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Phospho-ATM Protein Kinase (Ser1981) Polyclonal Antibody

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说明书
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说明书
实验方案
技术支持

产品信息

600-401-398

应用
建议稀释比
已发表文章

免疫印迹 (WB)

1:500- 1:2,000
-

免疫组化（石蜡） (IHC (P))

Assay-dependent
-

酶联免疫吸附实验 (ELISA)

1:10,000-1:50,000
-
产品规格

种属反应

Human, Mouse

宿主/亚型

Rabbit / IgG

分类

Polyclonal

类型

Antibody

抗原

This antibody was affinity purified from whole rabbit serum prepared by repeated immunizations with a synthetic peptide S-L-A-F-E-E-G-S-Q-S-T-T-I-S-S corresponding to aa 1974-1988 of human ATM conjugated to KLH using maleimide.
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偶联物

Unconjugated Unconjugated Unconjugated

形式

Liquid

浓度

1.1 mg/mL

纯化类型

Affinity chromatography

保存液

0.02M potassium phosphate, pH 7.2, with 0.15M NaCl

内含物

0.01% sodium azide

保存条件

-20° C, Avoid Freeze/Thaw Cycles

运输条件

Ambient (domestic); Wet ice (international)

产品详细信息

Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use.

This affinity-purified antibody is directed against human ATM and is useful in determining its presence in various assays. This polyclonal anti-ATM antibody detects native and over-expressed proteins found in various tissues and extracts. Reactivity is observed against human ATM and cross reactivity with ATM from other mammalian sources has not been tested.

靶标信息

Ataxia-telangiectasia Mutated (ATM) is a protein that belongs to the PI3/PI4 kinase family. Ataxia-telangiectasia is a rare autosomal recessive disorder characterized by progressive neurologic degeneration, immunologic deficiency, and an increased risk of lymphoid cancer. The ATM gene codes for a protein belonging to the phosphoinositide 3-kinase (PI3K) superfamily. ATM phosphorylates proteins instead of lipid and has many downstream targets that act as cell-cycle regulators including: P53, Mdm2, BRCA1, and SMC1. The ATM protein is responsible for repairing double-stranded DNA breaks that occur because of ionizing radiation and other mutagens. The ATM’s C-terminal region has extensive homology to the catalytic domains of phosphatidylinositol 3-kinases (PI3 kinases). Studies have shown that ATM becomes autophosphorylated and upregulated by exposure to ionizing radiation. AT cells are hypersensitive to ionizing radiation, impaired in mediating the inhibition of DNA synthesis and display delays in p53 induction. Further, DNA damage caused by ionizing irradiation activates ATM-kinase, leading to a cascade of kinase reactions that regulate cell cycle, apoptosis, and DNA damage repair. Studies have linked ATM to apoptosis along with Nbs1 and Chk2 in the E2F1 pathway.

仅用于科研。不用于诊断过程。未经明确授权不得转售。

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生物信息学

蛋白别名: A-T mutated; A-T mutated homolog; AT mutated; AT mutated protein; Ataxia t; ataxia telangiectasia gene mutated in human beings; Ataxia telangiectasia mutated; Ataxia telangiectasia mutated homolog; DKFZp781A0353; EC 2.7.1.37; MGC74674; Serine-protein kinase ATM; TEL1, telomere maintenance 1, homolog

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基因别名: AI256621; AT1; ATA; ATC; ATD; ATDC; ATE; ATM; C030026E19Rik; TEL1; TELO1

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UniProt ID: (Human) Q13315, (Mouse) E9QNY7

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Entrez Gene ID: (Human) 472, (Mouse) 11920

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功能
DNA binding protein serine/threonine kinase activity DNA-dependent protein kinase activity protein binding ATP binding 1-phosphatidylinositol-3-kinase activity protein complex binding protein dimerization activity protein N-terminus binding nucleotide binding protein kinase activity kinase activity transferase activity transferase activity, transferring phosphorus-containing groups phosphotransferase activity, alcohol group as acceptor histone serine kinase activity non-receptor serine/threonine protein kinase
参与通路
double-strand break repair via homologous recombination DNA double-strand break processing DNA synthesis involved in DNA repair strand displacement response to hypoxia somitogenesis pre-B cell allelic exclusion DNA replication DNA repair double-strand break repair via nonhomologous end joining protein phosphorylation cellular response to DNA damage stimulus DNA damage induced protein phosphorylation DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest telomere maintenance via telomerase cell cycle arrest mitotic spindle assembly checkpoint reciprocal meiotic recombination signal transduction brain development heart development determination of adult lifespan intrinsic apoptotic signaling pathway in response to DNA damage response to ionizing radiation regulation of autophagy histone phosphorylation peptidyl-serine phosphorylation negative regulation of B cell proliferation positive regulation of telomere maintenance via telomerase positive regulation of histone phosphorylation V(D)J recombination phosphatidylinositol-3-phosphate biosynthetic process peptidyl-serine autophosphorylation lipoprotein catabolic process regulation of apoptotic process positive regulation of apoptotic process positive regulation of DNA damage response, signal transduction by p53 class mediator positive regulation of neuron apoptotic process meiotic telomere clustering protein autophosphorylation oocyte development neuron apoptotic process regulation of telomerase activity histone mRNA catabolic process cellular response to gamma radiation cellular response to X-ray cellular response to nitrosative stress signal transduction involved in mitotic G2 DNA damage checkpoint replicative senescence establishment of RNA localization to telomere establishment of macromolecular complex localization to telomere regulation of cellular response to heat regulation of signal transduction by p53 class mediator negative regulation of TORC1 signaling negative regulation of telomere capping positive regulation of telomere maintenance via telomere lengthening positive regulation of telomerase catalytic core complex assembly DNA damage checkpoint telomere maintenance cell cycle female gamete generation phosphorylation histone-serine phosphorylation phosphatidylinositol phosphorylation regulation of cell cycle
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