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Merck

05-513

Anti-ATM Antibody, clone AM9

ascites fluid, clone AM9, Upstate®

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A propos de cet article

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
AM9, monoclonal
Application:
WB
Citations:
17
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biological source

mouse

conjugate

unconjugated

antibody form

ascites fluid

antibody product type

primary antibodies

clone

AM9, monoclonal

species reactivity

human

manufacturer/tradename

Upstate®

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... ATM(472)

General description

350kDa

Immunogen

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

Biochem/physiol Actions

ATM

Physical form

Ascites
mouse ascites containing 0.05% sodium azide

Preparation Note

2 years at -20°C

Analysis Note

routinely evaluated by immunoblot on nuclear extract from Raji cells

Other Notes

Replaces: 04-200

Legal Information

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

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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Classe de stockage

12 - Non Combustible Liquids

wgk

nwg

flash_point_f

Not applicable

flash_point_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
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
Shu Wu et al.
PLoS genetics, 16(6), e1008799-e1008799 (2020-06-06)
TRF2 and TRF1 are a key component in shelterin complex that associates with telomeric DNA and protects chromosome ends. BRM is a core ATPase subunit of SWI/SNF chromatin remodeling complex. Whether and how BRM-SWI/SNF complex is engaged in chromatin end
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

Numéro d'article de commerce international

RéférenceGTIN
05-51304053252516672

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