Paper instructions Please answer the question. There is a 300-word cap on this part( must bee 300 or less words); references do not count toward this word limit. Posts that demonstrate quality, clarity, depth, ; focus will be more positively evaluated than posts that are shy on these key elements.please also add pic after your explanation and make sure to add the pic source in APA format in reference section.
DNA Damage Response (DDR): Nucleotide Excision Repair
Through the DNA damage response system or DDR, cells have evolved to detect DNA lesions, sense their presence, and promote their repair in order to maintain genomic integrity and prevent from harmful mutations. (1) As Alan has pointed out the DDR mechanism of Mismatch repair (MMR), another DDR mechanism involves Nucleotide excision repair (NER) which involves repair of DNA damage occurring from chemicals, radiation, and other mutagens, UV light in particular. DNA damage induced by UV light causes something called a DNA in the commonly found form of thymine dimers that is recognized from its helix-distorting base lesions and repaired through one of NERs subpathways: 1) global genomic NER, which removes DNA lesions in the genome whether the sequence is transcribed or not, and 2) transcription coupled NER, which targets DNA lesions from transcribed DNA that block transcription. (1)
How the two subpathways differ is in the proteins each pathway has in how each pathway recognizes and repair the DNA lesion, but both pathways ultimately follow the DNA repair process the same. In Global genomic NER, the complexes involved in recognition include 1) DNA-damage binding (DDB) complexes and 2) XPC-Rad23-CETN2 complexes, which recognize helix distortions and damages caused by UV light. (2) In transcription-coupled NER, a stalled RNA polymerase at the DNA lesion signals this pathway. In principle, upon recognition of the damaged DNA, a single-stranded stretch of the DNA segment with the DNA lesion is removed while the undamaged ssDNA is left intact. Using the undamaged DNA as a template, DNA polymerase fills in the gap and a ligase completes NER to form the repaired dsDNA. NER dysfunction critically affects DNA repair, ultimately resulting in increased likelihood of cancer development.
Question: What potential does nucleotide excision repair have as a potential therapeutic target in cancer?
Reprinted from “Nucleotide Excision Repair”, by BioRender, September 2020, retrieved from https://app.biorender.com/biorender-templates/figures/5c8c7ba9d4f2ef3300632942/t-5ff89ea220fc0100a21c523e-nucleotide-excision-repair Copyright 2022 by BioRender.
References
Jackson, S. P., & Bartek, J. (2009). The DNA-damage response in human biology and disease. Nature, 461(7267), 10711078. https://doi.org/10.1038/nature08467
Kusakabe, M., Onishi, Y., Tada, H. et al. Mechanism and regulation of DNA damage recognition in nucleotide excision repair. Genes and Environ 41, 2 (2019). https://doi.org/10.1186/s41021-019-0119-6
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