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ATM and ATR SIGNALING PROTEINS

Exposure to mutagenic agents results in DNA damage that must be rigorously dealt with in order to prevent the cell from propagating mutations that can result in genomic instability and malignant transformation. To address the constant threat of genotoxic stress, animal cells have evolved a DNA damage response that is governed by a complex and highly-branched signaling network. The components of this network function to sense DNA lesions and transduce cellular signals that activate transcriptional programs for the initiation of DNA repair, cell death, or cell cycle arrest.

There are three cell cycle checkpoint pathways that arrest or delay DNA synthesis when genetic damage is sensed. The G1, S, and G2 cell cycle checkpoints are primarily regulated by the ATM (ataxia telangiectasia, mutated) and ATR (ATM and Rad3-related) protein kinases. ATM and ATR are members of the PI-3 family of serine-threonine kinases and function as essential links between the sensors and effectors of the DNA damage response. The roles of ATM and ATR partially overlap and are cooperative; however they are also known to play distinct roles in protecting the cell from DNA damage. ATM is mostly responsible for sending signals from DSBs (double-strand breaks) induced by ionizing radiation while the closely related ATR responds to UV damage or stalled replication forks.

ATM and ATR are known to phosphorylate common as well as specific substrates to activate checkpoint signaling. The list of reported substrates of ATM is sizable and continues to grow. The ever-expanding and elaborate downstream network of ATM illustrates both the versatility and complexity of this signaling pathway and presents many paths of research that will require further exploration for a complete understanding of the DNA damage response. Even more paths of research remain for understanding the upstream events that take place at the level of sensing DNA damage and grasping how this is linked to ATM and ATR activation. .

Detection of Human Gamma H2AX by IHC.

Samples: FFPE sections of human colon adenocarcinoma. Mock treatment (left) or lambda phosphatase-treatment (right).

Antibodies: Affinity purified rabbit anti-Gamma H2AX (Cat. No. IHC-00059) used at a dilution of 1:250. Detection: DAB staining using anti-Rabbit IHC antibody (Cat. No. A120-501P) at a dilution of 1:100.

Flow Cytometrical Analysis of gamma-H2AX in Etoposide Treated Jurkat Cells.

Cells were treated for 3 hrs in 5ug/ml etoposide, fixed in 1.5% PFA, and permeabilized in 90% Methanol. 1 X 106 cells were stained with 0.5 ug anti-KLH or anti-H2AX [A300-081A] and secondary FITC-conjugated goat anti-rabbit (in a 150ul reaction).

Black- etosposide treated, anti-KLH; Red- untreated, anti-gamma H2AX; Blue- etoposide treated , anti-gamma H2AX.