Cell Signaling Technology

Product Pathways - Growth Factors/Cytokines

BAFF (D7I1U) Rabbit mAb #19944

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H Endogenous 17,29,31 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

BAFF (D7I1U) Rabbit mAb recognizes endogenous levels of total BAFF protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with recombinant human BAFF protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from U-937 cells using BAFF (D7I1U) Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of 1 ng recombinant Human BAFF/TNFSF13B (hBAFF) #5233 using BAFF (D7I1U) Rabbit mAb.

IP

IP

Immunoprecipitation of BAFF from U-937 cell extracts using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2) or BAFF (D7I1U) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using BAFF (D7I1U) Rabbit mAb.


Background

BAFF, a member of the TNF superfamily of proteins, is a homotrimeric transmembrane protein, which is cleaved to produce a soluble cytokine (1). BAFF may also further oligomerize into 60-mer structures (1). BAFF is expressed by monocytes, neutrophils, macrophages, dendritic cells, activated T cells, and epithelial cells (1,2). BAFF plays a key role in B cell development, survival, and activation (1,3,4). BAFF binds to three distinct receptors, BAFF-R, TACI, and BCMA (1). These receptors are differentially expressed during B cell development and among B cell subsets (1,2,4). While BAFF-R and BCMA bind to the homotrimeric form of BAFF, TACI only binds to membrane bound or higher order BAFF structures (1). The BAFF/ BAFF-R interaction activates both canonical and non-canonical NF-κB pathways, PI3K/Akt, and mTOR (2,4). Activation of the noncanonical NF-κB pathway via BAFF-R is negatively regulated by TRAF3 (5). Research studies have shown that elevated levels of BAFF may exacerbate many autoimmune disorders, making it a potential therapeutic target (2).

  1. Mackay, F. and Schneider, P. (2009) Nat Rev Immunol 9, 491-502.
  2. Moisini, I. and Davidson, A. (2009) Clin Exp Immunol 158, 155-63.
  3. Schiemann, B. et al. (2001) Science 293, 2111-4.
  4. Khan, W.N. (2009) J Immunol 183, 3561-7.
  5. Gardam, S. et al. (2008) Immunity 28, 391-401.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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