RUNX1 (Acetyl Lys24) rabbit pAb

• Background:

  Alternative products:Additional isoforms seem to exist, caution:The fusion of AML1 with EAP in T-MDS induces a change of reading frame in the latter resulting in 17 AA unrelated to those of EAP., disease:A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelogenous leukemia (CML) . Translocation t (3;21) (q26; q22) with EAP, MSD1 or EVI1., disease:A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelomonocytic leukemia. Inversion inv (21) (q21; q22) with USP16., disease: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/MTG8/ETO., disease:A chromosomal aberration involving RUNX1/AML1 is a cause of therapy-related myelodysplastic syndrome (T-MDS) . Translocation t (3;21) (q26; q22) with EAP, MSD1 or EVI1., disease: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., disease: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., disease: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., domain:A proline/serine/threonine rich region at the C-terminus is necessary for transcriptional activation of target genes., function: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., PTM:Methylated., PTM:Phosphorylated in its C-terminus upon IL-6 treatment. Phosphorylation enhances interaction with MYST3., similarity:Contains 1 Runt domain., subunit:Heterodimer with CBFB. RUNX1 binds DNA as a monomer and through the Runt domain. DNA-binding is increased by heterodimerization. Isoform AML-1L can neither bind DNA nor heterodimerize. Interacts with TLE1 and THOC4. Interacts with ELF1, ELF2 and SPI1. Interacts via its Runt domain with the ELF4 N-terminal region. Interaction with ELF2 isoform 2 (NERF-1a) may act to repress RUNX1-mediated transactivation. Interacts with MYST3 and MYST4. Interacts with SUV39H1, leading to abrogate the transactivating and DNA-binding properties of RUNX1., tissue specificity:Expressed in all tissues examined except brain and heart. Highest levels in thymus, bone marrow and peripheral blood.

• Description:

  Alternative products: Additional isoforms seem to exist, Caution: The fusion of AML1 with EAP in T-MDS induces a change of reading frame in the latter resulting in 17 AA unrelated to those of EAP. Disease: A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelogenous leukemia (CML). Translocation t (3;21) (q26;q22) with EAP, MSD1 or EVI1. Disease: A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelomonocytic leukemia. Inversion inv (21) (q21;q22) with USP16. Disease: 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/MTG8/ETO. Disease: A chromosomal aberration involving RUNX1/AML1 is a cause of therapy-related myelodysplastic syndrome (T-MDS). Translocation t (3;21) (q26;q22) with EAP, MSD1 or EVI1. Disease: 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. Disease: 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. Disease: 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. Domain: A proline/serine/threonine rich region at the C-terminus is necessary for transcriptional activation of target genes. function: 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. PTM: Methylated. PTM: Phosphorylated in its C-terminus upon IL-6 treatment. Phosphorylation enhances interaction with MYST3. similarity: Contains 1 Runt domain. subunit: Heterodimer with CBFB. RUNX1 binds DNA as a monomer and through the Runt domain. DNA-binding is increased by heterodimerization. Isoform AML-1L can neither bind DNA nor heterodimerize. Interacts with TLE1 and THOC4. Interacts with ELF1, ELF2 and SPI1. Interacts via its Runt domain with the ELF4 N-terminal region. Interaction with ELF2 isoform 2 (NERF-1a) may act to repress RUNX1-mediated transactivation. Interacts with MYST3 and MYST4. Interacts with SUV39H1, leading to abrogate the transactivating and DNA-binding properties of RUNX1. tissue specificity: Expressed in all tissues examined except brain and heart. Highest levels in thymus, bone marrow and peripheral blood.

• Synonyms:

  Runt-related transcription factor 1 (Acute myeloid leukemia 1 protein;Core-binding factor subunit alpha-2;CBF-alpha-2;Oncogene AML-1;Polyomavirus enhancer-binding protein 2 alpha B subunit;PEA2-alpha B;PEBP2-alpha B;SL3-3 enhancer factor 1 alpha B subunit;SL3/AKV core-binding factor alpha B subunit)

• Gene ID:

  861

• UniProt:

  Q01196

• Cellular Locus:

  Nucleus.

• Host:

  Rabbit

• Species Reactivity:

  Human, Mouse, Rat

• Reactivity:

  Human; Mouse; Rat

• Immunogen:

  Synthesized peptide derived from human RUNX1 (Acetyl Lys24)

• Clonality:

  Polyclonal

• Isotype:

  IgG

• Source:

  Rabbit

• Applications:

  WB, ELISA

• Validated Applications:

  WB, ELISA

• Stability:

  -20°C/1 year

• Concentration:

  1 mg/mL

• Dilution:

  WB 1:1000-2000 ELISA 1:5000-20000

• Molecular Weight:

  50kD

• Storage Conditions:

  PBS with 0.02% sodium azide and 50% glycerol pH 7.4. Store at -20°C. Avoid repeated freeze-thaw cycles.

• Observed Molecular Weight:

  50 kD

• Subcellular Location:

  Nucleus.

• Other Product Names:

  Runt-related transcription factor 1 (Acute myeloid leukemia 1 protein; Core-binding factor subunit alpha-2; CBF-alpha-2; Oncogene AML-1; Polyomavirus enhancer-binding protein 2 alpha B subunit; PEA2-alpha B; PEBP2-alpha B; SL3-3 enhancer factor 1 alpha B subunit; SL3/AKV core-binding factor alpha B subunit)

• Gene ID (Human):

  861

• SwissProt (Human):

  Q01196