Ataxia telangiectasia mutated (ATM) is a serine/threonine-specific protein kinase that is activated by DNA double-strand breaks. It phosphorylates several key proteins that initiate activation of the DNA damage checkpoint, leading to cell cycle arrest, DNA repair or apoptosis. Several of these targets are p53, CHK2, BRCA1, and H2AX.
ATM triggers the G1/S checkpoint; ATR (Ataxia telangiectasia and Rad3-related) prevents G1/S stasis. In this single point in the cell cycle, it would appear that ATM and ATR function in opposition to one another.
Ataxia telangiectasia (AT) is a rare neurodegenerative, autosomal recessive disorder characterized by chromosome instability, radiosensitivity, immunodeficiency and a predisposition for cancer.
The ATR (ATM and Rad3-related) kinase and its downstream effector kinase, Chk1, are central regulators of the replication checkpoint. Loss of these checkpoint proteins causes replication fork collapse and chromosomal rearrangements. ATR are thought to be master controllers of cell cycle checkpoint signaling pathways that are required for cell response to DNA damage and for genome stability.

Western Blot: 1:2,000; Immunoprecipitation: 1 ?l;

Type: Primary
Antigen: ATM (ataxia telangiectasia mutated)
Clonality: Monoclonal
Clone: 1B10
Conjugation: Unconjugated
Epitope:
Host: Mouse
Isotype: IgG2b Kappa
Reactivity: Human, Mouse, Rat