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A6218

Anti-ATM antibody, Mouse monoclonal

Name: Anti-ATM antibody, Mouse monoclonal
Brand: SIGMA

clone SYML6A10, purified from hybridoma cell culture

Synonym(s):

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

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About This Item

MDL number:

MFCD01321740

UNSPSC Code:

12352203

NACRES:

NA.41

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

SYML6A10, monoclonal

form

buffered aqueous solution

mol wt

antigen ~350 kDa

species reactivity

human

technique(s)

immunocytochemistry: suitable
microarray: suitable
western blot: 1-2 μg/mL using total cell extract from a G-361 (human melanoma) cell line

isotype

IgG1

UniProt accession no.

Q13315

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ATM(472)

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General description

Ataxia-Telangiectasia Mutated (ATM) is a member of the phosphatidylinositol 3-kinase (PI-3) family of kinases. It is activated in response to DNA damage such as double stranded breaks.

Mouse Monoclonal Anti-ATM antibody binds to human ATM.

Immunogen

synthetic peptide corresponding to the C-terminal region of human ATM with N-terminally added cysteine, conjugated to KLH.

Application

Mouse Monoclonal Anti-ATM antibody can be used for western blot assays at 1-2μg/ml using G-361 cell extracts. The antibody can also be used for immunocytochemistry and microarray applications.

Physical form

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

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.

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Certificates of Analysis (COA)

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ATM, ATR and DNA-PK: initiators of the cellular genotoxic stress responses.

Jun Yang et al.

Carcinogenesis, 24(10), 1571-1580 (2003-08-16)

Exposure to genotoxic agents is a major cause of human cancer, and cellular responses to genotoxic stress are important defense mechanisms. These responses are very complex, involving many cellular factors that form an extensive signal transduction network. This network includes

A RASSF1A polymorphism restricts p53/p73 activation and associates with poor survival and accelerated age of onset of soft tissue sarcoma.

Karen S Yee et al.

Cancer research, 72(9), 2206-2217 (2012-03-06)

RASSF1A (Ras association domain containing family 1A), a tumor suppressor gene that is frequently inactivated in human cancers, is phosphorylated by ataxia telangiectasia mutated (ATM) on Ser131 upon DNA damage, leading to activation of a p73-dependent apoptotic response. A single-nucleotide

Lack of vitamin D receptor causes stress-induced premature senescence in vascular smooth muscle cells through enhanced local angiotensin-II signals.

Petya Valcheva et al.

Atherosclerosis, 235(2), 247-255 (2014-06-02)

The inhibition of the renal renin-angiotensin system by the active form of vitamin D contributes to the cardiovascular health benefits of a normal vitamin D status. Local production of angiotensin-II in the vascular wall is a potent mediator of oxidative

Wild-type p53-induced phosphatase 1 (Wip1) forestalls cellular premature senescence at physiological oxygen levels by regulating DNA damage response signaling during DNA replication.

Hiroyasu Sakai et al.

Cell cycle (Georgetown, Tex.), 13(6), 1015-1029 (2014-02-21)

Wip1 (protein phosphatase Mg(2+)/Mn(2+)-dependent 1D, Ppm1d) is a nuclear serine/threonine protein phosphatase that is induced by p53 following the activation of DNA damage response (DDR) signaling. Ppm1d(-/-) mouse embryonic fibroblasts (MEFs) exhibit premature senescence under conventional culture conditions; however, little

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