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首页> 外文期刊>Cellular Signalling >ErbB2 and ErbB4 Cbl binding sites can functionally replace the ErbB1 Cbl binding site
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ErbB2 and ErbB4 Cbl binding sites can functionally replace the ErbB1 Cbl binding site

机译：ErbB2和ErbB4 Cbl结合位点可以在功能上替代ErbB1 Cbl结合位点

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摘要

Poor downregulation of ErbB receptors is associated with enhanced downstream signaling and tumorigenesis. It has been suggested that poor downregulation of ErbB-2, -3 and -4 receptors when compared to ErbB1 is due to decreased recruitment of Cbl E3 ligase proteins. However, a highly conserved Cbl binding site is not only present in ErbB1/EGFR (FLQRpY(1045)SSDP), but also in ErbE12 (PLQRpY(1091)SEDP) and ErbB4 (STQRpY(1103)SADP). We therefore replaced the ErbB1 Cbl binding site by that of ErbB2 and ErbB4. Whereas retrovirally infected NIH3T3 cells containing the EGFR Y1045F mutation showed dramatically impaired Cbl recruitment, EGFR ubiquitination and delayed EGFR degradation, replacement of the EGFR Cbl binding site by that of ErbB2 or ErbB4 did not affect Cbl recruitment, receptor-ubiquitination, -degradation, -downregulation or ligand degradation. We conclude that poor downregulation of ErbB2 and ErbB4 receptors is not due to sequence variations in the Cbl binding site of these receptors.
机译：ErbB受体的下调不良与下游信号传导增强和肿瘤发生有关。已经提出，与ErbB1相比，ErbB-2，-3和-4受体的不良下调是由于Cbl E3连接酶蛋白的募集减少。但是，高度保守的Cbl结合位点不仅存在于ErbB1 / EGFR（FLQRpY（1045）SSDP）中，而且还存在于ErbE12（PLQRpY（1091）SEDP）和ErbB4（STQRpY（1103）SADP）中。因此，我们用ErbB2和ErbB4替换了ErbB1 Cbl结合位点。含有EGFR Y1045F突变的逆转录病毒感染的NIH3T3细胞显示Cbl募集显着受损，EGFR泛素化和EGFR降解延迟，而用ErbB2或ErbB4取代EGFR Cbl结合位点则不影响Cbl募集，受体泛素化，-降解，-下调或配体降解。我们得出的结论是，ErbB2和ErbB4受体的不良下调不是由于这些受体的Cbl结合位点的序列变异引起的。

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