ATM antibody (pSer1981)
-
- Target See all ATM Antibodies
- ATM (Ataxia Telangiectasia Mutated (ATM))
-
Binding Specificity
- pSer1981
-
Reactivity
- Human
-
Host
-
Sheep
-
Clonality
- Polyclonal
-
Conjugate
- This ATM antibody is un-conjugated
-
Application
- Western Blotting (WB), ELISA
- Supplier Product No.
- 600-601-400
- Supplier
- Rockland
- Purpose
- ATM phospho S1981 Antibody
- Cross-Reactivity (Details)
- This affinity-purified antibody is directed against human ATM and is useful in determining its presence in various assays. This polyclonal anti-ATM antibody recognizes the phosphorylated epitope in native and over-expressed proteins found in various tissues and extracts.
- Characteristics
- Synonyms: sheep anti-ATM pS1981 Antibody, AT mutated antibody, AT protein antibody, AT1 antibody, ATA antibody, Ataxia telangiectasia gene mutated in human beings antibody, Ataxia telangiectasia mutated antibody, ATC antibody
- Purification
- Affinity purified antibody
- Sterility
- Sterile filtered
- Immunogen
-
Immunogen: This antibody was affinity purified from whole sheep serum prepared by repeated immunizations with a synthetic peptide corresponding to a region near serine 1981 of human ATM conjugated to KLH using maleimide.
Immunogen Type: Conjugated Peptide
- Isotype
- IgG
- Top Product
- Discover our top product ATM Primary Antibody
-
-
- Application Notes
-
Application Note: Affinity purified sheep anti-ATM has been tested by ELISA and western blotting against native form phosphorylated ATM PK.
Western Blot Dilution: 1:500 - 1:2,000
ELISA Dilution: 1:2,000 - 1:10,000
Other: User Optimized
- Restrictions
- For Research Use only
-
- Format
- Liquid
- Concentration
- 1.0 mg/mL
- Buffer
-
Buffer: 0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2
Stabilizer: None
Preservative: 0.01 % (w/v) Sodium Azide - Preservative
- Sodium azide
- Precaution of Use
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
- Storage
- 4 °C,-20 °C
- Storage Comment
- Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use.
- Expiry Date
- 12 months
-
- Target
- ATM (Ataxia Telangiectasia Mutated (ATM))
- Alternative Name
- ATM (ATM Products)
- Background
- Background: ATM, the gene mutated in the hereditary disease ataxia-telangiectasia, codes for a protein kinase that acts as a master regulator of cellular responses to DNA double-strand breaks. ATM is normally inactive and the question of how it is activated in the event of DNA damage (due to ionizing radiation for instance) is central to understanding its function. ATM protein is now shown to be present in undamaged cells as an inactive dimer. Low doses of ionizing radiation, which induce only a few DNA breaks, activate at least half of the total ATM protein present, possibly in response to changes in chromatin structure. The ATM gene encodes a 370- kDa protein that belongs to the phosphoinositide 3-kinase (PI(3)K) superfamily, but which phosphorylates proteins rather than lipids. The 350-amino-acid kinase domain at the carboxy terminus of this large protein is the only segment of ATM with an assigned function. Exposure of cells to IR triggers ATM kinase activity and this function is required for arrests in G1, S and G2 phases of the cell cycle. Several substrates of the ATM kinase participate in these IR-induced cell-cycle arrests. These include p53, Mdm2 and Chk2 in the G1 checkpoint, Nbs1, Brca1, FancD2 and SMC1 in the transient IR-induced S-phase arrest, and Brca1 and hRad17 in the G2/M checkpoint. This antibody is similar to the rabbit host antibody discussed by Bakkenist, C. J. & Kastan, M. B. in Nature 421, 499-506 (2003).
- Gene ID
- 472
- NCBI Accession
- NP_000042
- UniProt
- Q13315
- Pathways
- p53 Signaling, Apoptosis, DNA Damage Repair, Inositol Metabolic Process, Positive Regulation of Response to DNA Damage Stimulus
-