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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. Zusätzlich bieten wir Ihnen BCL11B Antikörper (62) und und viele weitere Produktgruppen zu diesem Protein an.
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Thus, this study identifies BCL11B as a novel regulator of adipogenesis, which works, at least in part, by stimulating C/EBPbeta (zeige CEBPB ELISA Kits) activity and suppressing the Wnt (zeige WNT2 ELISA Kits)/beta-catenin (zeige CTNNB1 ELISA Kits) signaling pathway.
Bcl11b is associated with cell fate in the T-cell gene regulatory network.
Bcl11b, known as a T-lineage commitment factor, is essential for proper expression of ThPOK (zeige ZBTB7B ELISA Kits) and Runx3 (zeige RUNX3 ELISA Kits), central regulators for the CD4 (zeige CD4 ELISA Kits)-helper/CD8 (zeige CD8A ELISA Kits)-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 (zeige HNF1A ELISA Kits), GATA-3 (zeige GATA3 ELISA Kits) and Runx1 (zeige RUNX1 ELISA Kits)) 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.
These results suggest that the upregulation of miR (zeige MLXIP ELISA Kits)-650 contributes to the development of acute renal allograft rejection by suppression of BCL11B, which leads to apoptosis and inflammatory responses. Thus, miR (zeige MLXIP ELISA Kits)-650 and BCL11B may represent potential therapeutic targets for the prevention of acute renal allograft rejection.
In this present work, the authors identify and characterize a transcription factor i.e. HIC1 (zeige HIC1 ELISA Kits), which physically interacts with both Bcl11b/CTIP2 and HMGA1 (zeige HMGA1 ELISA Kits) to co-regulate specific subsets of cellular genes and the HIV-1 tat (zeige TAT ELISA Kits) gene.
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 (zeige CDKN1A ELISA Kits) and stemness-associated genes (Sox-2 (zeige SOX2 ELISA Kits)/Bmi-1 (zeige BMI1 ELISA Kits)).
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.
Human T-cell leukemia virus type 1 (HTLV-1) Tax (zeige CNTN2 ELISA Kits) directly binds to BCL11B. Tax (zeige CNTN2 ELISA Kits) enhances BCL11B degradation through proteasome pathway. Loss of BCL11B enhances cell growth in HTLV-1-infected cells.
Findings identify BCL11B Ser2 (zeige JAG2 ELISA Kits) 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 (zeige CTNNB1 ELISA Kits) target genes, whereas Bcl11b attenuation in Lgr5 (zeige LGR5 ELISA Kits)(+) crypt base columnar cells increased expression of beta-catenin (zeige CTNNB1 ELISA Kits) targets including c-Myc (zeige MYC ELISA Kits) and cyclin D1 (zeige CCND1 ELISA Kits).
Tax (zeige CNTN2 ELISA Kits) is responsible for suppressing BCL11B protein expression in HTLV-1-infected T-cells; Tax (zeige CNTN2 ELISA Kits)-mediated repression of BCL11B is another mechanism that Tax (zeige CNTN2 ELISA Kits) uses to promote oncogenesis of HTLV-1-infected T-cells.
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