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DNA damage-inducible transcript 3, also known as C/EBP homologous protein (CHOP), is a pro-apoptotic transcription factor that is encoded by the DDIT3 gene. [5] [6] It is a member of the CCAAT/enhancer-binding protein (C/EBP) family of DNA-binding transcription factors. [6]
DNA repair proteins are often activated or induced when DNA has sustained damage. However, excessive DNA damage can initiate apoptosis (i.e., programmed cell death) if the level of DNA damage exceeds the repair capacity. Apoptosis can prevent cells with excess DNA damage from undergoing mutagenesis and progression to cancer. [43]
The SOS response is a global response to DNA damage in which the cell cycle is arrested and DNA repair and mutagenesis are induced. The system involves the RecA protein (Rad51 in eukaryotes). The RecA protein, stimulated by single-stranded DNA, is involved in the inactivation of the repressor of SOS response genes thereby inducing the response ...
Nucleotide excision repair (NER) is a particularly important excision mechanism that removes DNA damage induced by ultraviolet light (UV). UV DNA damage results in bulky DNA adducts — these adducts are mostly thymine dimers and 6,4-photoproducts. Recognition of the damage leads to removal of a short single-stranded DNA segment that contains ...
Olaparib is combined with chemotherapeutics to inhibit single-strand break repair induced by DNA damage caused by the co-administered chemotherapy. Tumor cells relying on this residual DNA repair mechanism are unable to repair the damage and hence are not able to survive and proliferate, whereas normal cells can repair the damage with the ...
In this case, the term PRR would encompasses all processes that facilitate the replication of damaged DNA, including those that repair replication-induced double-strand breaks. Melanoma cells are commonly defective in postreplication repair of DNA damages that are in the form of cyclobutane pyrimidine dimers , a type of damage caused by ...
The active metabolites interact with DNA to cause DNA damage, mutation induction, and cancer development in liver endothelial cells and hepatocytes. The researchers discovered in the end that the "comfrey is mutagenic in liver, and PA contained in comfrey appear to be responsible for comfrey-induced toxicity and tumor induction,".
Conversely, certain bacteria utilize photolyase, powered by sunlight, to repair pyrimidine dimer-induced DNA damage. Unrepaired lesions may lead to erroneous nucleotide incorporation by polymerase machinery. Overwhelming DNA damage can precipitate mutations within an organism's genome, potentially culminating in cancer cell formation. [7]