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Key Documents

07-1286

Sigma-Aldrich

Anti-ATM Antibody

Upstate®, from rabbit

Sinónimos:

A-T, mutated, AT mutated, ataxia telangiectasia mutated, ataxia telangiectasia mutated (includes complementation groups A, C and D), ataxia telangiectasia mutated protein, ATM, human phosphatidylinositol 3-kinase homolog, serine-protein kinase ATM, TEL1,

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About This Item

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

biological source

rabbit

Quality Level

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

mouse, human

species reactivity (predicted by homology)

horse (based on 100% sequence homology), bovine (based on 100% sequence homology), rat (based on 100% sequence homology)

manufacturer/tradename

Upstate®

technique(s)

immunocytochemistry: suitable
western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

bovine ... Atm(526824)
human ... ATM(472)
mouse ... Atm(11920)
rat ... Atm(300711)

General description

ATM (Ataxia Telangiectasia Mutated kinase) and ATR (Ataxia Telangiectasia and Rad3-related kinase) are related kinases that regulate cell cycle checkpoints and DNA repair. ATM is activated in response to DNA damage and serves to arrest further cell division before the damage can be repaired. Mutation in the ATM gene results in the autosomal recessive disease ataxia telangiectasia (AT). The identified substrates for ATM include p53, p95/NBS1, MDM2, Chk2, BRCA1, CtIP, 4E-BP1 and Chk1. ATM activates p53, increasing p21/Cip1/Waf1 levels, thus blocking activation of Cdk2. That results in Rb hypophosphorylation and blockage of the G1/S transition. Separately, ATM also phosphorylates and activates Chk1, which phosphorylates Cdc25C. This inactivates Cdc25C and prevents it from dephosphorylating the inhibitory phosphotyrosine residue on cdc2/Cdk1, thus preventing the G2/M transition. The complex phenotype of cells derived from patients with AT suggests that ATM has additional cellular substrates. In unirradiated cells, ATM is present as an inactive homodimer or multimer. Double-stranded breaks in DNA caused by ionizing radiation cause rapid ATM kinase activation through dissociation of this complex and ATM autophosphorylation at Ser1981.

Specificity

Detects ATM.

Immunogen

Epitope: Abl-interacting domain
KLH-conjugated synthetic peptide corresponding to sequence derived from the Abl-interacting domain of human ATM.

Application

Anti-ATM Antibody detects level of ATM & has been published & validated for use in WB & IF.
Research Category
Epigenetics & Nuclear Function
Research Sub Category
Nuclear Receptors
Western Blotting Analysis: A 1:5,000 dilution from a representative lot detected ATM in 10 µg of HeLa nuclear extract.
Immunocytochemistry Analysis: A representative lot detected ATM in HeLa and NIH/3T3 cells.
Immunocytochemistry Analysis: 2 µg/mL from a representative lot detected ATM in NIH/3T3 cells.

Quality

Evaluated by Western Blotting in HeLa nuclear extract.

Western Blotting Analysis: A 1:500 dilution of this antibody detected ATM in 10 µg of HeLa nuclear extract.

Target description

>260 kDa observed. Uncharacterized band(s) may appear in some lysates.

Physical form

Antigen Affinity Purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.

Analysis Note

Control
HeLa nuclear extract

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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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Referencia del producto
Descripción
Precios

Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Differential roles for checkpoint kinases in DNA damage-dependent degradation of the Cdc25A protein phosphatase.
Jin, J; Ang, XL; Ye, X; Livingstone, M; Harper, JW
The Journal of Biological Chemistry null
Regulation of intra-S phase checkpoint by ionizing radiation (IR)-dependent and IR-independent phosphorylation of SMC3.
Luo, H; Li, Y; Mu, JJ; Zhang, J; Tonaka, T; Hamamori, Y; Jung, SY; Wang, Y; Qin, J
The Journal of Biological Chemistry null
Aloke Sarkar et al.
Haematologica (2020-02-08)
Ataxia telangiectasia mutated (ATM), a critical DNA damage sensor with protein kinase activity,is frequently altered in human cancers including mantle cell lymphoma (MCL). Loss of ATM protein is linked to accumulation of nonfunctional mitochondria and defective mitophagy, in both murine
B M Burgering et al.
Nature, 376(6541), 599-602 (1995-08-17)
A serine/threonine kinase, named protein kinase B (PKB) for its sequence homology to both protein kinase A and C, has previously been isolated. PKB, which is identical to the kinase Rac, was later found to be the cellular homologue of
Scott Ackler et al.
Oncogene, 21(2), 198-206 (2002-01-23)
AKT1/protein kinase Balpha is a protein-serine/threonine kinase that regulates multiple targets involved in cell survival and cell cycle progression in a variety of cell types including breast cancer cells. To explore the role of Akt1 in mammary gland function and

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