Mig6 Antibody #2440

Mig6 was identified as a gene which is induced when quiescent fibroblasts are treated by mitogens (1). During cell cycle progression, Mig6 expression levels are also regulated (1). Mig6 mRNA levels were found to increase upon stimulation by chronic stresses including diabetic nephropathy (2). Overexpression of this gene leads to the activation of stress-activated protein kinases (SAPKs)/c-Jun amino-terminal kinases (JNKs) (2). Furthermore, Mig6 was found to interact with epidermal growth factor receptor (EGFR) when stimulated by epidermal growth factor (EGF) (3). Deletion of the Mig6 gene in mice results in hyperactivation of EGFR and signaling through the mitogen-activated protein kinase (MAPK) pathway, causing overproliferation and abnormal differentiation of epidermal keratinocytes in these animals. Inhibition of endogenous EGFR signaling by Iressa abolished skin defects observed in Mig6^(-/-) mice, indicating that Mig6 is a specfic negative regulator of EGFR signaling (4). Furthermore, expression of Mig6 was significantly lower in skin, breast, pancreatic and ovarian cancers, suggesting a role of Mig6 as a tumor suppressor (4).