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BCL11B encodes a C2H2-type zinc finger protein and is closely related to BCL11A, a gene whose translocation may be associated with B-cell malignancies. Additionally we are shipping BCL11B Kits (7) and and many more products for this protein.
Showing 10 out of 54 products:
Human Polyclonal BCL11B Primary Antibody for ICC, IF - ABIN251041
Beguin, Crépel, Aniksztejn, Becq, Pelosi, Pallesi-Pocachard, Bouamrane, Pasqualetti, Kitamura, Cardoso, Represa: An epilepsy-related ARX polyalanine expansion modifies glutamatergic neurons excitability and morphology without affecting GABAergic neurons development. in Cerebral cortex (New York, N.Y. : 1991) 2013
Show all 3 Pubmed References
Bcl11b, known as a T-lineage commitment factor, is essential for proper expression of ThPOK (show ZBTB7B Antibodies) and Runx3 (show RUNX3 Antibodies), central regulators for the CD4 (show CD4 Antibodies)-helper/CD8 (show CD8A Antibodies)-cytotoxic lineage choice.
Authors provide insight into the mechanism that underpins the repositioning of regulatory elements; identify a non-coding RNA, named ThymoD, which acts to reposition the Bcl11 enhancer away from the lamina to the nuclear interior and sequester the Bcl11b promoter and enhancer region into a single-loop domain.
these results suggest that Bcl11b acts as a central intrinsic regulator of mammary epithelial stem cell quiescence.
BCL11B is expressed in both osteogenic and sutural mesenchyme of the developing craniofacial complex. Bcl11b(-/-) mice exhibit increased proliferation of osteoprogenitors, premature osteoblast differentiation, and enhanced skull mineralization leading to synostoses of facial and calvarial sutures.
this study shows that distinct, asynchronous and stage-specific transcription factors (TCF-1 (show HNF1A Antibodies), GATA-3 (show GATA3 Antibodies) and Runx1 (show RUNX1 Antibodies)) activate Bcl11b for T cell commitment
the expression and function of Bcl11b in the oral epithelium and demonstration that Bcl11b is an essential regulator for keratinocyte differentiation and the morphogenesis of papillary structure of the lingual epithelium.
BCL11B as a regulator of energy metabolism
Data uncover for the first time a specific role of Bcl11b in adult hippocampal neurogenesis and function.
BCL11B is extensively expressed in neocortical GABAergic interneurons of all three major subgroups and thus its expression is not restricted to subcerebral projections cells.
Bcl11b regulates development of different thymocyte subsets at multiple stages and prevents an excess of innate CD8 (show CD8A Antibodies) single-positive thymocytes.
Decreased transcript and increased promoter methylation levels of BCL11B gene were identified in ankylosing spondylitis patients.
this is the first study to show that the inhibition of Bcl11b suppresses glioma cell growth by regulating the expression of the cell cycle regulator p21 (show CDKN1A Antibodies) and stemness-associated genes (Sox-2 (show SOX2 Antibodies)/Bmi-1 (show BMI1 Antibodies)).
studies show BCL11B is a key regulator of the initial stages of human T-cell differentiation and delineate the BCL11B transcriptional program, enabling the dissection of the underpinnings of normal T-cell differentiation and providing a resource for understanding dysregulations in T-ALL
BCL11B showed increased but varied expression in advanced tumor stage. Analysis of four patients receiving SAHA treatment suggested a positive correlation between BCL11B expression and favorable response to SAHA treatment. In conclusion, BCL11B may serve as a therapeutic target and a useful marker for improving HDACi efficacy in advanced CTCL (show TSPYL2 Antibodies).
Human T-cell leukemia virus type 1 (HTLV-1) Tax (show CNTN2 Antibodies) directly binds to BCL11B. Tax (show CNTN2 Antibodies) enhances BCL11B degradation through proteasome pathway. Loss of BCL11B enhances cell growth in HTLV-1-infected cells.
Findings identify BCL11B Ser2 (show JAG2 Antibodies) phosphorylation as a new mandatory step in the interconnected posttranslational modifications converting BCL11B from a transcriptional repressor to an activator.
BCL11B introduction in human cell lines downregulated transcription of beta-catenin (show CTNNB1 Antibodies) target genes, whereas Bcl11b attenuation in Lgr5 (show LGR5 Antibodies)(+) crypt base columnar cells increased expression of beta-catenin (show CTNNB1 Antibodies) targets including c-Myc (show MYC Antibodies) and cyclin D1 (show CCND1 Antibodies).
Tax (show CNTN2 Antibodies) is responsible for suppressing BCL11B protein expression in HTLV-1-infected T-cells; Tax (show CNTN2 Antibodies)-mediated repression of BCL11B is another mechanism that Tax (show CNTN2 Antibodies) uses to promote oncogenesis of HTLV-1-infected T-cells.
low BCL11b expression was associated with poor prognosis; particularly in the standard risk group of thymic T-cell acute lymphoblastic leukemia
Integrated genome-wide genotyping and gene expression profiling reveals BCL11B as a putative oncogene (show RAB1A Antibodies) in acute myeloid leukemia (show BCL11A Antibodies) with 14q32 aberrations.
This gene encodes a C2H2-type zinc finger protein and is closely related to BCL11A, a gene whose translocation may be associated with B-cell malignancies. The specific function of this gene has not yet been determined. Two alternatively spliced transcript variants, which encode distinct isoforms, have been reported.
B-cell CLL/lymphoma 11B (zinc finger protein)
, B-cell CLL/lymphoma 11B
, B-cell CLL/lymphoma 11B, isoform 1
, B-cell leukemia/lymphoma 11B
, B-cell lymphoma/leukaemia 11B
, B-cell lymphoma/leukemia 11B
, COUP-TF interacting protein 2
, COUP-TF-interacting protein 2
, radiation-induced tumor suppressor gene 1 protein
, B-cell CLL/lymphoma 11B/T-cell receptor delta constant region fusion protein
, BCL11B/TRDC fusion
, zinc finger protein hRit1 alpha
, B-cell lymphoma/leukemia 11B (predicted), 3 prime
, B-cell lymphoma/leukemia 11B (predicted), 5 prime
, COUP-TF-interacting protein 2 long form