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Merck

A1106

Anti-ATM antibody,Mouse monoclonal

clone MAT3-4G10/8, purified from hybridoma cell culture

Synonyme(s) :

Anti-Ataxia-Telangiectasia Mutated

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A propos de cet article

UNSPSC Code:
12352203
NACRES:
NA.45
MDL number:
MFCD01321740

Principaux documents

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Nom du produit

Anti-ATM antibody,Mouse monoclonal, clone MAT3-4G10/8, purified from hybridoma cell culture

biological source

mouse

recombinant

expressed in mouse cell line

conjugate

unconjugated

antibody form

purified from hybridoma cell culture

antibody product type

primary antibodies

clone

MAT3-4G10/8, monoclonal

form

PBS solution

mol wt

antigen ~300 kDa

species reactivity

human, mouse

packaging

antibody small pack of 25 μL

concentration

~2 mg/mL

technique(s)

immunoprecipitation (IP): suitable
indirect ELISA: suitable
western blot: 0.1-0.2 μg/mL using HEK-293T total cel extract

isotype

IgG1

UniProt accession no.

Q13315

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

200

Gene Information

human ... ATM(472)
mouse ... Atm(11920)

Application

Monoclonal Anti-ATM antibody can be used in immunoblotting , ELISA and immunoprecipitation.

Biochem/physiol Actions

Anti-Ataxia-Telangiectasia Mutated (ATM) is responsible for the activation and stabilization of p53 in response to double-strand break (DSB). ATM phosphorylates p53 directly on Ser15 and concomitantly activates other kinases that phosphorylate the same molecule on additional sites. Furthermore, human homolog of double minute 2 (Hdm2) is phosphorylated by ATM on Ser395 and this phosphorylation inhibits Hdm2-mediated degradation of p53.
Monoclonal Anti-ATM antibody reacts specifically with mouse and human ATM.

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

Monoclonal Anti-ATM (mouse IgG1 isotype) is derived from the hybridoma MAT3-4G10/8 produced by the fusion of mouse myeloma cells (NSO) and splenocytes from BALB/c mice immunized with a peptide.

Immunogen

peptide spanning positions 1967-1988 of mouse ATM containing a cysteine at its NH2 terminus coupled to KLH.

Physical form

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

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Classe de stockage

10 - Combustible liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificats d'analyse (COA)

Lot/Batch Number
0000476087
0000476087
0000420018
0000420018
0000339705

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Consulter la Bibliothèque de documents

ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage
Maya R, et al.
Genes & Development, 15(9), 1067-1067 (2001)
Phosphorylation of Hdmx mediates its Hdm2- and ATM-dependent degradation in response to DNA damage
Pereg Y, et al.
Proceedings of the National Academy of Sciences of the USA, 102(14), 5056-5061 (2005)
Jasmin Roohi et al.
Journal of human genetics, 62(5), 581-584 (2017-01-27)
Ataxia-telangiectasia (A-T) is an autosomal recessive chromosome breakage disorder caused by mutations in the ATM gene. Typically, it presents in early childhood with progressive cerebellar dysfunction along with immunodeficiency and oculocutaneous telangiectasia. An increased risk of malignancy is also associated
Tatiana N Moiseeva et al.
DNA repair, 43, 9-17 (2016-05-29)
We describe a dynamic phosphorylation on serine-1940 of the catalytic subunit of human Pol ε, POLE1, following DNA damage. We also describe novel interactions between POLE1 and the iron-sulfur cluster assembly complex CIA proteins CIAO1 and MMS19. We show that
Domenico Delia et al.
Human molecular genetics, 13(18), 2155-2163 (2004-07-23)
Hypomorphic mutations of the MRE11 gene are the hallmark of the radiosensitive ataxia-telangiectasia-like disorder (ATLD). Here, we describe a new family with two affected siblings, ATLD5 and ATLD6, now aged 37 and 36, respectively. They presented with late onset cerebellar
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Contenu apparenté

Data Sheet - A1106

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