Thermo Fisher Scientific ATM Polyclonal Antibody, DyLight 488

Applications

Tested Dilution

Publications

Western Blot (WB)

1:500-1:1,000

-

Immunohistochemistry (Paraffin) (IHC (P))

Assay-Dependent

-

Immunocytochemistry (ICC/IF)

1:100

-

Flow Cytometry (Flow)

Assay-Dependent

-

ELISA (ELISA)

Assay-Dependent

-

Product Specifications

Species Reactivity

Dog, Human, Marsupial, Mouse, Rat

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

A fragment of human ATM protein expressed in E.coli. The fragment relates to the C-terminal region (within the last third of the protein sequence). if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:ATM,uniProtId:Q13315-1,ncbiNodeId:9606,antigenRange:3056,antigenLength:3056,antigenImageFileName:PA5-22690_ATM_Q13315-1_Rabbit.svg,antigenImageFileNamePDP:PA5-22690_ATM_Q13315-1_Rabbit_PDP.jpeg,sortOrder:1}\]; $mangular.isB2BCMGT = false; $mangular.isEpitopesModalImageMultiSizeEnabled = true;

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Conjugate

DyLight™ 488 DyLight™ 488 DyLight™ 488

Excitation/Emission Max

492/519 nm View spectra

Form

Liquid

Concentration

1.47 mg/mL

Purification

Antigen affinity chromatography

Storage buffer

50mM sodium borate

Contains

0.05% sodium azide

Storage conditions

4° C, store in dark

Shipping conditions

Ambient (domestic); Wet ice (international)

RRID

AB_11152836

Target Information

Ataxia-telangiectasia Mutated (ATM) is a protein that belongs to the PI3/PI4 kinase family. Ataxia-telangiectasia is a rare autosomal recessive disorder characterized by progressive neurologic degeneration, immunologic deficiency, and an increased risk of lymphoid cancer. The ATM gene codes for a protein belonging to the phosphoinositide 3-kinase (PI3K) superfamily. ATM phosphorylates proteins instead of lipid and has many downstream targets that act as cell-cycle regulators including: P53, Mdm2, BRCA1, and SMC1. The ATM protein is responsible for repairing double-stranded DNA breaks that occur because of ionizing radiation and other mutagens. The ATM`s C-terminal region has extensive homology to the catalytic domains of phosphatidylinositol 3-kinases (PI3 kinases). Studies have shown that ATM becomes autophosphorylated and upregulated by exposure to ionizing radiation. AT cells are hypersensitive to ionizing radiation, impaired in mediating the inhibition of DNA synthesis and display delays in p53 induction. Further, DNA damage caused by ionizing irradiation activates ATM-kinase, leading to a cascade of kinase reactions that regulate cell cycle, apoptosis, and DNA damage repair. Studies have linked ATM to apoptosis along with Nbs1 and Chk2 in the E2F1 pathway.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.