磷酸化急性髓细胞白血病1蛋白抗体

本公司是最专业磷酸化急性髓细胞白血病1蛋白抗体供应商，提供磷酸化急性髓细胞白血病1蛋白抗体的报价，泛素样蛋白Sumo2/3抗体咨询，技术服务，欢迎来电咨询选购。

英文名称  Anti-phospho-RUNX1(Ser303)

中文名称  磷酸化急性髓细胞白血病1蛋白抗体

别    名  RUNX1/AML1 (phospho S303); RUNX1(phospho S303); RUNX1(phospho Ser303); p-AML1 (S303); p-AML1 (Ser303); 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.

浓    度  1mg/1ml

规 格  0.2ml/200μg

磷酸化急性髓细胞白血病1蛋白抗体概述：

B淋巴细胞在抗原的刺激下，能够分化、增殖形成具有针对这种抗原分泌特异性抗体的能力。B细胞的这种能力和量是有限的，不可能持续分化增殖下去，因此产生免疫球蛋白的能力也是极其微小的。将这种B细胞与非分泌型的骨髓瘤细胞融合形成杂交瘤细胞，再进一步克隆化，这种克隆化的杂交瘤细胞是既具有瘤细胞的无限分裂的能力，又具有产生特异性抗体的B淋巴细胞的能力。将这种克隆化的杂交瘤细胞进行培养或注入小鼠腹水内即可获得大量的高效、单一的特异性抗体。这种技术即称为单克隆抗体技术。

抗体来源  Rabbit  

克隆类型  polyclonal

交叉反应  Human, Horse

产品类型  一抗  磷酸化抗体  

研究领域  细胞生物 发育生物学 信号转导 干细胞 表观遗传学  

蛋白分子量  predicted molecular weight: 49kDa

性    状  Lyophilized or Liquid

免 疫 原  KLH conjugated Synthesised phosphopeptide derived from human RUNX1 around the phosphorylation site of Ser303

亚    型  IgG

纯化方法  affinity purified by Protein A

储 存 液  Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4

产品应用   WB=1:100-500  ELISA=1:500-1000  IHC-P=1:100-500  IHC-F=1:100-500  ICC=1:100-500  IF=1:100-500

（石蜡切片需做抗原修复）

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

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.

Important Note  This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

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.

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.

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 ALYREF/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 KAT6A and KAT6B. Interacts with SUV39H1, leading to abrogation of transactivating and DNA-binding properties of RUNX1. Interacts with YAP1. Interacts with HIPK2 (By similarity). Interaction with CDK6 prevents myeloid differentiation, reducing its transcription transactivation activity.

Subcellular Location : Nucleus.

Tissue Specificity : Expressed in all tissues examined except brain and heart. Highest levels in thymus, bone marrow and peripheral blood.

Post-translational modifications : Phosphorylated in its C-terminus upon IL-6 treatment. Phosphorylation enhances interaction with KAT6A.

Methylated.

Phosphorylated in Ser-249 Thr-273 and Ser-276 by HIPK2 when associated with CBFB and DNA. This phosphorylation promotes subsequent EP300 phosphorylation.

DISEASE : 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.

磷酸化急性髓细胞白血病1蛋白抗体Note=A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelomonocytic leukemia. Inversion inv(21)(q21;q22) with USP16.

Similarity : Contains 1 Runt domain.

Database links : UniProtKB/Swiss-Prot: Q01196.3