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Invitrogen
Human ATM (aa 2946-3021) Control Fragment Recombinant Protein
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Product Details
RP-107548
Product Specifications
Species
Human
Expression System
E. coli
Amino acid sequence
LTIVEVLLYDPLFDWTMNPLKALYLQQRPEDETELHPTLNADDQECKRNLSDIDQSFNKVAERVLMRLQEKLKGVE
Tag
His-ABP-tag
Class
Recombinant
Type
Protein
Purity
>80% by SDS-PAGE and Coomassie blue staining
Conjugate
Form
Liquid
Concentration
≥5.0 mg/mL
Purification
purified
Storage buffer
1M urea/PBS, pH 7.4
Contains
no preservative
Storage conditions
-20°C, Avoid Freeze/Thaw Cycles
Shipping conditions
Wet ice
Product Specific Information
Highest antigen sequence indentity to the following orthologs: Mouse (91%), Rat (91%).
This recombinant protein control fragment may be used for blocking experiments with the corresponding antibody, PA5-84748. In IHC/ICC and WB experiments, we recommend a 100x molar excess of the protein fragment control based on the concentration and the molecular weight. Pre-incubate the antibody-protein control fragment mixture for 30 min at room temperature.
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; A-T mutated; AT mutated; AT mutated protein; Ataxia t; Ataxia telangiectasia mutated; DKFZp781A0353; EC 2.7.1.37; MGC74674; mutated in ataxia telangiectasia; Serine-protein kinase ATM; serine/threonine kinase ATM; TEL1, telomere maintenance 1, homolog; unnamed protein product
Gene Aliases: AT1; ATA; ATC; ATD; ATDC; ATE; ATM; TEL1; TELO1
UniProt ID: (Human) Q13315
Entrez Gene ID: (Human) 472
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