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Description
Human RET Protein, His TagProduct Specification Species Human Synonyms Proto oncogene tyrosine protein kinase receptor Ret, Cadherin family member 12, Proto oncogene c Ret, CDHF12, CDHR16, PTC Accession P07949 Amino Acid Sequence Protein sequence (P07949, Leu29 Arg635, with C His Tag)
Product Specification
| Species | Human |
| Synonyms | Proto-oncogene tyrosine-protein kinase receptor Ret, Cadherin family member 12, Proto-oncogene c-Ret, CDHF12, CDHR16, PTC |
| Accession | P07949 |
| Amino Acid Sequence | Protein sequence (P07949, Leu29-Arg635, with C-His Tag) LYFSRDAYWEKLYVDQAAGTPLLYVHALRDAPEEVPSFRLGQHLYGTYRTRLHENNWICIQEDTGLLYLNRSLDHSSWEKLSVRNRGFPLLTVYLKVFLSPTSLREGECQWPGCARVYFSFFNTSFPACSSLKPRELCFPETRPSFRIRENRPPGTFHQFRLLPVQFLCPNISVAYRLLEGEGLPFRCAPDSLEVSTRWALDREQREKYELVAVCTVHAGAREEVVMVPFPVTVYDEDDSAPTFPAGVDTASAVVEFKRKEDTVVATLRVFDADVVPASGELVRRYTSTLLPGDTWAQQTFRVEHWPNETSVQANGSFVRATVHDYRLVLNRNLSISENRTMQLAVLVNDSDFQGPGAGVLLLHFNVSVLPVSLHLPSTYSLSVSRRARRFAQIGKVCVENCQAFSGINVQYKLHSSGANCSTLGVVTSAEDTSGILFVNDTKALRRPKCAELHYMVVATDQQTSRQAQAQLLVTVEGSYVAEEAGCPLSCAVSKRRLECEECGGLGSPTGRCEWRQGDGKGITRNFSTCSPSTKTCPDGHCDVVETQDINICPQDCLRGSIVGGHEPGEPRGIKAGYGTCNCFPEEEKCFCEPEDIQDPLCDELCR |
| Expression System | HEK293 |
| Molecular Weight | Predicted MW: 69.5 kDa Observed MW: 100-120 kDa |
| Purity | ＞95% by SDS-PAGE |
| Endotoxin | <1EU/μg |
| Conjugation | Unconjugated |
| Physical Appearance | Lyophilized powder |
| Storage Buffer | Lyophilized from a 0.2 μm filtered solution of 0.2M PBS, pH7.4 with 3% trehalose. |
| Reconstitution | Reconstitute no more than 1 mg/mL according to the size in deionized water after rapid centrifugation. |
| Stability & Storage | 12 months from date of receipt, -20 to -70 °C as supplied. |
Background
The RET is a receptor tyrosine kinase crucial for normal cell development and survival. It is activated by binding to glial cell line-derived neurotrophic factor (GDNF) family ligands, leading to dimerization and autophosphorylation. This triggers downstream signaling pathways like MAPK and PI3K-AKT, which regulate proliferation, differentiation, and migration, particularly in neural crest and genitourinary lineages. Gain-of-function mutations in RET cause constitutive activation, driving oncogenesis in medullary thyroid cancer and other malignancies. Conversely, loss-of-function mutations are associated with developmental disorders like Hirschsprung's disease. RET is thus a critical therapeutic target in both oncology and neurodevelopment.
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