BCL11B Antibodies
Background
The BCL11B gene is a key gene encoding a C2H2-type zinc finger transcription factor, which is mainly expressed in the nervous system, immune system, and skin tissues. This gene plays a significant role in neural development, T lymphocyte differentiation, and epidermal formation by regulating the expression of downstream target genes. Patients with immunodeficiency syndromes often carry mutations in the BCL11B gene, and this gene's abnormality is also closely related to neurodevelopmental disorders and certain hematological malignancies. Since it was confirmed to be associated with severe combined immunodeficiency in 2012, BCL11B has become an important research subject in the fields of immunology and developmental biology. The study of its regulatory network provides a key theoretical basis for understanding the mechanism of cell fate determination and developing gene therapy strategies for related diseases.
Structure of BCL11B
The protein encoded by the BCL11B gene has a molecular weight of approximately 92 kDa. This value may have slight variations among different tissues and cell types, and it is mainly related to post-transcriptional modifications. The BCL11B protein consists of 894 amino acids and forms a characteristic DNA-binding region through its C2H2 type zinc finger domain. This protein is located in the cell nucleus. Its zinc finger domain contains multiple tandemly arranged zinc finger motifs, each of which is stabilized by zinc ions to maintain its spatial conformation, enabling specific recognition of DNA sequences. Zinc fingers 1-3 are mainly responsible for DNA recognition and binding, while zinc fingers 4-6 are involved in protein-protein interactions. This structure enables BCL11B to precisely regulate the expression of downstream target genes.
Fig. 1 Structure and variants in BCL11B.1
Key structural properties of BCL11B:
- Contains 6 C2H2 type zinc finger domains
- The amino-terminal region rich in proline is the transcriptional activation domain
- The zinc fingers 3-5 form the core for specific DNA recognition
- The carboxyl-terminal contains the domain for binding to the NuRD complex
- The nuclear localization signal mediates its entry into the cell nucleus
- The phosphorylation sites regulate the stability and transcriptional activity of the protein
Functions of BCL11B
The core function of the BCL11B gene is to regulate neural development and immune cell differentiation. However, it also plays a significant role in various physiological processes, including maintaining nervous system function, participating in T lymphocyte development, and influencing the self-renewal of hematopoietic stem cells.
| Function | Description |
| Neurodevelopmental regulation | BCL11B is highly expressed in cortical neurons and regulates the migration, differentiation, and survival of neurons, which is crucial for the normal development of the cerebral cortex. |
| T-cell differentiation determination | As a transcription factor specific to the T lymphocyte lineage, BCL11B determines the differentiation of lymph progenitor cells towards T cells rather than NK cells, and is a key switch in T-cell development. |
| Immune homeostasis maintenance | Regulates the function of regulatory T cells (Treg), participates in the formation of peripheral immune tolerance, and prevents the occurrence of autoimmune reactions. |
| Tumor suppression | Often mutates or is deleted in T-cell acute lymphoblastic leukemia, functioning as a tumor suppressor gene, inhibiting malignant transformation. |
| Neuroprotective effect | Participates in maintaining the survival of neurons in the adult brain, and its downregulation is associated with the occurrence and development of neurodegenerative diseases. |
The expression of BCL11B is highly cell-specific, and its regulatory network undergoes dynamic changes in different developmental stages and cell types. This precise spatiotemporal expression characteristic determines its multifunctionality in the development of multiple organs.
Applications of BCL11B and BCL11B Antibody in Literature
1. Vedovato-dos-Santos, J. Heather, et al. "BCL11B-related disease: a single phenotypic entity?." European Journal of Human Genetics 33.4 (2025): 451-460. https://doi.org/10.1038/s41431-025-01824-x
The systematic review confirmed that BCL11B-related diseases are a single phenotypic entity. Based on four new cases, craniosynostosis was identified as an important diagnostic clue for this disease, expanding the genetic phenotypic spectrum and providing clinical guidance for the diagnosis of rare diseases and genetic counseling.
2. Lennon, Matthew J., et al. "Bcl11b—a critical neurodevelopmental transcription factor—roles in health and disease." Frontiers in cellular neuroscience 11 (2017): 89. https://doi.org/10.3389/fncel.2017.00089
The article indicates that BCL11B is a zinc finger protein transcription factor with dual regulatory functions, playing a crucial role in the development of central nervous system, immune system, etc. Abnormalities in this gene are associated with Huntington's disease, Alzheimer's disease, HIV and T-cell malignancies, but the underlying mechanism remains to be elucidated.
3. Przybylski, Grzegorz K., Julia Przybylska, and Yangqiu Li. "Dual role of BCL11B in T-cell malignancies." Blood Science 6.4 (2024): e00204. https://doi.org/10.1097/BS9.0000000000000204
The article indicates that BCL11B has both tumor-suppressing and tumor-promoting effects in T-cell malignancies, depending on the expression level. When expressed at high levels, inhibiting this gene can cause tumor apoptosis and induce the transformation of T-NK cells, suggesting that targeting BCL11B is a potential therapeutic strategy.
4. Li, Yehua, et al. "BMP suppresses Wnt signaling via the Bcl11b-regulated NuRD complex to maintain intestinal stem cells." The EMBO Journal 43.23 (2024): 6032-6051. https://doi.org/10.1038/s44318-024-00276-1
The article indicates that BCL11B is inhibited by BMP signals and enhances the Wnt pathway by suppressing the NuRD complex, thereby maintaining intestinal stem cells and promoting damage repair. The absence of this gene can inhibit the proliferation of colorectal cancer, revealing the regulatory mechanism of the BMP-BCL11B-Wnt axis in regeneration and tumors.
5. Daher, Marie-Thérèse, et al. "Bcl11b/Ctip2 in skin, tooth, and craniofacial system." Frontiers in cell and developmental biology 8 (2020): 581674. https://doi.org/10.3389/fcell.2020.581674
The article indicates that BCL11B is a key transcription factor that regulates cell proliferation and differentiation, and is involved in the development of skin, fat, teeth and cranial sutures. Its mutation leads to premature closure of cranial sutures, and the polymorphism in the 3' regulatory region is related to cardiovascular homeostasis, revealing the core role of this gene in the formation of multiple organs.
Creative Biolabs: BCL11B Antibodies for Research
Creative Biolabs specializes in the production of high-quality BCL11B antibodies for research and industrial applications. Our portfolio includes monoclonal and polyclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.
- Custom BCL11B Antibody Development: Tailor-made solutions to meet specific research requirements.
- Bulk Production: Large-scale antibody manufacturing for industry partners.
- Technical Support: Expert consultation for protocol optimization and troubleshooting.
- Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.
For more details on our BCL11B antibodies, custom preparations, or technical support, contact us at info@creative-biolabs.com.
Reference
- Vedovato-dos-Santos, J. Heather, et al. "BCL11B-related disease: a single phenotypic entity?." European Journal of Human Genetics 33.4 (2025): 451-460. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.1038/s41431-025-01824-x
Anti-BCL11B antibodies
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- AActivation
- AGAgonist
- APApoptosis
- BBlocking
- BABioassay
- BIBioimaging
- CImmunohistochemistry-Frozen Sections
- CIChromatin Immunoprecipitation
- CTCytotoxicity
- CSCostimulation
- DDepletion
- DBDot Blot
- EELISA
- ECELISA(Cap)
- EDELISA(Det)
- ESELISpot
- EMElectron Microscopy
- FFlow Cytometry
- FNFunction Assay
- GSGel Supershift
- IInhibition
- IAEnzyme Immunoassay
- ICImmunocytochemistry
- IDImmunodiffusion
- IEImmunoelectrophoresis
- IFImmunofluorescence
- IGImmunochromatography
- IHImmunohistochemistry
- IMImmunomicroscopy
- IOImmunoassay
- IPImmunoprecipitation
- ISIntracellular Staining for Flow Cytometry
- LALuminex Assay
- LFLateral Flow Immunoassay
- MMicroarray
- MCMass Cytometry/CyTOF
- MDMeDIP
- MSElectrophoretic Mobility Shift Assay
- NNeutralization
- PImmunohistologyp-Paraffin Sections
- PAPeptide Array
- PEPeptide ELISA
- PLProximity Ligation Assay
- RRadioimmunoassay
- SStimulation
- SESandwich ELISA
- SHIn situ hybridization
- TCTissue Culture
- WBWestern Blot




