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An Overview of DNA Damage and Repair

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A cell’s DNA is constantly being damaged – up to one million alterations per cell each day1. This assault by environmental factors includes exposure to X-rays, ultraviolet radiation from the sun, and mutagenic chemicals (such as those present in cigarettes). DNA damage also spontaneously occurs as a result of a cell’s metabolic processes. For example, DNA replication errors during cell division can result in the wrong nucleotide being added to the growing chain, and reactive oxygen species generated during normal cellular processes lead to a variety of alterations such as oxidation, alkylation, and hydrolysis of bases2.

The integrity of a cell’s genetic information relies on the identification and repair of this constant DNA insult. Once identified, damaged single-stranded DNA can be repaired by a direct reversal of the damage (direct repair) or by the far more common mechanism of removing the affected free bases or nucleotides and synthesizing new DNA to fill in the gap (excision repair)3. Double-stranded DNA breaks, an especially deleterious form of damage that causes chromosomal rearrangements, are repaired through either homologous recombination or non-homologous end joining mechanisms2, 3.

One mechanism by which the repair processes are initiated is through the transcription factor p53. Termed the “guardian of the genome,” p53 alerts the cell to damaged DNA, halts the progression of the cell cycle in order to enable repair processes, or induces cell death if the damage is deemed too severe. Failure to repair DNA damage may have disastrous consequences, including the introduction of mutations that induce tumor growth. In fact, a mutation in p53 is found in up to 40% of cancers, and this protein pathway is a target of many chemotherapeutic agents4, 5, 6. Thus, appropriate identification and repair of damaged DNA is vital to the health of an organism.


Contributed by Allison A. Curley, Ph.D.


Detection of human DNA-PKcs in FFPE lung carcinoma by IHC.

Detection of human DNA-PKcs in FFPE lung carcinoma by IHC. Antibody: Rabbit anti-DNA-PKcs (A300-518A). Secondary: HRP-conjugated goat anti-mouse IgG (A90-116P). Substrate: DAB.

Detection of human 53BP1 by WB of immunoprecipitates from 293T lysate.

Detection of human 53BP1 by WB of immunoprecipitates from 293T lysate. Antibodies: Rabbit anti-53BP1 recombinant monoclonal [BL-250-1H11] (A700-011) and rabbit anti-53BP1 (A300-272A). Secondary: ReliaBLOT® reagents (WB120).



Below is the current listing of Bethyl antibodies for studying DNA damage and repair:


DNA Damage/Repair


1. Lodish H, Berk A, Matsudaira P, Kaiser CA, Krieger M, Scott MP, Zipursky SL, Darnell J. 2004. Molecular biology of the cell. 5th Ed. New York, NY: WH Freeman.

2. Clancy, S. 2008. DNA damage & repair: mechanisms for maintaining DNA integrity. Nature Ed. 2008;1(1):103.

3. Postel-Vinay S, Vanhecke E, Olaussen KA, Lord CJ, Ashworth A, Soria JC. 2012. The potential of exploiting DNA-repair defects for optimizing lung cancer treatment. Nat Rev Clin Oncol. Feb 14;9(3):144-155.

4. Vousden KH, Prives C. 2009. Blinded by the light: the growing complexity of p53. Cell. May 1;137(3):413-431.

5. Goh AMCoffill CRLane DP. 2011. The role of mutant p53 in human cancer. J Pathol. Jan;223(2):116-126.

6. Borrás CGómez-Cabrera MCViña J. 2011. The dual role of p53: DNA protection and antioxidant. Free Radic Res. Jun;45(6):643-652.