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生物源
mouse
共軛
unconjugated
抗體表格
purified immunoglobulin
抗體產品種類
primary antibodies
無性繁殖
SYR6D4, monoclonal
形狀
buffered aqueous solution
分子量
antigen 350 kDa
物種活性
human
技術
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
microarray: suitable
western blot: 1-2 μg/mL using a whole cell extract of an ATM high-producer human melanoma cell line
同型
IgG1
UniProt登錄號
運輸包裝
dry ice
儲存溫度
−20°C
目標翻譯後修改
unmodified
基因資訊
human ... ATM(472)
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一般說明
Ataxia-telangiectasia (A-T) is a rare human autosomal recessive disease with a pleiotropic phenotype characterized by cerebellar degeneration, oculocutaneous telangiectasias, immune dysfunction, genomic instability, cancer predisposition, radiation sensitivity, and premature aging. The gene mutated in A-T, ATM (A-T, mutated), encodes a 350-370 kDa protein. The C-terminal region of the protein has extensive homology to the catalytic domain of PI-3 kinase. ATM is predominantly nuclear and localizes to cytoplasmic vesicles. ATM expression is absent or expressed at very low levels in A-T cells.
Ataxia-telangiectasia, mutated (ATM) is a protein kinase that may regulate cell cycle and the response to DNA damage. ATM is known to associate with β-adaptin and β-NAP and hence, may modulate intracellular transport of proteins and vesicles. Mouse Monoclonal Anti-ATM antibody recognizes human ATM (approx. 350kDa).
應用
Anti-ATM antibody, Mouse monoclonal has been used in:
- immunoblotting
- immunocytochemistry
- immunoprecipitation
Endogenous ATM was immunoprecipitated from whole cell lysates using monoclonal anti-ATM (SYR6D4). Immunoprecipitates were used for an ATM kinase assay.
Mouse Monoclonal Anti-ATM antibody can be used for western blot at 1-2μg/mL using a whole cell extracts of melanoma cell lines. The antibody can also be used for microarray, immunocytochemistry and immunoprecipitation assays.
生化/生理作用
Ataxia-telangiectasia (A-T) cells exhibit hypersensitivity to ionizing radiation and multiple defects responding to DNA double-strand breaks. In addition, A-T cells exhibit a variety of cellular abnormalities in culture, including cytoskeletal defects, abnormalities in the plasma membrane and defects in intracellular signaling. ATM kinase activity is enhanced immediately after exposure of cells to DNA double strand break (DSB)-inducing agents and a fraction of it is localized to nuclear aggregates, colocalized with the phosphorylated form of histone H2AX and Nbs1 protein. It binds to β-adaptin, one of the components of the AP-2 adaptor complex, which is involved in clathrin-mediated endocytosis of receptors.
外觀
Solution 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
免責聲明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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儲存類別代碼
10 - Combustible liquids
水污染物質分類(WGK)
WGK 3
閃點(°F)
Not applicable
閃點(°C)
Not applicable
Nuclear retention of ATM at sites of DNA double strand breaks
The Journal of Biological Chemistry, 276(41), 38224-38230 (2001)
Ataxia-telangiectasia, an evolving phenotype
DNA Repair, 3(8-9), 1187-1196 (2004)
Cytoplasmic ATM in neurons modulates synaptic function
Current Biology, 19(24), 2091-2096 (2009)
Advances in cancer research, 83, 209-254 (2001-10-23)
One of the cornerstones of the web of signaling pathways governing cellular life and differentiation is the DNA damage response. It spans a complex network of pathways, ranging from DNA repair to modulation of numerous processes in the cell. DNA
Proceedings of the National Academy of Sciences of the United States of America, 95(17), 10146-10151 (1998-08-26)
Inherited mutations in the ATM gene lead to a complex clinical phenotype characterized by neuronal degeneration, oculocutaneous telangiectasias, immune dysfunction, and cancer predisposition. Using the yeast two-hybrid system, we demonstrate that ataxia telangiectasia mutated (ATM) binds to beta-adaptin, one of
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