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Dialkylating agents can react with two different 7-N-guanine residues, and, if these are in different strands of DNA, the result is cross-linkage of the DNA strands, which prevents uncoiling of the DNA double helix. If the two guanine residues are in the same strand, the result is called limpet attachment of the drug molecule to the DNA.
Epigenetic alterations can accompany DNA repair of oxidative damage or double-strand breaks. In human cells, oxidative DNA damage occurs about 10,000 times a day and DNA double-strand breaks occur about 10 to 50 times a cell cycle in somatic replicating cells (see DNA damage (naturally occurring)). The selective advantage of DNA repair is to ...
TF II H participates in nucleotide excision repair (NER) by opening the DNA double helix after damage is initially recognized. NER is a multi-step pathway that removes a wide range of different damages that distort normal base pairing, including bulky chemical damages and UV-induced damages.
Purified XPB has been shown to unwind DNA with 3’-5’ polarity. The function of the XPB(ERCC3) protein in NER is to assist in unwinding the DNA double helix after damage is initially recognized. NER is a multi-step pathway that removes a wide range of different DNA damages that distort normal base pairing.
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 ...
The siDNA family, led by Dbait, consists of 32 base pairs deoxyribonucleotide forming an intramolecular double helix, which mimicks DNA double-strand break lesions. In the event of a double-stranded break in the genome, the cell most commonly repairs the damaged segment via non-homologous end joining (NHEJ).
This complex separates the DNA helix for a short distance on either side of the site of damage. It then acts as an endonuclease to incise the damaged DNA strand on the 5' side of the damaged site. [20] Mutant cells with deficient ERCC1-XPF are not only defective in NER, but also in the repair of double-strand breaks and inter-strand crosslinks.
DNA crosslinking lesions can also be formed when under conditions of oxidative stress, in which free oxygen radicals generate reactive intermediates in DNA, and these lesions have been implicated in aging and cancer. Tandem DNA lesions are formed at a substantial frequency by ionizing radiation and metal-catalyzed H 2 O 2 reactions. Under ...