ERBB2 信号通路中的 PI3K 事件
中文名称
通路描述
ERBB2:ERBB3 和 ERBB2:ERBB4 异二聚体通过直接结合 PI3K 调节亚基 p85 磷酸化的 C 端酪氨酸残基 (ERBB3 的 Y1054, Y1197, Y1222, Y1224, Y1276 和 Y1289; JM-A CYT1 异构体的 Y1056 和 JM-B CYT1 异构体的 Y1046) 激活 PI3K 信号通路。调节亚基 p85 随后招募 PI3K 催化亚基 p110，形成活性 PI3K，将 PIP2 转化为 PIP3，并介导 AKT 信号通路的激活 (Junttila et al. 2009, Kainulainen et al. 2000)。ERBB2 和 EGFR 的异二聚体间接招募 PI3K，通过 GRB2:GAB1 复合物 (Jackson et al. 2004)，再次导致 PIP3 介导的 AKT 信号通路激活。
英文描述
PI3K events in ERBB2 signaling ERBB2:ERBB3 and ERBB2:ERBB4cyt1 heterodimers activate PI3K signaling by direct binding of PI3K regulatory subunit p85 (Yang et al. 2007, Cohen et al. 1996, Kaushansky et al. 2008) to phosphorylated tyrosine residues in the C-tail of ERBB3 (Y1054, Y1197, Y1222, Y1224, Y1276 and Y1289) and ERBB4 CYT1 isoforms (Y1056 in JM-A CYT1 isoform and Y1046 in JM-B CYT1 isoform). Regulatory subunit p85 subsequently recruits catalytic subunit p110 of PI3K, resulting in the formation of active PI3K, conversion of PIP2 to PIP3, and PIP3-mediated activation of AKT signaling (Junttila et al. 2009, Kainulainen et al. 2000). Heterodimers of ERBB2 and EGFR recruit PI3K indirectly, through GRB2:GAB1 complex (Jackson et al. 2004), which again leads to PIP3-mediated activation of AKT signaling.
所含基因
13 个基因