Summary:
Recombinant human TFRC protein
Cat：P05798
| 【Derived From】： E.coli |
| 【Endotoxin】： Not measured |
| 【Amino Acid】： 101-450aa |
| 【Purity】： ≥85% by SDS-PAGE. |
| 【Name】： TFRC |
| 【Full Name】： transferrin receptor (p90，CD71) |
| 【Uniprot】： P02786 |
| 【Gene ID】： 7037 |
| 【Species Reactivity】： Human Mouse Rat (Orangutan Horse Cat Dog Pig Chicken) |
| 【Mol Mass】： 39kDa |
| 【Application】： Immunology research |
| 【Purification】： NI-NTA affinity purification |
| 【Bioactive】： N0 |
| 【Tag】： With a 6×His tag at the N/C-terminus. |
| 【Concentration】： 1mg/ml by SDS-PAGE. |
Store:
| 【Reconstitution】： Reconstituted protein solution can be diluted with distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. (It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water.) |
| 【Storage】： Reconstituted protein solution can be stored at 4-7℃ for 1-2 weeks， stored at < -20℃ for 1 year. |
| 【Formulation】： Powder: Lyophilized from a 0.2 μm filtered solution of 2-8M Urea, 20mM Tris-HCl, 150mM NaCl, 1mM DTT, PH7.2-8.0. |
Background:
Cellular uptake of iron occurs via receptor-mediated endocytosis of ligand-occupied transferrin receptor into specialized endosomes (PubMed:26214738).Endosomal acidification leads to iron release. The apotransferrin-receptor complex is then recycled to the cell surface with a return to neutral pH and the concomitant loss of affinity of apotransferrin for its receptor. Transferrin receptor is necessary for development of erythrocytes and the nervous system (By similarity).A second ligand, the heditary hemochromatosis protein HFE, competes for binding with transferrin for an overlapping C-terminal binding site. Positively regulates T and B cell proliferation through iron uptake (PubMed:26642240).Acts as a lipid sensor that regulates mitochondrial fusion by regulating activation of the JNK pathway (PubMed:26214738).When dietary levels of stearate (C18:0) are low, promotes activation of the JNK pathway, resulting in HUWE1-mediated ubiquitination and subsequent degradation of the mitofusin MFN2 and inhibition of m
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