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RISS 인기검색어
- 검색키워드
- 저자 : Gaddameedhi, Shobhan (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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Choi, Jun-Hyuk,Gaddameedhi, Shobhan,Kim, So-Young,Hu, Jinchuan,Kemp, Michael G.,Sancar, Aziz Oxford University Press 2014 Nucleic acids research Vol.42 No.4
<P>The nucleotide excision repair pathway removes ultraviolet (UV) photoproducts from the human genome in the form of short oligonucleotides ∼30 nt in length. Because there are limitations to many of the currently available methods for investigating UV photoproduct repair <I>in vivo</I>, we developed a convenient non-radioisotopic method to directly detect DNA excision repair events in human cells. The approach involves extraction of oligonucleotides from UV-irradiated cells, DNA end-labeling with biotin and streptavidin-mediated chemiluminescent detection of the excised UV photoproduct-containing oligonucleotides that are released from the genome during excision repair. Our novel approach is robust, with essentially no signal in the absence of UV or a functional excision repair system. Furthermore, our non-radioisotopic methodology allows for the sensitive detection of excision products within minutes following UV irradiation and does not require additional enrichment steps such as immunoprecipitation. Finally, this technique allows for quantitative measurements of excision repair in human cells. We suggest that the new techniques presented here will be a useful and powerful approach for studying the mechanism of human nucleotide excision repair <I>in vivo</I>.</P>
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Kemp, Michael G.,Gaddameedhi, Shobhan,Choi, Jun-Hyuk,Hu, Jinchuan,Sancar, Aziz American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.38
<P>Ultraviolet (UV) photoproducts are removed from genomic DNA by dual incisions in humans in the form of 24- to 32-nucleotide-long oligomers (canonical 30-mers) by the nucleotide excision repair system. How the small, excised, damage-containing DNA oligonucleotides (sedDNAs) are processed in cells following the dual incision event is not known. Here, we demonstrate that sedDNAs are localized to the nucleus in two biochemically distinct forms, which include chromatin-associated, transcription factor II H-bound complexes and more readily solubilized, RPA-bound complexes. Because the nuclear mobility and repair functions of transcription factor II H and RPA are influenced by post-incision gap-filling events, we examined how DNA repair synthesis and DNA ligation affect sedDNA processing. We found that although these gap filling activities are not essential for the dual incision/sedDNA generation event <I>per se</I>, the inhibition of DNA repair synthesis and ligation is associated with a decrease in UV photoproduct removal rate and an accumulation of RPA-sedDNA complexes in the cell. These findings indicate that sedDNA processing and association with repair proteins following the dual incisions may be tightly coordinated with gap filling during nucleotide excision repair <I>in vivo</I>.</P>
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Hu, Jinchuan,Choi, Jun-Hyuk,Gaddameedhi, Shobhan,Kemp, Michael G.,Reardon, Joyce T.,Sancar, Aziz American Society for Biochemistry and Molecular Bi 2013 The Journal of biological chemistry Vol.288 No.29
<P>Nucleotide excision repair is the sole mechanism for removing the major UV photoproducts from genomic DNA in human cells. <I>In vitro</I> with human cell-free extract or purified excision repair factors, the damage is removed from naked DNA or nucleosomes in the form of 24- to 32-nucleotide-long oligomers (nominal 30-mer) by dual incisions. Whether the DNA damage is removed from chromatin <I>in vivo</I> in a similar manner and what the fate of the excised oligomer was has not been known previously. Here, we demonstrate that dual incisions occur <I>in vivo</I> identical to the <I>in vitro</I> reaction. Further, we show that transcription-coupled repair, which operates in the absence of the XPC protein, also generates the nominal 30-mer in UV-irradiated XP-C mutant cells. Finally, we report that the excised 30-mer is released from the chromatin in complex with the repair factors TFIIH and XPG. Taken together, our results show the congruence of <I>in vivo</I> and <I>in vitro</I> data on nucleotide excision repair in humans.</P>
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