RET is a receptor tyrosine-protein kinase involved in diverse cellular processes, including cell proliferation, migration, differentiation, and neuronal navigation. Unlike most receptor tyrosine kinases, RET activation requires both its ligands—GDNF family growth factors (GDNF, NRTN, ARTN, PSPN, and GDF15)—and their respective coreceptors (GFRA1, GFRA2, GFRA3, GFRA4, and GFRAL). Ligand-coreceptor binding triggers RET autophosphorylation and activates downstream signaling pathways such as MAPK and AKT.
In somatotrophs, RET functions as a dependence receptor via GDNF-GFRA1 signaling, promoting cell survival and downregulating growth hormone production in the presence of GDNF but inducing apoptosis in its absence. RET is essential for intestinal organogenesis through ARTN-GFRA3 signaling, contributing to enteric nervous system development, renal organogenesis, and Peyer’s patch formation during embryogenesis. In the brainstem, RET mediates GDF15-GFRAL signaling, inducing aversive responses like nausea and appetite loss in response to stress.
RET modulates cell adhesion and migration through integrins (e.g., ITGB1 and ITGB3) and caspase-dependent cleavage in sympathetic neurons. It also triggers apoptosis in a ligand-independent manner via caspase cleavage. Additionally, RET supports the differentiation of rapidly adapting mechanoreceptors, neural crest development, nociceptor survival and size regulation, and phosphorylates PTK2/FAK1, further emphasizing its role in cellular and developmental regulation.
| Product Name | Recombinant Human RET Protein (His Tag) |
| Accession | P07949 |
| Host Species | Human |
| Gene | RET |
| Source | HEK293 |
