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Recombinant Human BAFF R/TNFRSF13C Fc Chimera Protein, CF  50 UG图1

Recombinant Human BAFF R/TNFRSF13C Fc Chimera Protein, CF 50 UG

2024-11-24 19:25IP属地 广东省东莞市 电信00留言

1162-BR

 

Formulation Lyophilized from a 0.2 μm filtered solution in PBS.


Reconstitution Reconstitute at 100 μg/mL in sterile PBS.



Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.


Stability & Storage:       Use a manual defrost freezer and avoid repeated freeze-thaw cycles.      

  • 12 months from date of receipt, -20 to -70 °C as supplied.

  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.

  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.


Background: BAFF R/TNFRSF13C

B-cell activating factor (BAFF), also known as BlyS, TALL-1, TNAK, and zTNF4, is a TNF ligand superfamily member and has been designated TNFSF13B. Produced by macrophages, dendritic cells, and T lymphocytes, BAFF promotes the survival of B cells and is essential for B cell maturation (1-4). 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. Whereas TACI and BCMA bind BAFF and another TNF superfamily ligand, APRIL (a proliferation-inducing ligand), BAFF R selectively binds BAFF. The BAFF R extracellular domain lacks the TNF receptor canonical cysteine-rich domain (CRD) and contains only a partial CRD with four cysteine residues. Human and mouse BAFF R share 56% aa sequence identity. 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. In contrast, BCMA- or TACI-deficient mice have no major defect in B-cell development. While the function of BCMA is not defined, TACI has been shown to control B-cell homeostasis and T-cell-independent immune responses.

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