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Phospho-ATM (Ser1893) Polyclonal Antibody
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FIGURE: 1 / 1
Phospho-ATM (Ser1893) Antibody (PA5-64544) in WB
Western Blot analysis of Phospho-ATM (Ser1893) was performed using lysates of K562 cell (Left) and K562 cell treated with 100 ng/mL LPS for 30 min (Right). The membrane was probed with Phospho-ATM (Ser1893) Polyclonal Antibody (Product # PA5-64544) using a dilution of 1:1,000.
Please note: We are reviewing Western blot images included in the antibody testing data in our catalog, including those provided by third parties. Unless expressly labeled or annotated as “raw-unedited”, Western blot images included in the antibody testing data in our catalog may have been edited, optimized or otherwise adjusted for presentation.
Product Details
PA5-64544
Product Specifications
Species Reactivity
Human
Host/Isotype
Rabbit
/ IgG
Class
Polyclonal
Type
Antibody
Immunogen
A synthesized peptide derived from human ATM (Phospho-Ser1893), range 1885-1990.
Conjugate
Unconjugated
Unconjugated
Unconjugated
Form
Liquid
Concentration
1 mg/mL
Amount
100 µg
Purification
Antigen affinity chromatography
Storage buffer
PBS, pH 7.4, with 50% glycerol
Contains
0.02% sodium azide
Storage conditions
-20°C
Shipping conditions
Ambient (domestic); Wet ice (international)
RRID
Product Specific Information
Phospho-ATM (Ser1893) Polyclonal Antibody detects endogenous levels of ATM only when phosphorylated at Ser1893.
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.
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Bioinformatics
Protein Aliases: A-T mutated; AT mutated protein; Ataxia t; Ataxia telangiectasia mutated; DKFZp781A0353; EC 2.7.1.37; MGC74674; Serine-protein kinase ATM
Gene Aliases: ATM
Entrez Gene ID: (Human) 472
Disclaimer
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Performance Guarantee
If an Invitrogen™ antibody doesn't perform as described on our website or datasheet,we'll replace the product at no cost to you, or provide you with a credit for a future purchase.*
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