Article Abstract:
Common fragile sites are specific chromosomal loci that form gaps on metaphase chromosomes exposed to replication stress that shows DNA replication. Replication stress leads to formation of RAD51 and phosphorylated DNA-Pkcs, key components of the homologous recombination (HR) and nonhomologous end-joining (NHEJ), double-strand break (DSR) repair pathways and studies shows that HR and NHEJ repair pathways can be coupled to repair DSK and to maintain site stability.
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Article Abstract:
The article discusses the distinctive repair pathways and the mechanisms involved in the mending of the nonhomologous DNA end-joining (NHEJ). The mechanistic flexibility of the bacteria is found to play an extremely significant role in NHEJ, which can be further employed in the infectious disease researches.
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Article Abstract:
A human cell must constantly repair over 10,000 DNA lesions per day to counteract endogenous sources of DNA damage. Recent studies on the cellular machinery that facilitates DNA repair within the context of chromatin are reviewed.
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