BACH2 Antibody (Rabbit mAb) [N18E12]

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000 IP1:100 FCM1:50

Application
WB, IP, FCM, ELISA

Reactivity
Human, Mouse

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
93 kDa

Positive Control	Human non-Hodgkin's lymphoma tissue; Human tonsil tissue; WEHI-231 cells; Ramos cells; NAMALWA cells; Mouse PBMC cells; Human PBMC cells
Negative Control	Human pancreas tissue; J774A.1 cells; THP-1 cells; HL-60 cells

Datasheet & SDS

Biological Description

Specificity
BACH2 Antibody (Rabbit mAb) [N18E12] detects endogenous levels of total BACH2 protein.

Clone
N18E12

Synonym(s)
Transcription regulator protein BACH2, BTB and CNC homolog 2, BACH2

Background
BACH2, BTB and CNC homology 2, belongs to the BTB-basic leucine zipper family of transcriptional repressors, requiring heterodimerization with small Maf proteins such as MAFK to bind DNA at Maf recognition elements and repress target gene transcription, and it is predominantly expressed in B and T lymphocytes where it operates across two distinct branches of adaptive immunity. In germinal center B cells, BACH2 forms a complex with MAFK that binds chromatin at gene sets governing the germinal center response, and chromatin immunoprecipitation sequencing shows substantial overlap between BACH2 and BCL6 binding sites, including shared occupancy of regulatory sequences controlling PRDM1, the master driver of plasma cell differentiation. BCL6 and BACH2 cooperate through both physical and biochemical mechanisms, recruiting each other to shared DNA-binding sites or to proximal regulatory elements, and BCL6 additionally stabilizes BACH2 protein, so that the two factors' expression levels correlate positively within germinal center B cells; combined heterozygous loss of both factors, but not loss of either alone, produces a profound reduction in germinal center formation and accelerates premature plasmacytic differentiation, marked by elevated expression of Prdm1, Xbp1, and CD138, demonstrating that BCL6 and BACH2 function as a cooperative repressive unit rather than through independent, additive contributions. In the T cell compartment, BACH2 represses a broad network of effector-differentiation genes to stabilize regulatory T cell identity, restraining CD4-positive T cell differentiation toward inflammatory effector lineages while supporting Foxp3-dependent regulatory programming, and this repression extends to interleukin-2 receptor signaling: BACH2 directly represses CD25, the IL-2 receptor alpha chain, and this repression is required for the quiescence, survival, and long-term maintenance of resting regulatory T cells, with loss of BACH2 producing elevated CD25 and IL-2R signaling that only partially compensates for impaired Treg survival. BACH2-mediated CD25 repression additionally shapes T follicular regulatory cell development, coupling BACH2's transcriptional repressor activity to the balance between regulatory and effector states across multiple T cell subsets rather than to a single lineage decision. Across both B and T lymphocyte compartments, BACH2 functions as a rheostat restraining terminal effector or plasma cell differentiation in favor of quiescent, memory, or regulatory cell fates, and dysregulation of the BACH2-BCL6 balance or of BACH2-dependent Treg stabilization is implicated in autoimmune susceptibility and B-cell malignancy.

Background

BACH2, BTB and CNC homology 2, belongs to the BTB-basic leucine zipper family of transcriptional repressors, requiring heterodimerization with small Maf proteins such as MAFK to bind DNA at Maf recognition elements and repress target gene transcription, and it is predominantly expressed in B and T lymphocytes where it operates across two distinct branches of adaptive immunity. In germinal center B cells, BACH2 forms a complex with MAFK that binds chromatin at gene sets governing the germinal center response, and chromatin immunoprecipitation sequencing shows substantial overlap between BACH2 and BCL6 binding sites, including shared occupancy of regulatory sequences controlling PRDM1, the master driver of plasma cell differentiation. BCL6 and BACH2 cooperate through both physical and biochemical mechanisms, recruiting each other to shared DNA-binding sites or to proximal regulatory elements, and BCL6 additionally stabilizes BACH2 protein, so that the two factors' expression levels correlate positively within germinal center B cells; combined heterozygous loss of both factors, but not loss of either alone, produces a profound reduction in germinal center formation and accelerates premature plasmacytic differentiation, marked by elevated expression of Prdm1, Xbp1, and CD138, demonstrating that BCL6 and BACH2 function as a cooperative repressive unit rather than through independent, additive contributions. In the T cell compartment, BACH2 represses a broad network of effector-differentiation genes to stabilize regulatory T cell identity, restraining CD4-positive T cell differentiation toward inflammatory effector lineages while supporting Foxp3-dependent regulatory programming, and this repression extends to interleukin-2 receptor signaling: BACH2 directly represses CD25, the IL-2 receptor alpha chain, and this repression is required for the quiescence, survival, and long-term maintenance of resting regulatory T cells, with loss of BACH2 producing elevated CD25 and IL-2R signaling that only partially compensates for impaired Treg survival. BACH2-mediated CD25 repression additionally shapes T follicular regulatory cell development, coupling BACH2's transcriptional repressor activity to the balance between regulatory and effector states across multiple T cell subsets rather than to a single lineage decision. Across both B and T lymphocyte compartments, BACH2 functions as a rheostat restraining terminal effector or plasma cell differentiation in favor of quiescent, memory, or regulatory cell fates, and dysregulation of the BACH2-BCL6 balance or of BACH2-dependent Treg stabilization is implicated in autoimmune susceptibility and B-cell malignancy.

References
https://pubmed.ncbi.nlm.nih.gov/32082072/ https://pubmed.ncbi.nlm.nih.gov/24277074/

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%