BATF Antibody [C3L16] | Primary Antibodies

Application: Reactivity: Mouse, Human

Usage Information

Dilution
WB1:1000 IP1:30 IF1:100 FCM1:500

Application
WB, IP, IF, FCM

Reactivity
Mouse, Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
14 kDa

Positive Control	KARPAS-299 cells; A20 cells
Negative Control	HeLa cells

Datasheet & SDS

Biological Description

Specificity
BATF Antibody [C3L16] detects endogenous levels of total BATF protein.

Clone
C3L16

Synonym(s)
Basic leucine zipper transcriptional factor ATF-like; B-cell-activating transcription factor; SF-HT-activated gene 2 protein; B-ATF; SFA-2; BATF

Background
BATF (Basic Leucine Zipper ATF-Like Transcription Factor) is a member of the AP-1/ATF family of bZIP transcription factors, functioning primarily in immune cell gene regulation. The protein consists of 125 amino acids, featuring a basic DNA-binding domain (residues 18–35) that recognizes AP-1 consensus motifs (TGASTCA), and a leucine zipper region (residues 68–89) that mediates inhibitory heterodimerization with Jun proteins, thereby modulating activator binding. BATF expression is induced by T cell receptor (TCR) engagement or IL-6/STAT3 signaling, peaking in mature T follicular helper (Tfh), Th17, and effector CD8 T cells. As a pioneering factor, BATF opens chromatin at thousands of sites, cooperating with IRF4 and JunB to activate critical effector genes such as Tbx21, Eomes, Prdm1, and Gzmb. This drives CD8 T cell cytotoxicity, cytokine production (IFNγ, IL-2), and metabolic reprogramming via Sirt1. BATF is essential for Il17a, Rorc, and Maf expression, with knockout models showing resistance to autoimmune diseases like EAE due to the absence of IL-17 responses. In Tfh cells, BATF induces Bcl6 and Cxcr5, facilitating germinal center formation and high-affinity antibody production. BATF regulates class-switch recombination by binding to AID and Prdm1 promoters upon activation, controlling IgG/IgA production during infection. BATF target genes are temporally clustered during the effector-to-memory transition of CD8 T cells, with enrichments in TCR signaling, cytokine receptors, cellular homing, and apoptosis regulation. BATF deficiency impairs effector differentiation and compromises viral control, as seen in LCMV infection models. In cancer, BATF reprograms regulatory T cell (Treg) epigenomes to enhance anti-tumor immunity. Dysregulation of BATF contributes to autoimmunity (e.g., lupus) through hyperactive Th17/Tfh responses, while deficiency confers protection against EAE and colitis.

Background

BATF (Basic Leucine Zipper ATF-Like Transcription Factor) is a member of the AP-1/ATF family of bZIP transcription factors, functioning primarily in immune cell gene regulation. The protein consists of 125 amino acids, featuring a basic DNA-binding domain (residues 18–35) that recognizes AP-1 consensus motifs (TGASTCA), and a leucine zipper region (residues 68–89) that mediates inhibitory heterodimerization with Jun proteins, thereby modulating activator binding. BATF expression is induced by T cell receptor (TCR) engagement or IL-6/STAT3 signaling, peaking in mature T follicular helper (Tfh), Th17, and effector CD8 T cells. As a pioneering factor, BATF opens chromatin at thousands of sites, cooperating with IRF4 and JunB to activate critical effector genes such as Tbx21, Eomes, Prdm1, and Gzmb. This drives CD8 T cell cytotoxicity, cytokine production (IFNγ, IL-2), and metabolic reprogramming via Sirt1. BATF is essential for Il17a, Rorc, and Maf expression, with knockout models showing resistance to autoimmune diseases like EAE due to the absence of IL-17 responses. In Tfh cells, BATF induces Bcl6 and Cxcr5, facilitating germinal center formation and high-affinity antibody production. BATF regulates class-switch recombination by binding to AID and Prdm1 promoters upon activation, controlling IgG/IgA production during infection. BATF target genes are temporally clustered during the effector-to-memory transition of CD8 T cells, with enrichments in TCR signaling, cytokine receptors, cellular homing, and apoptosis regulation. BATF deficiency impairs effector differentiation and compromises viral control, as seen in LCMV infection models. In cancer, BATF reprograms regulatory T cell (Treg) epigenomes to enhance anti-tumor immunity. Dysregulation of BATF contributes to autoimmunity (e.g., lupus) through hyperactive Th17/Tfh responses, while deficiency confers protection against EAE and colitis.

References
https://pubmed.ncbi.nlm.nih.gov/24584090/ https://pubmed.ncbi.nlm.nih.gov/21572431/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%