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CBFA2T2 Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IF, E |
|---|---|
| Primary Accession | O43439 |
| Other Accession | NP_001028171.1, NP_005084.1 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 67133 Da |
| Antigen Region | 1-29 aa |
| Gene ID | 9139 |
|---|---|
| Other Names | Protein CBFA2T2, ETO homologous on chromosome 20, MTG8-like protein, MTG8-related protein 1, Myeloid translocation-related protein 1, p85, CBFA2T2, EHT, MTGR1 |
| Target/Specificity | This CBFA2T2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-29 amino acids from the N-terminal region of human CBFA2T2. |
| Dilution | IF~~1:10~50 WB~~1:2000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | CBFA2T2 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | CBFA2T2 |
|---|---|
| Synonyms | EHT, MTGR1 |
| Function | Transcriptional corepressor which facilitates transcriptional repression via its association with DNA-binding transcription factors and recruitment of other corepressors and histone-modifying enzymes (PubMed:12559562, PubMed:15203199). Via association with PRDM14 is involved in regulation of embryonic stem cell (ESC) pluripotency (PubMed:27281218). Involved in primordial germ cell (PCG) formation. Stabilizes PRDM14 and OCT4 on chromatin in a homooligomerization- dependent manner (By similarity). Can repress the expression of MMP7 in a ZBTB33-dependent manner (PubMed:23251453). May function as a complex with the chimeric protein RUNX1/AML1-CBFA2T1/MTG8 (AML1-MTG8/ETO fusion protein) which is produced in acute myeloid leukemia with the chromosomal translocation t(8;21). May thus be involved in the repression of AML1-dependent transcription and the induction of G- CSF/CSF3-dependent cell growth. May be a tumor suppressor gene candidate involved in myeloid tumors with the deletion of the 20q11 region. Through heteromerization with CBFA2T3/MTG16 may be involved in regulation of the proliferation and the differentiation of erythroid progenitors by repressing the expression of TAL1 target genes (By similarity). Required for the maintenance of the secretory cell lineage in the small intestine. Can inhibit Notch signaling probably by association with RBPJ and may be involved in GFI1-mediated Paneth cell differentiation (By similarity). |
| Cellular Location | Nucleus. |
| Tissue Location | Ubiquitously expressed in fetal and adult tissues. Highly expressed in adult brain, heart, lung, kidney, lymph node, appendix, thymus, testis, uterus, small intestine, prostate and thymus |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
In acute myeloid leukemia, especially in the M2 subtype, the t(8;21)(q22;q22) translocation is one of the most frequent karyotypic abnormalities. The translocation produces a chimeric gene made up of the 5'-region of the RUNX1 (AML1) gene fused to the 3'-region of the CBFA2T1 (MTG8) gene. The chimeric protein is thought to associate with the nuclear corepressor/histone deacetylase complex to block hematopoietic differentiation. The protein encoded by this gene binds to the AML1-MTG8 complex and may be important in promoting leukemogenesis. Several transcript variants are thought to exist for this gene, but the full-length natures of only three have been described.
References
Guastadisegni, M.C., et al. Leukemia 24(8):1516-1519(2010)
Ossovskaya, V.S., et al. J. Neurosci. Methods 177(2):322-333(2009)
Venkatesan, K., et al. Nat. Methods 6(1):83-90(2009)
Olsson, A., et al. Biochim. Biophys. Acta 1779(10):590-598(2008)
Kumar, R., et al. Mol. Cancer Res. 4(9):655-665(2006)
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