Hamilton, ON (July 8, 2010) By solving the three-dimensional structure of a protein involved in repairing DNA errors, a group of McMaster University researchers have revealed new avenues to develop assessment tools and alternative treatments for people living with hereditary colorectal cancers.
The finding, published in the journal Molecular Cell, is an important step forward in the field of molecular and structural biology. The McMaster researchers uncovered how a specific protein, known as MutL, works within a cell to unleash the series of events that repair DNA when the replication machinery makes a mistake.
The research team was led by Alba Guarn, an associate professor in the Department of Biochemistry and Biomedical Sciences at McMaster, and involved researchers in Europe and the United States. The lead author of the study was Monica Pillon, a master's student in the Guarn laboratory.
Errors in DNA can arise from many types of damage including external harm, such as UV radiation or carcinogens, as well as by intrinsic cellular processes such as DNA replication. Failure to correct these errors leads to mutations, which results in cancer or a number of severe genetic disorders.
To prevent this from happening, cells posses a variety of DNA repair systems that correct these errors or trigger cell death when the damage cannot be fixed.
In this study, the investigators examined the DNA mismatch repair pathway, which corrects errors that have escaped proofreading during DNA replication. Specifically, they examined the protein MutL a matchmaker protein that recruits other enzymes and proteins within the cell to recognize, remove and correct mismatched DNA.
Research has shown that mutations on the genes that encode mismatch repair proteins give rise to two forms of familial cancer hereditary non-polyposis colorectal cancer and Turcot Syndrome, which is associated with colorectal cancer as wel
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