B-Cell CLL/lymphoma 11B (Zinc Finger Protein) (BCL11B) ELISA Kits

Mouse (Murine) B-Cell CLL/lymphoma 11B (Zinc Finger Protein) (BCL11B) interaction partners

1. Bcl11b controls both GATA3-mediated gene activation and repression in Th2 cells.

2. We show that Bcl11b in pro-T cells blocked expression of the E-protein antagonist Id2 (encoded by Id2) and the innate-response regulator PLZF (encoded by Zbtb16).

3. stimulation of MAP kinase and (or) Wnt signaling pathways differentially affects gene expression of some Bcl11b target and maturation-associated genes.

4. Study identified the maturation enhancer E4m, validated its role in regulating CD4 expression, and isolate Bcl11b as an important activator for E4m.

5. Mice lacking Bcl11b in mature T-cells have a diminished capacity to mount Th2 responses during helminth infection and allergic asthma, showing reduced Th2 cytokines and Gata3, and elevated Runx3.

6. Thus, this study identifies BCL11B as a novel regulator of adipogenesis, which works, at least in part, by stimulating C/EBPbeta activity and suppressing the Wnt/beta-catenin signaling pathway.

7. Bcl11b is associated with cell fate in the T-cell gene regulatory network.

8. Bcl11b, known as a T-lineage commitment factor, is essential for proper expression of ThPOK and Runx3, central regulators for the CD4-helper/CD8-cytotoxic lineage choice.

9. 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.

10. key regulator of Invariant natural killer T-cell effector subsets, their function, identity, and survival

11. these results suggest that Bcl11b acts as a central intrinsic regulator of mammary epithelial stem cell quiescence.

12. 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.

13. this study shows that distinct, asynchronous and stage-specific transcription factors (TCF-1, GATA-3 and Runx1) activate Bcl11b for T cell commitment

14. 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.

15. BCL11B as a regulator of energy metabolism

16. Data uncover for the first time a specific role of Bcl11b in adult hippocampal neurogenesis and function.

17. BCL11B is extensively expressed in neocortical GABAergic interneurons of all three major subgroups and thus its expression is not restricted to subcerebral projections cells.

18. Bcl11b regulates development of different thymocyte subsets at multiple stages and prevents an excess of innate CD8 single-positive thymocytes.

19. sustains mature Type 2 innate lymphoid cells genetic and functional programs and lineage fidelity

20. Data indicate kinetic changes in relative phosphorylation on 18 of 23 serine and threonine residues and sumoylation on one of two lysine resides in B-cell lymphoma-leukemia 11B protein BCL11B.

Human B-Cell CLL/lymphoma 11B (Zinc Finger Protein) (BCL11B) interaction partners

1. An interaction between a novel 3'-BCL11B gene desert locus and daily sodium consumption.

2. Results confirm the BCL11B dimerization hypothesis and prove its importance for BCL11B function. By mapping the relevant regions to the CCHC domain, authors describe a previously unidentified mechanism of transcription factor homodimerization.

3. BCL11B regulates mammary cell differentiation.

4. These results suggest that the upregulation of miR-650 contributes to the development of acute renal allograft rejection by suppression of BCL11B, which leads to apoptosis and inflammatory responses. Thus, miR-650 and BCL11B may represent potential therapeutic targets for the prevention of acute renal allograft rejection.

5. In this present work, the authors identify and characterize a transcription factor i.e. HIC1, which physically interacts with both Bcl11b/CTIP2 and HMGA1 to co-regulate specific subsets of cellular genes and the HIV-1 tat gene.

6. Decreased transcript and increased promoter methylation levels of BCL11B gene were identified in ankylosing spondylitis patients.

7. 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 and stemness-associated genes (Sox-2/Bmi-1).

8. 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

9. 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.

10. Human T-cell leukemia virus type 1 (HTLV-1) Tax directly binds to BCL11B. Tax enhances BCL11B degradation through proteasome pathway. Loss of BCL11B enhances cell growth in HTLV-1-infected cells.

11. Findings identify BCL11B Ser2 phosphorylation as a new mandatory step in the interconnected posttranslational modifications converting BCL11B from a transcriptional repressor to an activator.

12. BCL11B introduction in human cell lines downregulated transcription of beta-catenin target genes, whereas Bcl11b attenuation in Lgr5(+) crypt base columnar cells increased expression of beta-catenin targets including c-Myc and cyclin D1.

13. Tax is responsible for suppressing BCL11B protein expression in HTLV-1-infected T-cells; Tax-mediated repression of BCL11B is another mechanism that Tax uses to promote oncogenesis of HTLV-1-infected T-cells.

14. low BCL11b expression was associated with poor prognosis; particularly in the standard risk group of thymic T-cell acute lymphoblastic leukemia

15. Integrated genome-wide genotyping and gene expression profiling reveals BCL11B as a putative oncogene in acute myeloid leukemia with 14q32 aberrations.

16. a comprehensive review of the roles of Bcl11b in progenitors, effector T cells, regulatory T cells, and invariant NKT cells, as well as its impact on immune diseases.

17. overexpressed in mycosis fungoides lesions

18. CTIP2 controls P-TEFb function in physiological and pathological conditions.

19. BCL11B is up-regulated by EWS/FLI and contributes to the transformed phenotype in Ewing sarcoma.

20. a reduction in the level of the BCL11B protein is a key event in the multistep progression of ATLL leukemogenesis