BATF (D7C5) Rabbit mAb (PE Conjugate) #27120
- F
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Description
Product Usage Information
| Application | Dilution |
|---|---|
| Flow Cytometry (Fixed/Permeabilized) | 1:50 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human BATF protein
Background
Basic leucine zipper transcriptional factor ATF-like (BATF) is a basic leucine zipper (bZIP) transcription factor and is part of the AP-1/ATF family that forms inhibitory dimers with members of the Jun family (1-3). Expression of BATF is largely restricted with highest levels found in mature T cells, and it is induced in B cells following immune responses including viral infection (1,2). BATF expression is also induced by IL-6 via a Stat3-dependent mechanism (4). BATF plays an important role in the differentiation of immune cell lineages (5-7). Studies of BATF-deficient mice have demonstrated a critical role for BATF in the formation of IL-17-expressing Th17 cells, in part, by regulating the expression of IL-17 (5,6). BATF knockouts are resistant to experimental autoimmune encephalomyelitis (EEA), consistent with the role of Th17 cells in this model for autoimmunity (5). Additional studies have found that BATF is important in generating antibody class switching. BATF is required for the generation of follicular helper T cells (Tfh), by regulating BCL6 and c-Maf (6,7). In B cells, BATF controls the expression of activation-induced cytidine deaminase (AID) and regulates class-switched antibody responses (7). Taken together, these studies suggest that BATF is a key regulator of distinct populations of immune cells.
- Dorsey, M.J. et al. (1995) Oncogene 11, 2255-65.
- Hasegawa, H. et al. (1996) Biochem Biophys Res Commun 222, 164-70.
- Echlin, D.R. et al. (2000) Oncogene 19, 1752-63.
- Senga, T. et al. (2002) Oncogene 21, 8186-91.
- Schraml, B.U. et al. (2009) Nature 460, 405-9.
- Betz, B.C. et al. (2010) J Exp Med 207, 933-42.
- Ise, W. et al. (2011) Nat Immunol 12, 536-43.
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