RET
RET (ret proto-oncogene, also known as PTC, CDHF12, RET51, CDHR16, HSCR1, MEN2A, MTC1 and MEN2B) is a transmembrane receptor tyrosine kinase. It transduces signals from GDNF and related ligands to regulate cell differentiation, growth, migration and survival. Browse Assay Genie's current range of RET research reagents below, or read on for the biology behind the target.
RET is a transmembrane receptor that belongs to the protein kinase superfamily and the Tyr protein kinase family, with the enzyme classification EC 2.7.10.1. Binding of ligands such as GDNF (glial cell-line derived neurotrophic factor) and other related proteins stimulates receptor dimerisation and activation of downstream signalling pathways. These pathways play a role in cell differentiation, growth, migration and survival. In the UniProt record, the RET protein localises to the cell membrane and to endosome membranes.
The RET gene is important in development of the nervous system and of organs and tissues derived from the neural crest. UniProt also notes that RET acts in complex with GFRAL: isoform 1 in complex with GFRAL induces higher activation of the MAPK signalling pathway than isoform 2 in complex with GFRAL. This makes isoform composition a relevant consideration when studying RET signalling output.
RET is a proto-oncogene that can undergo oncogenic activation through both cytogenetic rearrangement and activating point mutations. Mutations in the gene are associated with Hirschsprung disease and central hypoventilation syndrome, and have been identified in patients with renal agenesis. The alias list reflects this history: HGNC records previous names of multiple endocrine neoplasia and medullary thyroid carcinoma 1, and Hirschsprung disease 1, which correspond to the symbols MEN2A, MEN2B, MTC1 and HSCR1. HGNC places RET in the cadherin related and Ret proto-oncogene gene groups.
RET is important in development of the nervous system and of organs and tissues derived from the neural crest.
RET can be activated oncogenically through cytogenetic rearrangement and activating point mutations, making it a study subject in cancer biology.
Ligand binding, including GDNF, drives RET dimerisation and downstream pathways controlling differentiation, growth, migration and survival.
Mutations in RET are associated with Hirschsprung disease and central hypoventilation syndrome, and have been found in patients with renal agenesis.
RET is a transmembrane receptor tyrosine kinase. Ligands such as GDNF and related proteins stimulate its dimerisation and activation, triggering downstream pathways that influence cell differentiation, growth, migration and survival. It is important in development of the nervous system and neural crest-derived tissues.
RET has aliases including PTC, CDHF12, RET51, CDHR16, HSCR1, MEN2A, MTC1 and MEN2B. Previous names include multiple endocrine neoplasia and medullary thyroid carcinoma 1, and Hirschsprung disease 1, reflecting the disease associations of the gene. UniProt also describes isoforms 1 and 2.
Mouse and rat both have a Ret ortholog, so the receptor is studied in rodent models; check the datasheet of any product for its validated reactivity. In humans, RET mutations are associated with Hirschsprung disease and central hypoventilation syndrome, and the gene can be oncogenically activated.
Ligands, co-receptors and other signalling proteins linked to RET biology, with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P07949; product specifications from Assay Genie datasheets.