RET Protein, Mouse (HEK293, His)

RET protein is a receptor tyrosine-protein kinase that plays a crucial role in various cellular processes, including cell proliferation, neuronal navigation, cell migration, and cell differentiation when it binds with glial cell-derived neurotrophic factor family ligands. It phosphorylates PTK2/FAK1 and regulates the balance between cell death and survival, as well as positional information. During intestine organogenesis, RET protein is essential for coordinating molecular mechanisms and is involved in the development of the enteric nervous system and renal organogenesis in embryonic life. Additionally, it promotes the formation of Peyer's patch-like structures, which are vital components of the gut-associated lymphoid tissue. RET protein modulates cell adhesion through its cleavage by caspase in sympathetic neurons and facilitates cell migration in an integrin-dependent manner, involving proteins such as ITGB1 and ITGB3. Furthermore, RET protein is implicated in the development of the neural crest. In the absence of ligand, it exhibits activity that triggers apoptosis via receptor intracellular caspase cleavage. Moreover, RET protein acts as a dependence receptor, promoting survival and downregulating growth hormone production in somatotrophs when the ligand GDNF is present, but inducing apoptosis in the absence of GDNF. It also regulates nociceptor survival and size and triggers the differentiation of rapidly adapting mechanoreceptors. In various diseases, such as neuroendocrine cancers, RET protein acts as a mediator by modulating cell migration regulated by aberrant integrins. Additionally, RET protein interacts with the GDF15-receptor GFRAL in the brainstem to mediate GDF15-induced cell signaling, leading to the inhibition of food intake. Furthermore, RET protein activates the MAPK and AKT signaling pathways.