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Merck
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Key Documents

05-513

Sigma-Aldrich

Anti-ATM Antibody, clone AM9

ascites fluid, clone AM9, Upstate®

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

ascites fluid

Type de produit anticorps

primary antibodies

Clone

AM9, monoclonal

Espèces réactives

human

Fabricant/nom de marque

Upstate®

Technique(s)

western blot: suitable

Isotype

IgG

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ATM(472)

Spécificité

ATM

Immunogène

Full-length human ATM

Application

Detect ATM also known as Ataxia Telangiectasia Mutated with Anti-ATM Antibody, clone AM9 (Mouse Monoclonal Antibody), that has been demonstrated to work in WB.
Research Category
Epigenetics & Nuclear Function
Research Sub Category
Cell Cycle, DNA Replication & Repair

Qualité

routinely evaluated by immunoblot on nuclear extract from Raji cells

Description de la cible

350kDa

Liaison

Replaces: 04-200

Forme physique

Ascites
mouse ascites containing 0.05% sodium azide

Stockage et stabilité

2 years at -20°C

Informations légales

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

Clause de non-responsabilité

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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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Chen Wang et al.
Translational oncology, 10(2), 190-196 (2017-02-10)
The ataxia telangiectasia mutated (ATM) protein kinase plays a central role in the cellular response to DNA damage. Loss or inactivation of both copies of the ATM gene (ATM) leads to ataxia telangiectasia, a devastating childhood condition characterized by neurodegeneration
Characterization of mre11 loss following HSV-1 infection.
Gregory, DA; Bachenheimer, SL
Virology null
T K Pandita et al.
Molecular and cellular biology, 19(7), 5096-5105 (1999-06-22)
A-T (ataxia telangiectasia) individuals frequently display gonadal atrophy, and Atm-/- mice show spermatogenic failure due to arrest at prophase of meiosis I. Chromosomal movements take place during meiotic prophase, with telomeres congregating on the nuclear envelope to transiently form a
Scott L Baughan et al.
Cancer genetics, 264-265, 40-49 (2022-03-31)
Variants of unknown significance (VUS) remain a constant challenge in the diagnosis of hereditary cancer and the counseling of patients with pedigrees suggestive of such a syndrome. In order to assess some of this limitation, several variants in the DNA
K Nakagawa et al.
Molecular and cellular biology, 19(4), 2828-2834 (1999-03-19)
Microinjection of the restriction endonuclease HaeIII, which causes DNA double-strand breaks with blunt ends, induces nuclear accumulation of p53 protein in normal and xeroderma pigmentosum (XP) primary fibroblasts. In contrast, this induction of p53 accumulation is not observed in ataxia

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