Name :
Recombinant Human RET Protein (aa 658-1114, His & GST Tag)
Biological Activity :
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 Immunotherapy Immune Checkpoint Immunotherapy Targeted Therapy
Biological Activity :
The specific activity was determined to be 17 nmol/min/mg using synthetic TRK-C-derived Peptide (R11-VYSTDYYRLFNPS) as substrate.
Expression Host :
Human
Source :
Baculovirus-Insect Cells
Tag :
Protein Accession No. :
P07949-1
NCBI Gene ID :
Synonyms :
Synonyms :
ret proto-oncogene
Amino Acid Sequence :
Molecular Weight :
The recombinant human RET (aa 658-1114)/GST chimera consists of 694 amino acids and has a calculated molecular mass of 76.7 kDa. It migrates as an approximately 70 kDa band in SDS-PAGE under reducing conditions.
Purity :
> 90 % as determined by SDS-PAGE
State of Matter :
Product Concentration :
Storage and Stability :
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.
Endotoxin Level :
< 1.0 EU per μg of the protein as determined by the LAL method
Protein 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.
Buffer Solution :
Supplied as sterile 20mM Tris, 500mM NaCl, 10% gly, pH 8.0Please contact us for any concerns or special requirements.Please refer to the specific buffer information in the hardcopy of datasheet.
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.
Redissolution :
A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.
Synonyms :
CDHF12 Protein, Human; CDHR16 Protein, Human; HSCR1 Protein, Human; MEN2A Protein, Human; MEN2B Protein, Human; MTC1 Protein, Human; PTC Protein, Human; RET-ELE1 Protein, Human; RET51 Protein, Human RET 背景信息 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 Immunotherapy Immune Checkpoint Immunotherapy Targeted Therapy
References & Citations :
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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