Render Target: SSR
Render Timestamp: 2024-11-14T22:37:22.802Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-30 01:53:58.237
Product last modified at: 2024-11-07T19:45:13.191Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

ATR (E1S3S) Rabbit mAb #13934

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 300
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    ATR (E1S3S) Rabbit mAb recognizes endogenous levels of total ATR protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro1456 of human ATR protein.

    Background

    Ataxia telangiectasia mutated kinase (ATM) and ataxia telangiectasia and Rad3-related kinase (ATR) are PI3 kinase-related kinase (PIKK) family members that phosphorylate multiple substrates on serine or threonine residues that are followed by a glutamine in response to DNA damage or replication blocks (1-3). Despite the essential role of ATR in cell cycle signaling and DNA repair processes, little is known about its activation. ATR was long thought to exist in a constitutively active state in cells, with DNA damage-induced signaling occurring via recruitment of ATR to single stranded DNA and sites of replication stress. Phosphorylation of ATR at serine 428 in response to UV-induced DNA damage has been suggested as a means of activating ATR (4,5). Recent work has shown autophosphorylation of ATR at threonine 1989. Like ATM Ser1981, phosphorylation of ATR Thr1989 occurs in response to DNA damage, indicating that phosphorylation at this site is important in ATR-mediated signaling (6,7).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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