Background:

alternative products:Additional isoforms seem to exist|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)

Classification:

Primary antibody

Alternative names:

RUNX1 ;Acetyl Lys24; 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

Species reactivity:

Human, Mouse, Rat

Host:

Rabbit

Isotype:

IgG

Immunogen:

Synthesized peptide derived from human RUNX1 (Acetyl Lys24)

Concentration:

1 mg/ml

Molecular weight:

49830

Applications:

WB, ELISA

Storage:

-20°C for 1 year

More info:

Email: info@sobekbio.com

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