急性髓细胞白血病1蛋白抗体
英文名称 RUNX1
中文名称 急性髓细胞白血病1蛋白抗体
别 名 Acute myeloid leukemia 1; Acute myeloid leukemia 1 protein; alpha subunit core binding factor; AML 1; AML1 EVI 1; Aml1 oncogene; AMLCR 1; AMLCR1; CBFA 2; CBFA2; Core binding factor alpha 2 subunit; Core binding factor runt domain alpha subunit 2; EVI 1; EVI1; HGNC; Oncogene AML 1; PEA2 alpha; PEBP2 alpha B; PEBP2A2; PEBP2aB; Polyomavirus enhancer binding protein 2 alpha B subunit; Run1; Runt related transcription factor 1; RUNX 1; SL3 3 enhancer factor 1 alpha B subunit; SL3/AKV core binding factor alpha B subunit; RUNX1_HUMAN.
研究领域 肿瘤 心血管 细胞生物 细胞凋亡
抗体来源 Rabbit
克隆类型 Polyclonal
交叉反应 Human, Mouse, Rat, Dog, Cow, Horse, Rabbit,
产品应用 WB=1:500-2000 ELISA=1:500-1000 Flow-Cyt=1ug/Test
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 50kDa
细胞定位 细胞核
性 状 Lyophilized or Liquid
浓 度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human RUNX1:101-200/453
亚 型 IgG
纯化方法 affinity purified by Protein A
储 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
PubMed PubMed
产品介绍 AML1/Runx1 binds DNA as a monomer and through the Runt domain. DNA binding is increased by heterodimerization with CBFB. Isoform AML1L can neither bind DNA nor heterodimerize and interferes with the transactivation activity of AML1/Runx1. 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, IL3 and GMCSF promoters. The alpha subunit binds DNA and appears to have a role in the development of normal hematopoiesis. AML1/Runx1 is expressed in a wide variety of tissues and is expressed at the highest levels in thymus, bone marrow and peripheral blood. Defects in AML1/Runx1 are the cause of familial platelet disorder with associated myeloid malignancy, an autosomal dominant disease characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukemia。