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001-es BibID:	BIBFORM051534
035-os BibID:	(Scopus)84896538802 (WoS)000332701400043
Első szerző:	Ba, Xueqing
Cím:	8-oxoguanine DNA glycosylase-1 augments proinflammatory gene expression by facilitating the recruitment of site-specific transcription factors / Xueqing Ba, Attila Bacsi, Jixian Luo, Leopoldo Aguilera-Aguirre, Xianlu Zeng, Zsolt Radak, Allan R. Brasier, Istvan Boldogh
Dátum:	2014
ISSN:	0022-1767 1550-6606
Megjegyzések:	Among the insidious DNA base lesions, 8-oxo-7,8-dihydroguanine (8-oxoG) is one of the most abundant, a lesion that arises through the attack by reactive oxygen species on guanine, especially when located in cis-regulatory elements. 8-oxoG is repaired by the 8-oxoguanine glycosylase 1 (OGG1)-initiated DNA base excision repair pathway. In this study, we investigated whether 8-oxoG repair by OGG1 in promoter regions is compatible with a prompt gene expression and a host innate immune response. For this purpose, we used a mouse model of airway inflammation, supplemented with cell cultures, chromatin immunoprecipitation, small interfering RNA knockdown, real-time PCR, and comet and reporter transcription assays. Our data show that exposure of cells to TNF-? altered cellular redox, increased the 8-oxoG level in DNA, recruited OGG1 to promoter sequences, and transiently inhibited base excision repair of 8-oxoG. Promoter-associated OGG1 then enhanced NF-?B/RelA binding to cis-elements and facilitated recruitment of specificity protein 1, transcription initiation factor II-D, and p-RNA polymerase II, resulting in the rapid expression of chemokines/cytokines and inflammatory cell accumulation in mouse airways. Small interfering RNA depletion of OGG1 or prevention of guanine oxidation significantly decreased TNF-?-induced inflammatory responses. Taken together, these results show that nonproductive binding of OGG1 to 8-oxoG in promoter sequences could be an epigenetic mechanism to modulate gene expression for a prompt innate immune response.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk OGG1 8-oxoG trans-ACTING FACTORS INNATE IMMUNE RESPONSE
Megjelenés:	Journal of Immunology. - 192 : 5 (2014), p. 2384-2394. -
További szerzők:	Bácsi Attila (1967-) (immunológus) Luo, Jixian Aguilera-Aguirre, Leopoldo Zeng, Xianlu Radák Zsolt Brasier, Allan R. Boldogh István
Pályázati támogatás:	4.2.2.A-11/1/KONV-2012-0023 TÁMOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM069722
Első szerző:	Pan, Lang
Cím:	Oxidized Guanine Base Lesions Function in 8-Oxoguanine DNA Glycosylase-1-mediated Epigenetic Regulation of Nuclear Factor ?B-driven Gene Expression / Lang Pan, Bing Zhu, Wenjing Hao, Xianlu Zeng, Spiros A. Vlahopoulos, Tapas K. Hazra, Muralidhar L. Hegde, Zsolt Radak, Attila Bacsi, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:	2016
ISSN:	0021-9258 1083-351X
Megjegyzések:	A large percentage of redox-responsive gene promoters containevolutionarily conserved guanine-rich clusters; guaninesare the bases most susceptible to oxidative modification(s). Consequently,7,8-dihydro-8-oxoguanine (8-oxoG) is one of themost abundant base lesions in promoters and is primarilyrepaired via the 8-oxoguanine DNA glycosylase-1 (OOG1)-initiatedbase excision repair pathway. In view of a prompt cellularresponse to oxidative challenge, we hypothesized that the8-oxoG lesion and the cognate repair protein OGG1 are utilizedin transcriptional gene activation. Here, we document TNF -induced enrichment of both 8-oxoG and OGG1 in promoters ofpro-inflammatory genes, which precedes interaction of NF- Bwith its DNA-binding motif. OGG1 bound to 8-oxoG upstreamfrom the NF- B motif increased its DNA occupancy by promotingan on-rate of both homodimeric and heterodimeric forms ofNF- B. OGG1 depletion decreased both NF- B binding andgene expression, whereas Nei-like glycosylase-1 and -2 had amarginal effect. These results are the first to document a novelparadigm wherein the DNA repair protein OGG1 bound to itssubstrate is coupled to DNA occupancy of NF- B and functionsin epigenetic regulation of gene expression.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban 8-oxoguanine DNA glycosylase1 8-oxoguanine NF-kappaB gene expression inflammation
Megjelenés:	Journal Of Biological Chemistry 291 : 49 (2016), p. 25553-25566. -
További szerzők:	Zhu, Bing Hao, Wenjing Zeng, Xianlu Vlahopoulos, Spiros A. Hazra, Tapas K. Hegde, Muralidhar L. Radák Zsolt Bácsi Attila (1967-) (immunológus) Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:	United States National Institute of Environmental Health and Sciences (grant number: RO1 ES018948 to IB) Egyéb United States National Institute of Allergic and Infectious Diseases (grant number: PO1-AI062885, to ARB and IB) Egyéb United States National Institute of Environmental Health and Sciences Center Grant (grant number: P30 ES006676 to ARB, IB) Egyéb National Science Foundation of China (grant number: 31571339 to XB) Egyéb
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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