RET Proteins, Antibodies, cDNA Clones Research Reagents

RET (Ret Proto-Oncogene) is a protein coding gene located on human chromosome 10q11.21. RET is also known as PTC, MTC1, HSCR1, MEN2A, MEN2B, CDHF12, CDHR16 and RET-ELE1. The human RET gene encodes a 124319 Da protein containing 1114 amino acids. Biased expression in adrenal (RPKM 10.2), prostate (RPKM 1.3) and 9 other tissues Among its related pathways are Neuroscience and GDNF-Family Ligands and Receptor Interactions. RET is related to calcium ion binding and protein kinase activity. FLT4 is an important paralog of RET gene. RET is associated with some diseases, including Multiple Endocrine Neoplasia, Type Iia and Thyroid Carcinoma, Familial Medullary.

RET Protein (2)

    RET Antibody (4)

      RET cDNA Clone (16)


      In cloning vector

      In lentiviral vector


      In expression vector

      RET qPCR Primer (1)

      RET Lysate (2)

        RET Background

        RET proto-oncogene, also known as RET, is a cell-surface molecule that transduce signals for cell growth and differentiation. It contains 1 cadherin domain and 1 protein kinase domain. RET proto-oncogene belongs to the protein kinase superfamily, tyr protein kinase family. RET proto-oncogene is involved in numerous cellular mechanisms including cell proliferation, neuronal navigation, cell migration, and cell differentiation upon binding with glial cell derived neurotrophic factor family ligands. It phosphorylates PTK2/FAK1 and regulates both cell death/survival balance and positional information. RET is required for the molecular mechanisms orchestration during intestine organogenesis; involved in the development of enteric nervous system and renal organogenesis during embryonic life; promotes the formation of Peyer's patch-like structures; modulates cell adhesion via its cleavage; involved in the development of the neural crest. RET proto-oncogene is active in the absence of ligand, triggering apoptosis. RET acts as a dependence receptor; in the presence of the ligand GDNF in somatotrophs (within pituitary), promotes survival and downregulates growth hormone (GH) production, but triggers apoptosis in absence of GDNF. It also regulates nociceptor survival and size; triggers the differentiation of rapidly adapting (RA) mechanoreceptors; mediated several diseases such as neuroendocrine cancers. Defects in RET may cause colorectal cancer, hirschsprung disease type 1, medullary thyroid carcinoma, multiple neoplasia type 2B, susceptibility to pheochromocytoma, multiple neoplasia type 2A, thyroid papillary carcinoma and congenital central hypoventilation syndrome.

        RET References

        • Schulten HJ, et al. (2011) Mutational screening of RET, HRAS, KRAS, NRAS, BRAF, AKT1, and CTNNB1 in medullary thyroid carcinoma. Anticancer Res. 31(12):4179-83.
        • Ciampi R, et al. (2012) Chromosome 10 and RET gene copy number alterations in hereditary and sporadic Medullary Thyroid Carcinoma. Mol Cell Endocrinol. 348(1):176-82.
        • Garcia-Lavandeira M, et al. (2012) Craniopharyngiomas express embryonic stem cell markers (SOX2, OCT4, KLF4, and SOX9) as pituitary stem cells but do not coexpress RET/GFRA3 receptors. J Clin Endocrinol Metab. 97(1):E80-7.
        • Stine ZE, et al. (2011) Steroid hormone modulation of RET through two estrogen responsive enhancers in breast cancer. Hum Mol Genet. 20(19):3746-56.
        • Sharma BP, et al. (2011) RET gene mutations and polymorphisms in medullary thyroid carcinomas in Indian patients. J Biosci. 36(4):603-11.

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