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Cdc42 (show CDC42 Proteins) inhibition is required for Mig-6 suppression of cell migration induced by EGF (show EGF Proteins)
ectopic expression of Gene 33 triggers DNA damage response in an ATM serine/threonine kinase (ATM)-dependent fashion and through pathways dependent or not dependent on ABL proto-oncogene 1 non-receptor tyrosine kinase (c-Abl).
our data suggest that dormant cancer cells with a high MIG6 expression level might be one of the causes of EGFR (show EGFR Proteins)-TKI resistance in EGFR (show EGFR Proteins) mutant lung cancer cells.
Down-regulation of Mig-6 induces Cyclin D1 (show CCND1 Proteins) expression and activates the MAPK-ERK (show MAPK1 Proteins) signaling pathway. Our study shows that the expression of Mig-6 protein is low in hepatocellular carcinoma, which predicts a poor prognosis.
PIPKIgammai5, NEDD4-1 (show NEDD4 Proteins), and Mig6 form a novel molecular nexus that controls EGFR (show EGFR Proteins) activation and downstream signaling.
Low MIG6 expression is associated with lung cancer.
MIG6 down regulation may promote the migration and invasiveness of MEK (show MAP2K1 Proteins) inhibited mutant NRAS (show NRAS Proteins) melanoma.
MIG6 is a potent tumor suppressor for mutant EGFR (show EGFR Proteins)-driven lung tumor initiation and progression in mice and provides a possible mechanism by which mutant EGFR (show EGFR Proteins) can partially circumvent this tumor suppressor in human lung adenocarcinoma.
Crystal structures of human EGFR (show EGFR Proteins)-Mig6 complexes show how Mig6 rearranges after phosphorylation by EGFR (show EGFR Proteins) to effectively irreversibly inhibit the same receptor that catalyzed its phosphorylation.
MIG-6 efficiently reduces cellular transformation driven by oncogenic BRAF (show BRAF Proteins) by orchestrating a negative feedback circuit directed towards the EGFR (show EGFR Proteins).
Studies indicate that progesterone receptor transgenic (Pgrcre/+) mitogen inducible gene 6 (Mig-6over) phosphatase and tensin homolog protein (Ptenf/f) knockout mice exhibited an increase of phospho-ERK1/2 and its target genes.
mouse Mig-6 ablation in the liver results in multiple metabolic phenotypes such as fatty liver, fasting hyperglycemia, and hypercholesterolemia but in lower bodyweight and improved insulin (show INS Proteins) sensitivity.
Liver-specific ablation of Mig-6 caused hyperglycemia by hepatic insulin (show INS Proteins) resistance.
This microarray analysis also revealed that 324 genes are regulated by P4 as well as Mig-6. Cited2 (show CITED2 Proteins), the developmentally important transcription factor, was identified as being regulated by the P4-Mig-6 axis
Mig-6 plays a critical role in the development of atherosclerosis.
our findings suggest that Mig-6 regulates ERK1/2 phosphorylation and that it is crucial for progression of PTEN-mutant endometrial cancers, providing a mechanistic rationale for the evaluation of ERK1/2 inhibitors
MIG-6 expression in chondrocytes is important for the maintenance of cartilage and joint homeostasis.
Cartilage-specific deletion of Mig-6 results in osteoarthritis-like disorder with excessive articular chondrocyte proliferation.
This treatment had no effect in PR(cre/+)Mig-6(f/f) mice where Mig-6 was deleted in both the epithelial and stromal compartments of the uterus.
Fibroblast growth factor signaling requires Xmig6 for muscle differentiation in Xenopus embryos. Fibroblast growth factor signaling may involve XGPCR4 (show GPR84 Proteins) in gastrulation.
ERRFI1 is a cytoplasmic protein whose expression is upregulated with cell growth (Wick et al., 1995
mitogen-inducible gene 6 protein
, receptor-associated late transducer
, mitogen-inducible gene 6 protein homolog
, gene 33 polypeptide
, ERBB receptor feedback inhibitor 1
, mitogen-inducible gene 6-like protein
, ERBB receptor feedback inhibitor 1-like