BCL11B Antibody, FITC conjugated

Code CSB-PA880159HC01HU
Size US$166
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Product Details

Full Product Name
Rabbit anti-Homo sapiens (Human) BCL11B Polyclonal antibody
Uniprot No.
Target Names
BCL11B
Alternative Names
ATL1 alpha antibody; ATL1 antibody; ATL1 beta antibody; ATL1 gamma antibody; ATL1-delta antibody; B cell CLL/lymphoma 11B/T cell receptor delta constant region fusion protein antibody; B cell lymphoma/leukemia 11B antibody; B-cell CLL/lymphoma 11B (zinc finger protein) antibody; B-cell CLL/lymphoma 11B antibody; B-cell lymphoma/leukemia 11B antibody; BC11B_HUMAN antibody; BCL-11B antibody; Bcl11b antibody; BCL11B/TRDC fusion antibody; COUP TF interacting protein 2 antibody; COUP-TF interacting protein 2 antibody; COUP-TF-interacting protein 2 antibody; Ctip 2 antibody; CTIP-2 antibody; CTIP2 antibody; hRIT1 alpha antibody; hRit1 antibody; Radiation induced tumor suppressor gene 1 antibody; Radiation induced tumor suppressor gene 1 protein antibody; Radiation-induced tumor suppressor gene 1 protein antibody; Rit 1 antibody; Rit1 antibody; zinc finger protein hRit1 alpha antibody; ZNF856B antibody
Raised in
Rabbit
Species Reactivity
Human
Immunogen
Recombinant Human B-cell lymphoma/leukemia 11B protein (500-550AA)
Immunogen Species
Homo sapiens (Human)
Conjugate
FITC
Clonality
Polyclonal
Isotype
IgG
Purification Method
>95%, Protein G purified
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, PH 7.4
Form
Liquid
Troubleshooting and FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time
Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

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Target Background

Function
Key regulator of both differentiation and survival of T-lymphocytes during thymocyte development in mammals. Essential in controlling the responsiveness of hematopoietic stem cells to chemotactic signals by modulating the expression of the receptors CCR7 and CCR9, which direct the movement of progenitor cells from the bone marrow to the thymus. Is a regulator of IL2 promoter and enhances IL2 expression in activated CD4(+) T-lymphocytes. Tumor-suppressor that represses transcription through direct, TFCOUP2-independent binding to a GC-rich response element. May also function in the P53-signaling pathway.
Gene References into Functions
  1. 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. PMID: 29039465
  2. 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. PMID: 27725726
  3. Decreased transcript and increased promoter methylation levels of BCL11B gene were identified in ankylosing spondylitis patients. PMID: 28794504
  4. 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). PMID: 26096706
  5. 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 PMID: 28232744
  6. 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. PMID: 28288848
  7. 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. PMID: 28669733
  8. Findings identify BCL11B Ser2 phosphorylation as a new mandatory step in the interconnected posttranslational modifications converting BCL11B from a transcriptional repressor to an activator. PMID: 27161321
  9. 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. PMID: 25827435
  10. 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. PMID: 25613934
  11. low BCL11b expression was associated with poor prognosis; particularly in the standard risk group of thymic T-cell acute lymphoblastic leukemia PMID: 25023966
  12. Integrated genome-wide genotyping and gene expression profiling reveals BCL11B as a putative oncogene in acute myeloid leukemia with 14q32 aberrations. PMID: 24441149
  13. 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. PMID: 25128552
  14. overexpressed in mycosis fungoides lesions PMID: 23682716
  15. CTIP2 controls P-TEFb function in physiological and pathological conditions. PMID: 23852730
  16. BCL11B is up-regulated by EWS/FLI and contributes to the transformed phenotype in Ewing sarcoma. PMID: 23527175
  17. a reduction in the level of the BCL11B protein is a key event in the multistep progression of ATLL leukemogenesis PMID: 23383087
  18. BLC11B is an oncogene in T-ALL pathogenesis. PMID: 23040356
  19. BCL11B gene silencing alone does not affect hematopoietic stem/progenitor cell proliferation and differentiation in vitro. PMID: 23168072
  20. REVIEW: describes phenotypes given by loss of Bcl11b and roles of Bcl11b in cell proliferation, differentiation and apoptosis, taking tissue development and lymphomagenesis into consideration PMID: 22450536
  21. Bcl11b phospho-deSUMO switch was identified, the basis of which was phosphorylation-dependent recruitment of the SUMO hydrolase SENP1 to phospho-Bcl11b, coupled to hydrolysis of SUMO-Bcl11b PMID: 22700985
  22. Common genetic variation in a locus in the BCL11B gene desert that is thought to harbor 1 or more gene enhancers is associated with higher CFPWV and increased risk for cardiovascular disease. PMID: 22068335
  23. BCL11B directly interacts with P2 promoter region of HDM2 and inhibits HDM2 promoter activity in a p53-dependent manner. PMID: 22245141
  24. BCL11B is a haploinsufficient tumor suppressor that collaborates with all major T-ALL oncogenic lesions in human thymocyte transformation. PMID: 21878675
  25. This study proposed that the expression of CTIP2 in the anterior neocortex may mark the early location of the human motor cortex, including its corticospinal projection neurons, allowing further study of their early differentiation. PMID: 21060114
  26. BCL11B might play a role in anti-apoptosis in T-ALL cells through up-regulation of its downstream genes BCL2L1 and CREBBP. PMID: 21080944
  27. Increased expression of bcl11b leads to chemoresistance and G1 arrest. PMID: 20824091
  28. CTIP2 expression could be linked to disease progression and/or maintenance in human atopic dermatitis and allergic contact dermatitis PMID: 19366371
  29. CTIP2 mediates transcriptional repression with SIRT1 in mammmalian cells PMID: 12930829
  30. To our knowledge, this is the first report implicating BCL11B in hematological malignancies. PMID: 15104287
  31. BCL11B is involved in hematological neoplasms of T-cells but not acute myeloid leukemia. PMID: 15325104
  32. BCL11B appears to play a key role in T-cell differentiation, BCL11B disruption and disturbed expression may contribute to the development of T-cell malignancies in man. PMID: 15668700
  33. transcriptional repression fuction is mediated by NuRD complex PMID: 16091750
  34. CTIP2 recruits histone deacetylase (HDAC)1 and HDAC2 to promote local histone H3 deacetylation at the HIV-1 promoter region. PMID: 17245431
  35. Data document homeobox gene dysregulation by a novel regulatory region at 3'-BCL11B responsive to histone deacetylase inhibition and highlight a novel class of potential therapeutic target amid noncoding DNA. PMID: 17308084
  36. Bcl11b has a role in response to DNA replication stress and damages PMID: 17369851
  37. We propose that sequestration and/or decreased expression of Bcl11b in HD is responsible, at least in part, for the dysregulation of striatal gene expression observed in HD and may contribute to the specificity of pathology observed in this disease. PMID: 18595722
  38. The authors provide evidence that the transcription factor BCL11B represses expression from the HIV-1 long terminal repeat (LTR) in T lymphocytes through direct association with the HIV-1 long terminal repeat. PMID: 18768194
  39. A statistically significant increase in the expression of CTIP2 was detected in poorly differentiated samples of head and neck tumors. PMID: 19399189
  40. CTIP2 is a constitutive p21 gene suppressor that cooperates with SUV39H1 and histone methylation to silence the p21 gene transcription. PMID: 19581932

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Involvement in disease
Immunodeficiency 49 (IMD49)
Subcellular Location
Nucleus.
Tissue Specificity
Highly expressed in brain and in malignant T-cell lines derived from patients with adult T-cell leukemia/lymphoma.
Database Links

HGNC: 13222

OMIM: 606558

KEGG: hsa:64919

STRING: 9606.ENSP00000349723

UniGene: Hs.709690

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