IndraLab
Statements
reach
"Interaction of RET protein with its ligands (glial cell derived neurotrophic factor (GDNF), neurturin (NRTN), and artemin (ARTN)) and its co-receptors (GDNF receptor alpha proteins (GFRα1-4)) activates the Phosphoinositide-3-kinase-protein kinase B (PI3K-PKB/AKT), RAS mitogen-activated protein kinase (RAS/MAPK) and phospholipase Cγ (PLCγ) signaling pathways, which control the survival, migration, proliferation, differentiation, and maturation of the vagal and sacral neural crest cells into enteric neurons."
reach
"Previous studies have shown that a subset of ERalpha positive breast cancers express high levels of mRNA transcripts encoding RET and that RET signaling in ERalpha positive breast cancer cell lines can result in the activation of MAPK and AKT, which are important regulators of ERalpha phosphorylation [XREF_BIBR, XREF_BIBR]."
"Activation of RET, either by ligand or through specific mutations, results in phosphorylation of multiple tyrosine residues that, in turn, interact with specific adaptor molecules to trigger downstream signaling. Four of the tyrosines phosphorylated on RET activation, tyrosines 905, 1015, 1062, and 1096, have been well characterized, and are known to interact with a number of adaptor molecules to stimulate signaling through phosphatidylinositol kinase (PI3K)/AKT, PLC-gamma, RAS/extracellular signal-regulated kinase (ERK), p38MAPK, JNK and ERK5."