|Other Names||Runt-related transcription factor 1, Acute myeloid leukemia 1 protein, Core-binding factor subunit alpha-2, CBF-alpha-2, Oncogene AML-1, Polyomavirus enhancer-binding protein 2 alpha B subunit, PEA2-alpha B, PEBP2-alpha B, SL3-3 enhancer factor 1 alpha B subunit, SL3/AKV core-binding factor alpha B subunit, RUNX1, AML1, CBFA2|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP3672a was selected from the region of human Phospho-RUNX1-S276. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||CBF binds to the core site, 5'-PYGPYGGT-3', of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers, LCK, IL-3 and GM-CSF promoters. The alpha subunit binds DNA and appears to have a role in the development of normal hematopoiesis. Isoform AML-1L interferes with the transactivation activity of RUNX1. Acts synergistically with ELF4 to transactivate the IL-3 promoter and with ELF2 to transactivate the mouse BLK promoter. Inhibits KAT6B- dependent transcriptional activation. Controls the anergy and suppressive function of regulatory T-cells (Treg) by associating with FOXP3. Activates the expression of IL2 and IFNG and down- regulates the expression of TNFRSF18, IL2RA and CTLA4, in conventional T-cells (PubMed:17377532).|
|Tissue Location||Expressed in all tissues examined except brain and heart. Highest levels in thymus, bone marrow and peripheral blood|
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Provided below are standard protocols that you may find useful for product applications.
AML1/Runx1 binds DNA as a monomer and through the Runt domain. DNA binding is increased by heterodimerization with CBFB. Isoform AML1L can neither bind DNA nor heterodimerize and interferes with the transactivation activity of AML1/Runx1. CBF binds to the core site, 5'-PYGPYGGT-3', of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T cell receptor enhancers, LCK, IL3 and GMCSF promoters. The alpha subunit binds DNA and appears to have a role in the development of normal hematopoiesis. AML1/Runx1 is expressed in a wide variety of tissues and is expressed at the highest levels in thymus, bone marrow and peripheral blood. Defects in AML1/Runx1 are the cause of familial platelet disorder with associated myeloid malignancy, an autosomal dominant disease characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukemia.
Roberts,K.E., et.al., Gastroenterology (2010) In pressKonn,Z.J., et.al., Genes Chromosomes Cancer 49 (3), 253-259 (2010)
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