The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Best use within three months from the date of receipt of this protein.
Concentration information loading...
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
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 MYST4-dependent transcriptional activation.
Expressed in all tissues examined except brain and heart. Highest levels in thymus, bone marrow and peripheral blood.
Note=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.
Contains 1 Runt domain.
A proline/serine/threonine rich region at the C-terminus is necessary for transcriptional activation of target genes.
Phosphorylated in its C-terminus upon IL-6 treatment. Phosphorylation enhances interaction with MYST3. Methylated.