Human CellExp GFRA1 /GDNFRA, human recombinant protein
GFRA1, GDNFRA, RETL1, TRNR1, GDNFR, GFR-ALPHA-1, RET1L
|Calculated MW||This protein is fused with 6×His tag at the C-terminus, has a calculated MW of 45.5 kDa. The predicted N-terminus is Asp 25. DTT-reduced Protein migrates as 55-60 kDa due to glycosylation.|
|Other Names||GFRA1, GDNFRA, RETL1, TRNR1, GDNFR, GFR-ALPHA-1, RET1L|
|Results||Measured by its binding ability in a functional ELISA. Immobilized Recombinant Human GDNF at 1 µg/mL binds rhGFRA1 with an apparent KD <10 nM.|
|Application Notes||Centrifuge the vial prior to opening. Reconstitute in sterile PBS, pH 7.4 to a concentration of 50 µg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 month. For extended storage, it is recommended to store at -20°C.|
|Storage||-20°C; Lyophilized from 0.22 µm filtered solution in PBS, pH 7.4. Normally Mannitol or Trehalose is added as protectants before lyophilization.|
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Provided below are standard protocols that you may find useful for product applications.
GDNF family receptor alpha-1 (GFRA1) also known as RET ligand 1 (RETL1), TGF-beta-related neurotrophic factor receptor 1 (TRNR1), is a novel glycosylphosphatidylinositol (GPI)-linked cell surface receptor, and belongs to the glial cell line-derived neurotrophic factor (GDNF) receptor subfamily. The GDNF family ligands comprises GDNF, Neurturin (NTN), Artemin, and Persephin. GDNF and NTN are two structurally related, potent neurotrophic factors that play key roles in the control of neuron survival and differentiation. GFRA1 mediates the association with and activation of the RET tyrosine kinase receptor (RTK), and subsequently initiates the RET signaling pathway. GFR alpha-mediated signaling plays an important role in the survival, differentiation, and migration of central and peripheral neurons, and is essential for the development of kidneys and the enteric nervous system, as well as the inflammatory response in some carcinomas.
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Shefelbine S.E.,et al.Hum. Genet. 102:474-478(1998).
Hishiki T.,et al.Submitted (OCT-1997) to the EMBL/GenBank/DDBJ databases.
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