The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Additional notesBest use within three months from the date of receipt of this protein.
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Preparation and Storage
Stability and Storage
Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
pH: 8.00 Constituents: 0.31% Glutathione, 0.79% Tris HCl
Acute myeloid leukemia 1
Acute myeloid leukemia 1 protein
alpha subunit core binding factor
AML1 EVI 1
AML1 EVI 1 fusion protein
CBF alpha 2
Core binding factor alpha 2 subunit
Core binding factor runt domain alpha subunit 2
Core-binding factor subunit alpha-2
Oncogene AML 1
PEA2 alpha B
PEBP2 alpha B
Polyomavirus enhancer binding protein 2 alpha B subunit
Polyomavirus enhancer-binding protein 2 alpha B subunit
Runt related transcription factor 1
Runt-related transcription factor 1
SL3 3 enhancer factor 1 alpha B subunit
SL3-3 enhancer factor 1 alpha B subunit
SL3/AKV core binding factor alpha B subunit
SL3/AKV core-binding factor alpha B subunit
FunctionCBF 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 MYST4-dependent transcriptional activation.
Tissue specificityExpressed in all tissues examined except brain and heart. Highest levels in thymus, bone marrow and peripheral blood.
Involvement in diseaseNote=A chromosomal aberration involving RUNX1/AML1 is a cause of M2 type acute myeloid leukemia (AML-M2). Translocation t(8;21)(q22;q22) with RUNX1T1. Note=A chromosomal aberration involving RUNX1/AML1 is a cause of therapy-related myelodysplastic syndrome (T-MDS). Translocation t(3;21)(q26;q22) with EAP or MECOM. Note=A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelogenous leukemia (CML). Translocation t(3;21)(q26;q22) with EAP or MECOM. Note=A chromosomal aberration involving RUNX1/AML1 is found in childhood acute lymphoblastic leukemia (ALL). Translocation t(12;21)(p13;q22) with TEL. The translocation fuses the 3'-end of TEL to the alternate 5'-exon of AML-1H. Note=A chromosomal aberration involving RUNX1 is found in acute leukemia. Translocation t(11,21)(q13;q22) that forms a MACROD1-RUNX1 fusion protein. Defects in RUNX1 are the cause of familial platelet disorder with associated myeloid malignancy (FPDMM) [MIM:601399]. FPDMM is an autosomal dominant disease characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukemia. Note=A chromosomal aberration involving RUNX1/AML1 is found in therapy-related myeloid malignancies. Translocation t(16;21)(q24;q22) that forms a RUNX1-CBFA2T3 fusion protein. Note=A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelomonocytic leukemia. Inversion inv(21)(q21;q22) with USP16.
Sequence similaritiesContains 1 Runt domain.
DomainA proline/serine/threonine rich region at the C-terminus is necessary for transcriptional activation of target genes.
Post-translational modificationsPhosphorylated in its C-terminus upon IL-6 treatment. Phosphorylation enhances interaction with MYST3. Methylated.