Key features and details
- Rabbit polyclonal to RUNX1 / AML1
- Suitable for: WB
- Reacts with: Mouse, Human
- Isotype: IgG
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Batches of this product that have a concentration < 1mg/ml may have BSA added as a stabilising agent. If you would like information about the formulation of a specific lot, please contact our scientific support team who will be happy to help.
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab35962 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.25 µg/ml. Detects a band of approximately 53 kDa (predicted molecular weight: 49 kDa).|
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.
modificationsPhosphorylated in its C-terminus upon IL-6 treatment. Phosphorylation enhances interaction with MYST3.
- Information by UniProt
- Acute myeloid leukemia 1 antibody
- Acute myeloid leukemia 1 protein antibody
- alpha subunit core binding factor antibody
All lanes : Anti-RUNX1 / AML1 antibody (ab35962) at 1 µg/ml
Lane 1 : Jurkat nuclear extract lysate (ab14844)
Lane 2 : MOLT4 (Human acute lymphoblastic leukemia cell line) Whole Cell Lysate
Lysates/proteins at 10 µg per lane.
All lanes : Goat Anti-Rabbit IgG H&L (HRP) (ab97051) at 1/10000 dilution
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size: 49 kDa
Observed band size: 52,54,55 kDa why is the actual band size different from the predicted?
Additional bands at: 47 kDa, 75 kDa. We are unsure as to the identity of these extra bands.
Exposure time: 10 seconds
RUNX2 recombinant protein full length, with N-terminal HIS tag, expressed in E.Coli.
RUNX3 overexpression and empty vector control lysates created in HEK293T cells. The protein contains a C-terminal DDK tag.
ab35962 has been referenced in 7 publications.
- Serrano-Coll H et al. Notch Signaling Pathway Expression in the Skin of Leprosy Patients: Association With Skin and Neural Damage. Front Immunol 11:368 (2020). PubMed: 32265900
- Liang Z et al. Down-regulation of lncRNA-NEF indicates poor prognosis in intrahepatic cholangiocarcinoma. Biosci Rep 39:N/A (2019). PubMed: 31015363
- Shi X et al. Clonal expansion and myeloid leukemia progression modeled by multiplex gene editing of murine hematopoietic progenitor cells. Exp Hematol 64:33-44.e5 (2018). WB . PubMed: 29751067
- Zhao H et al. KSRP specifies monocytic and granulocytic differentiation through regulating miR-129 biogenesis and RUNX1 expression. Nat Commun 8:1428 (2017). PubMed: 29127290
- Zape JP et al. Cell cycle dynamics and complement expression distinguishes mature haematopoietic subsets arising from hemogenic endothelium. Cell Cycle 16:1835-1847 (2017). PubMed: 28820341
- Cheng Y et al. RUNX1 promote invasiveness in pancreatic ductal adenocarcinoma through regulating miR-93. Oncotarget 8:99567-99579 (2017). PubMed: 29245924
- Tsunoda T et al. Immune-related zinc finger gene ZFAT is an essential transcriptional regulator for hematopoietic differentiation in blood islands. Proc Natl Acad Sci U S A 107:14199-204 (2010). IHC-P ; Mouse . PubMed: 20660741