E3 ubiquitin ligases in ErbB receptor quantity control.
E3 ubiquitin ligases in ErbB receptor quantity control.
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DOI：
10.1016/j.semcdb.2010.09.006
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发表时间：
2010-12
影响因子：
7.3
通讯作者：
Carraway KL 3rd
中科院分区：
文献类型：
--
作者：
Carraway KL 3rd
通过ErbB家族生长因子受体酪氨酸激酶的信号传导对于多种组织类型的发育和稳态是必需的。然而，受体介导的细胞信号传导的强度必须在精确的范围内;信号传导不足可导致发育异常或组织萎缩，而过度信号传导可导致增生和最终肿瘤事件。虽然已经描述了调节下游信号传导事件的过多机制，但似乎细胞也利用各种机制来调节其ErbB受体水平。此类机制统称为“ErbB受体数量控制”。值得注意的是，过去几年的研究强调了转录后过程，特别是蛋白质降解在ErbB数量控制中的作用。在这里讨论了ErbB定向的E3泛素连接酶的参与，包括Nrdp 1介导的ErbB 3降解，Nedd 4家族E3连接酶介导的ErbB 4降解和CHIP介导的ErbB 2降解。提出的假设是，蛋白质降解为基础的ErbB的数量控制机制发挥核心作用，在正常细胞中抑制受体过表达，这种机制的损失可能会促进ErbB依赖性肿瘤的发病或进展。
Signaling through ErbB family growth factor receptor tyrosine kinases is necessary for the development and homeostasis of a wide variety of tissue types. However, the intensity of receptor-mediated cellular signaling must fall within a precise range; insufficient signaling can lead to developmental abnormalities or tissue atrophy, while over-signaling can lead to hyperplastic and ultimately neoplastic events. While a plethora of mechanisms have been described that regulate downstream signaling events, it appears that cells also utilize various mechanisms to regulate their ErbB receptor levels. Such mechanisms are collectively termed “ErbB receptor quantity control.” Notably, studies over the past few years have highlighted roles for post-transcriptional processes, particularly protein degradation, in ErbB quantity control. Here the involvement of ErbB-directed E3 ubiquitin ligases is discussed, including Nrdp1-mediated ErbB3 degradation, ErbB4 degradation mediated by Nedd4 family E3 ligases, and CHIP-mediated ErbB2 degradation. The hypothesis is forwarded that protein degradation-based ErbB quantity control mechanisms play central roles in suppressing receptor overexpression in normal cells, and that the loss of such mechanisms could facilitate the onset or progression of ErbB-dependent tumors.
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影响因子：
3.8
作者：
Gerbin, Candice S.;Landgraf, Ralf
通讯作者：
Landgraf, Ralf
DOI：
10.1073/pnas.91.17.8132
发表时间：
1994-08-16
影响因子：
11.1
作者：
GUY, PM;PLATKO, JV;CARRAWAY, KL
通讯作者：
CARRAWAY, KL
影响因子：
3.7
作者：
Fry WH;Kotelawala L;Sweeney C;Carraway KL 3rd
通讯作者：
Carraway KL 3rd
影响因子：
3.7
作者：
Blobel CP;Carpenter G;Freeman M
通讯作者：
Freeman M
影响因子：
56.9
作者：
Cadwell, K;Coscoy, L
通讯作者：
Coscoy, L