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Merck
CN

A6093

Anti-ATM antibody, Mouse monoclonal

clone SYR6D4, purified from hybridoma cell culture

别名:

Monoclonal Anti-ATM antibody produced in mouse, Anti-Ataxia-Telangiectasia Mutated

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UNSPSC Code:
12352203
NACRES:
NA.41
MDL number:
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产品名称

Anti-ATM antibody, Mouse monoclonal, clone SYR6D4, purified from hybridoma cell culture

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

SYR6D4, monoclonal

form

buffered aqueous solution

mol wt

antigen 350 kDa

species reactivity

human

technique(s)

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

isotype

IgG1

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... ATM(472)

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Application

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.

Biochem/physiol Actions

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.

Disclaimer

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.

General description

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).

Physical form

Solution 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

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存储类别

10 - Combustible liquids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Nuclear retention of ATM at sites of DNA double strand breaks
Andegeko Y, et al.
The Journal of Biological Chemistry, 276(41), 38224-38230 (2001)
Ataxia-telangiectasia, an evolving phenotype
Chun HH and Gatti RA
DNA Repair, 3(8-9), 1187-1196 (2004)
Cytoplasmic ATM in neurons modulates synaptic function
Li J, et al.
Current Biology, 19(24), 2091-2096 (2009)
Y Shiloh et al.
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
D S Lim et al.
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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