IRS2是致癌基因，编码蛋白胰岛素受体底物2（IRS2）是细胞内胰岛素受体（INSR）信号传导的媒介之一。激活INSR后，IRS2被磷酸化并被激活，导致对AKT和MAPK通路的激活。IRS2的失调导致肥胖和糖尿病，IRS2缺陷会损害大脑的生长。IRS1在鳞状细胞癌等多个肿瘤实体中具有致癌功能，IRS1高表达IRS1与不良预后有关。Nedd4诱导的泛素化或IRS2增强了IGF信号级联及其有丝分裂活性。在大肠癌中观察到IRS2扩增，这增加了抗EGFR治疗的易感性。

IRS2 (Insulin receptor substrate 2) is one of the mediators of Insulin receptor (INSR) signalling in cells. Upon activation of INSR, IRS2 is phosphorylated and activated leading to the activation of the AKT and MAPK pathway. Dysregulation or IRS2 leads to obesity and diabetes and IRS2 deficiency impairs brain growth. IRS1 has oncogenic functions in multiple tumor entities such as squamous cell carcinoma and high IRS1 expression is associated with adverse prognosis. Nedd4-induced ubiquitination or IRS2 enhances IGF signalling and its mitotic activity. IRS2 amplifications have been observed in colorectal cancer which result in increased susceptibility to anti-EGFR therapy.

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