Western blot: 1: 500 - 1: 1000. Immunohistochemistry on paraffin sections: 1: 50 - 1: 200. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user.
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 all tissues examined except brain and heart, 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.Synonyms: 1, AML-1, AML1, AML1-EVI-1, AMLCR1, Acute myeloid leukemia 1 protein, CBF-alpha-2, CBFA2, Core-binding factor subunit alpha-2, EVI-1, PEA2-alpha B, PEBP2-alpha B, PEBP2A2, Polyomavirus enhancer-binding protein 2 alpha B subunit, Runt-related transcription factor, SL3-3 enhancer factor 1 alpha B subunit, SL3/AKV core-binding factor alpha B subunit