two'oncogenes' were apparently captured during independent recombination events, v-erbA is not (structurally linked or) related to v-erbB, and is not oncogenic when expressed independently, although it can augment v-erbB-mediated transformation events [9-13]. Although the contribution of the o-erbA product to the transformed phenotype is poorly understood at this time, it is clear that the cellular homolog of this oncogene is a member of the steroid hormone receptor family and the avian c-erbA product appears to be functionally equivalent to the human T 3 receptor [14, 15]. In contrast, expression of the v-erbB product is sufficient to transform both erythroblasts and fibroblasts in vitro, and to induce erythroleukemia and fibrosarcomas, in vivo [9, 16, 17]. Identification of the cellular homolog of v-erbB has revealed a large gene spanning greater than 20 kb of genomic sequence [18]. Identification of the normal cellular erbB homolog was rapidly followed by the observation of structural homology between the viral erbB product and a portion of the human epidermal growth-factor receptor [19]. Further structural analyses have revealed that the normal avian c-erbB product and the human epidermal growth-factor receptor are structurally homologous (Refs. 20-22; and unpublished data), and the avian c-erbB product may represent a functional equivalent of this growthfactor receptor.In this study, we compare the structural and functional properties of the oncogenic products to the properties of the normal receptor. Since the properties of the human EGF receptor have been reviewed extensively [23-25] in this report, we emphasize the properties of the avian oncogenic products. We also critically examine the molecular mechanisms involved in activating the oncogenic potential of this growth-factor receptor, and finally, consider the possible modes of action involved in relaying both the normal and aberrant mitogenic signals propagated by these molecules.
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胰岛素受体的蛋白酪氨酸激酶活性对于胰岛素介导的受体下调是必需的。
DOI：
--
发表时间：
1987
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Russell,DS;Gherzi,R;Johnson,EL;Chou,CK;Rosen,OM
通讯作者：
Rosen,OM
用于将外源脱氧核糖核酸序列插入禽种系的逆转录病毒载体的设计。
影响因子：
4.4
作者：
S. Hughes;E. Kosik;A. Fadly;D. Salter;L. Crittenden
通讯作者：
L. Crittenden
功能性表皮生长因子的内化：A-431 细胞中的受体/激酶复合物。
影响因子：
4.8
作者：
S. Cohen;R. Fava
通讯作者：
R. Fava
表皮生长因子受体的自磷酸化和蛋白激酶 C 磷酸化。
DOI：
10.1016/s0021-9258(17)38602-7
发表时间：
1985
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
J. Downward;M. Waterfield;P. Parker
通讯作者：
P. Parker
与禽成红细胞增多症病毒癌基因 erbB 相关的鸡 DNA 位点的分子克隆和表征。
影响因子：
11.4
作者：
A. Sergeant;S. Saule;D. Leprince;A. Begue;C. Rommens;D. Stéhelin
通讯作者：
D. Stéhelin