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Anti-ATM (Ser-1981), Phosphospecific Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC |
|---|---|
| Primary Accession | Q13315 |
| Reactivity | Bovine |
| Host | Mouse |
| Clonality | Mouse Monoclonal |
| Isotype | IgG1 |
| Clone Names | M366 |
| Calculated MW | 350687 Da |
| Gene ID | 472 |
|---|---|
| Other Names | ataxia telangiectasia mutated, AT1 ATDC TEL1 TELO1 |
| Target/Specificity | Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. Activation of ATM after DNA damage involves Cdk5 mediated phosphorylation of Ser-794 followed by autophosphorylation at Ser-1891. Active ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis and DNA repair. The Cdk5–ATM pathway regulates phosphorylation and function of the ATM targets p53 and H2AX in postmitotic neurons. Other known substrates of ATM include Chk2, Chk1, CtIP, 4E-BP1, BRCA1, RPA3, SMC1, FANCD2, Rad17, Artemis, Nbs1, and the I-2 regulatory subunit of PP1. Thus, activation of Cdk5 by DNA damage may be an important initiator of ATM-dependent regulation of cell cycle checkpoints. |
| Dilution | WB~~1:1000 IHC~~1:100~500 |
| Format | Protein A Purified |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Anti-ATM (Ser-1981), Phosphospecific Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Shipping | Blue Ice |
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Provided below are standard protocols that you may find useful for product applications.
Background
Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. Activation of ATM after DNA damage involves Cdk5 mediated phosphorylation of Ser-794 followed by autophosphorylation at Ser-1891. Active ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis and DNA repair. The Cdk5–ATM pathway regulates phosphorylation and function of the ATM targets p53 and H2AX in postmitotic neurons. Other known substrates of ATM include Chk2, Chk1, CtIP, 4E-BP1, BRCA1, RPA3, SMC1, FANCD2, Rad17, Artemis, Nbs1, and the I-2 regulatory subunit of PP1. Thus, activation of Cdk5 by DNA damage may be an important initiator of ATM-dependent regulation of cell cycle checkpoints.
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