|Tested species reactivity||Human, Mouse, Rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Peptide sequence around phosphorylation site of Serine 435( S-N-S(p)-P-T) derived from Human AML1.|
|Storage buffer||PBS, pH 7.4, with 50% glycerol|
|Contains||0.02% sodium azide|
|Tested Applications||Dilution *|
|Western Blot (WB)||1:500-1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
A suggested positive control for Western blot is 293 or HepG2 cells.
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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.