Grb2 interacts with SGEF and antagonizes the ability of SGEF to enhance EGF-induced ERK1/2 activation
Grb2 interacts with SGEF and antagonizes the ability of SGEF to enhance EGF-induced ERK1/2 activation
复制标题
Grb2 与 SGEF 相互作用并拮抗 SGEF 增强 EGF 诱导的 ERK1/2 激活的能力。
DOI：
10.1007/s11010-013-1945-7
复制
发表时间：
2014-04-01
影响因子：
4.3
通讯作者：
Zhou, Jianguang
中科院分区：
文献类型：
--
作者：
Wang, Hongtao;Li, Shanhu;Zhou, Jianguang
以前，我们证明了SGEF增强EGFR的稳定性;然而，SGEF介导的EGFR下游信号传导尚未得到很好的理解。在这里，我们表明，SGEF增强EGF诱导的ERK 1/2激活独立的鸟嘌呤核苷酸交换（GEF）的活动。我们进一步表明，SGEF与Grb 2相互作用，Grb 2是EGFR的关键下游转导子。令人惊讶的是，我们发现Grb 2与SGEF的相互作用拮抗SGEF增强EGF诱导的ERK 1/2活化的能力。总之，这项研究报告了SGEF的一种新功能，排除了GEF，并为Grb 2在EGFR信号转导中的复杂作用提供了重要的见解。
Previously, we demonstrated that SGEF enhances EGFR stability; however, SGEF-mediated downstream signaling of EGFR is not well understood. Here, we show that SGEF enhances EGF-induced ERK1/2 activation independent of its guanine nucleotide exchange (GEF) activity. We further show that SGEF interacts with Grb2, a critical downstream transducer of EGFR. Surprisingly, we found that interaction of Grb2 to SGEF antagonizes the ability of SGEF to enhance EGF-induced ERK1/2 activation. Taken together, this study reports a novel function of SGEF that excludes GEF and also provides important insights into the complex role of Grb2 in EGFR signal transduction.