Bcl11a Antibodies

B-cell lymphoma/leukemia 11A (Bcl11a)

Functions as a myeloid and B-cell proto-oncogene.

May play important roles in leukemogenesis and hematopoiesis.

A vital element in lymphopoiesis, is needed for B-cell formation in fetal liver. May function as a modulator of the transcriptional repression activity of ARP1.

Gene Information

Mouse
Gene Name:	Bcl11a
Uniprot:	Q9QYE3
Entrez:	14025

Family

Belongs to:
No superfamily

Alternative Names

B-cell CLL/lymphoma 11A (zinc finger protein) isoform 2; B-cell CLL/lymphoma 11A (zinc finger protein); B-cell CLL/lymphoma 11A; B-cell lymphoma/leukemia 11A; BCL11A B-cell CLL/lymphoma 11A (zinc finger protein) isoform 1; BCL-11A; BCL11A-S; BCL11A-XL; C2H2-type zinc finger protein; COUP-TF-interacting protein 1; CTIP1ecotropic viral integration site 9; ecotropic viral integration site 9 homolog; Ecotropic viral integration site 9 protein homolog; EVI-9; EVI9FLJ34997; HBFQTL5; KIAA1809BCL11A-L; Zinc finger protein 856; ZNF856FLJ10173

Molecular Weight

Mass (kDA):
83.855 kDA

Genomic Context

Mouse
Location:	11|11 A3.2
Sequence:	11;

Tissue Specificity

Isoforms are expressed in a tissue-specific fashion. Isoforms 1, isoform 2, and isoform 3 are expressed at similar levels in testis, kidney and spleen. Isoform 1 is expressed in the stomach, and isoform 2 is expressed exclusively in the lung. Overexpression following proviral integration in hematopoietic cells results in the generation of myeloid leukemia.

Diseases

• Anemia, Sickle Cell
• Leukemia
• Beta Thalassemia
• Lymphoma
• Malignant Neoplasms
• Neoplasms
• Anemia
• B-cell Lymphomas
• Lymphoid Leukemia
• Chronic Lymphocytic Leukemia
• Thalassemia
• Chromosomal Translocation
• Diabetes Mellitus

• Diabetes Mellitus, Non-insulin-dependent
• Hemoglobinopathies
• Hemoglobin F Disease
• Hodgkin Disease
• Myeloid Leukemia
• Cell Transformation, Neoplastic
• Diffuse Large B-cell Lymphoma

Pathways

• Pathogenesis
• Cell Development
• Gene Silencing
• Interphase
• Cell Proliferation
• Secretion
• Cell Fate Specification
• Translation
• Insulin Secretion
• Localization
• Methylation
• Innervation
• Cell Activation

• Developmental Process
• Dna Hypomethylation
• Brain Development
• Aging
• Neurogenesis
• B Cell Activation
• Ribosome Assembly

PTMs

• Deacetylation
• Phosphorylation

• Acetylation
• Methylation

• Sumoylation

Research Areas

• Apoptosis
• Cancer
• Inhibitors, Activators and Regulators
• Transcription Factors and Regulators
• Tumor Suppressors

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Bcl11a

Best Uses of the Anti-Ctip1 BCL11A Marker in Boster Bio

This article describes the Anti-Ctip1 CCL11A marker and how it regulates this gene using transcription factors. It will also show how this antibody reacts with Human protein. The following are the best uses of this antibody. Listed below are a few. These guidelines will help you maximize your results using this antibody. This information is useful for many research applications.

Anti-Ctip1 BCL11A Signer

The Anti-Ctip1 BCL11A marker in Boster Bio has been tested in flow cytometry, immunohistochemistry, and western blot assays. It was found to react with human cells. It is available in the A00741 catalog.

Although its function is not known, it is believed to play a role regulating hemoglobin levels. It is a transcription factor essential for the coordination of the development and maintenance of erythroid cells. It can be found in multiprotein complexes and transcription factors.

BCL11A interacts chromatin-modifying and histone desmethylases proteins. These proteins occupy the chromatin and regulate transcription. CPN survival is dependent on BCL11A expression in the early stages of postnatal life. Massive apoptosis occurs when Bcl11a is ablated in CPN. There are no known effective drugs for BCL11A.

ChIP analysis of erythroid cells has identified a variety of proteins that interact with BCL11A. Functional RNAi screens identified HbF regulators. Therefore, knocking out one or two critical components could result in the complete functional protein complex being disrupted. By knocking out BCL11A, a decrease in HbF expression is observed. The knockdown or loss of one component could lead to destabilization and/or impairment of chromatin occupancy.

BCL11A plays a role in silencing HbF. It also regulates hematopoietic functions. This gene may provide clues on therapeutic approaches for patients suffering from b-hemoglobinopathies. These results highlight the importance of BCL11A in the treatment of hemophilia. But there are also challenges.

Applications

The BCL11A marker has numerous applications, including the detection of breast cancer, colon cancer, lung cancer, and other malignancies. Analyzing individual cells' mRNA levels can reveal Bcl11A expression. Decreased mRNA levels mean a decrease in protein expression. This is a significant decrease if the protein level is less than five percent. It can also be interpreted as a decrease or omission of protein expression, which could mean a decrease of 20 percent to 30 percent or 40 percent.

BCL11A is involved in regulation of fetal blood hemoglobin. In addition to being a stage-specific regulator of fetal hemoglobin expression, BCL11A is a repressor of g-globin induction. In the human genome assembly, the BCL11A gene maps to chromosome 2 at 60,716,189-60,728,612 (Fig. 1). Its upstream distal regulatory region consistently contains three DNAse 1-hypersensitive sites.

BCL11A deletion selectively eliminates lymphoid competent HSCs. The resulting Bcl11a// cell is lymphoid-deficient. Restricted Bcl11a// HSCs have a limited self-renewal ability. For these reasons, the BCL11A marker is essential for studies of these cell types. If the BCL11A genes is deleted, lymphoid development is decreased and the phenotype for myeloerythroids increases.

Evidence is mounting that the HSC compartment may be heterogeneous. Part of the Bcl11a deficient HSCs show lineage restriction, bias, and other symptoms. It has been also shown that the Bcl11a-deficient HSCs have a lymphoid defect that is dependent on Bcl11a function. The HSC compartment was previously difficult to dissect unbiased transcriptomically due to its rarity. RNA-seq technology, however, has solved this problem.

Regulation

The BCL11A marker can be used in molecular biology for many purposes. BCL11A regulates many protein functions, including cyclin-dependent kinase inhibitor 1A (p21), early Bcell factor 1A (Ebf1) as well as paired box 5 (px5). It is also associated to cell proliferation, differentiation and death. Its exact functions are still unknown.

Because of its role in the switchover of hemoglobin from fetal to adult, the BCL11A genes has attracted increased interest. The BCL11A protein regulates both b and the g-globin genes. It has been demonstrated to suppress fetal hemoglobin as well as promoting adult hemoglobin. KLF1 activates b-globin and suppresses g-globin expression. It also interacts with a transcription factor called repressor element-1 silencing factor.

Regulation via transcription factors

The Boster Bio Anti-Ctip1 BCL11A antibody (catalog number A00741) has been tested in Flow Cytometry, Immunohistochemistry, and Western Blot. It reacts with Human samples as well as known positive and negative ones. The resulting data is summarized in Table 1, below. The results from the above experiment show that the antibody is effective for detecting BCL11A in a variety of cell types and tissues.

Regulation by the CRISPR-Cas9

Scientists have identified which CRISPR/Cas9 markers are most useful. Scientists have identified deletions in this gene that were caused by CRISPR/Cas9 encoded RNAs. This is critical for the development tissues. This gene is enriched for expression of the endodermis markers genes GATA4 or NES, which promote stem cell proliferation in vitro.

The BCL11A gene regulates hemoglobin production in the erythroid lineage. BCL11A can be disrupted in HSCs to stop it from being expressed. However, knockdowns of BCL11A resulted in a significant increase S/G2-phase HSCs in NSG mice. This is associated with stem cell exhaustion. The BCL11A gene can be targeted by autologous CRISPR-Cas9-modified CD34+ hHSPCs, which differentiate into the various types of blood cells. This enhances HbF production in red blood cells compensates patients with SCD for their reduced adult hemoglobin.

The Cas9-gRNA complex improves the efficiency of gene-editing and reduces off-target effects. Its two components, Cas9RNA RNA and Cas9gRNARNARNA can be delivered into cells via a variety different methods, including by electroporation. CRISPR/Cas9 encoded RNA has been shown in human cells to cause cell death and a cytosolic, dsDNA-induced innate immuno response.

The +1 NHEJ editing is the best way to edit this gene, as it permits donor-free gene therapy. Multiple machine learning models are available to predict the outcome of editing and help choose the most effective gRNA. One machine learning model was trained in order to predict the frequency and type of BCL11A gene edits in 100 cancer cells. Another model was trained to detect edits using NHEJ +1.