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A team led by a Baylor University researcher has published a breakthrough article that provides a better understanding of the dynamic process by which sunlight-induced DNA damage is recognized by the molecular repair machinery in cells as needing repair.
Ultraviolet light from the sun is a ubiquitous carcinogen that can inflict structural damage to the cellular DNA. As DNA carries important blueprints for cellular functions, failure in removing and restoring damaged parts of DNA in a timely fashion can have detrimental outcomes and lead to skin cancers in humans, said lead author Jung-Hyun Min, Ph.D., associate professor of chemistry and biochemistry in Baylor's College of Arts & Sciences.
Min - Team - Repair - Protein - Rad4/XPC
Min and her team showed how the repair protein Rad4/XPC would bind to one such UV-induced DNA damage—6-4 photoproduct—to mark the damaged site along the DNA in preparation for the rest of the nucleotide excision repair (NER) process in cells.
The study—"Structure and mechanism of pyrimidine-pyrimidone (6-4) photoproduct recognition by the Rad4/XPC nucleotide excision repair complex"—is published in the journal Nucleic Acids Research (NAR) as a "breakthrough article."
Articles - Studies - Questions - Field - Acids
Breakthrough articles present high-impact studies answering long-standing questions in the field of nucleic acids research and/or opening new areas and mechanistic hypotheses for investigation. They are the very best papers published at NAR, constituting 1 to 2 percent of those received by the journal.
UV light threatens the integrity of the genome by generating cellular DNA damage known as intra-strand crosslink damage, Min said. Two major types of these lesions are cyclobutane pyrimidine dimer (CPD), which makes up about 70 percent of such damage; and 6-4 photoproduct (6-4PP), which constitutes about 30 percent.
DNA - Repair - System - NER - Lesions
The cellular DNA repair system (NER), which is responsible for clearing these lesions, works much faster for 6-4PP than CPD, Min said. This is because a DNA damage-sensing protein (called Rad4/XPC) that initiates NER is more efficient...
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