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Recombinant Human BAFFR (C-6His)
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Recombinant Human BAFFR (C-6His)

PHH2402-50ug · 50ug

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Catalog No: PHH2402-50ug
Pack Size: 50ug
Brand: EnkiLife

Description

EnkiLife provides the Recombinant Human BAFFR (C-6His) protein,aslo know as BAFF R,BAFFR,BR3,CD268,TNFRSF13C, which features high purity, high activity, and high stability. It can be applied in scientific research, biopharmaceuticals, and other fields.Purity:Greater than 95% as determined by reducing SDS-PAGE;Endotoxin Level:<1 EU/µg as determined by LAL test.;Construction:Recombinant Human Tumor Necrosis Factor Receptor Superfamily Member 13C is produced by our Mammalian expression system and the target gene encoding Ser7-Ala71 is expressed with a 6His tag at the C-terminus.Accession:Q96RJ3. Expression Host:Human cells.Species:Human.Predicted Molecular Mass:7.4 KDa. Background:Tumor necrosis factor receptor superfamily, member 13C (TNFRSF13C) also known as B-cell-activating factor receptor (BAFFR) and CD268 antigen, is a member of the tumor necrosis factor receptor superfamily. BAFF promotes the survival of B cells and is essential for B cell maturation. BAFF binds to three TNF receptor superfamily members: B-cell maturation antigen (BCMA/TNFRSF17), transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI/TNFRSF13B) and BAFF receptor (BAFF R/BR3/TNFRSF13C). These receptors are type III transmembrane proteins that lack a signal peptide. BAFF R is highly expressed in spleen, lymph node and resting B cells. It is also expressed at lower levels in activated B cell, in resting CD4+ T cells, in thymus and peripheral blood leukocytes. BAFF knockout mice lack mature B cells. Similarly, A/WySnJ mice that are defective in BAFF-R intracellular signaling also lack mature B cells, suggesting that BAFF R is the critical receptor for BAFF during B lymphopoiesis. It has been proposed that abnormally high levels of BAFFR/TNFRSF13C (CD268) may contribute to the pathogenesis of autoimmune diseases by enhancing the survival of autoreactive B cells.

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