Investigating The Role Of Mismatch Repair Protein hMSH2 In Resolving Various Dna Damage Intermediates

Abstract

The aetiology of human cancer has been linked to a wide range of chemicals and newlinephysical factors, including UV light and X-radiation. These chemicals cause DNA damage newlinewhich is a critical first stage in the carcinogenesis process. Although evolutionary processes newlinehave produced DNA repair tools that are effective at fixing broken DNA, replication of newlinedamaged DNA may occur prior to repair, especially when it is triggered frequently. newlineMismatch paired bases, minor deletions or insertions and DNA single or double-strand breaks newlinecan all trigger many repair pathways. These repair pathways interact with one another to newlinecomplete the DNA repair process. Defective DNA repair, which results in the persistence of newlineDNA damage, can result in gene mutations, chromosome rearrangements, genomic instability newlineand ultimately, carcinogenesis. DNA repair defects are widespread in carcinogenesis and play newlinean important role in cancer progression. Mismatch repair is reduced by genetic abnormalities newlinein DNA mismatch repair genes, which increases the incidence of colon and uterine tumours. newlineMismatch repair is a key step in the prevention of genomic instability. Furthermore, proteins newlinein this pathway have the unique potential to function in the DNA damage response, initiating newlineapoptosis when irreversible damage occurs. Over billions of years, the DNA mismatch repair newline(MMR) machinery has evolved. On a strand-by-strand basis, it recognises and corrects errors newlineinduced by DNA polymerase activity during replication, such as base/base mismatches and newlineinsertion/deletion changes. From bacteria to humans, the hMSH2 protein belongs to a highly newlineconserved family of postreplication mismatch repair components. newline