RET Protein, Human, Recombinant (aa 658-1114, His & GST)

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.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy

Pack Size	Availability	Price/USD	Quantity
50 μg	5 days	$ 498.00

Description

Species	Human
Expression System	Baculovirus-Insect Cells
Tag	His,GST
Accession Number	P07949-1
Synonyms	HSCR1, RET51, CDHR16, RET-ELE1, ret proto-oncogene, MEN2A, PTC, MTC1, CDHF12, MEN2B
Construction	A DNA sequence encoding the cytoplasmic domain of human RET (P07949-1) (His 658-Ser 1114) was fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.
Protein Purity	> 90 % as determined by SDS-PAGE
Molecular Weight	76.7 kDa (predicted)

Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Formulation	Supplied as sterile 20mM Tris, 500mM NaCl, 10% gly, pH 8.0. Pleasecon tact usfor any concerns or special requirements. Please refer to the specific buffer information in the hard copy of CoA.
Reconstitution	A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.
Stability & Storage	Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Shipping	Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice. Shipment made at ambient temperature may seriously affect the activity of the ordered products.
Research 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.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy