CCL

Összesen 5 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM091749
Első szerző:Boldogh István
Cím:OGG1 at the Crossroads of Inflammation and DNA Base Excision Repair / I. Boldogh, L. Pan, S. Vlahopoulos, X. Zheng, K. Wang, T. K. Hazra, M. L. Hegde, A. Bacsi, Z. Radak, A. R. Brasier, X. Ba
Dátum:2020
Megjegyzések:Oxidative modification(s) to nucleic acid bases are an unavoidable consequence of reactions by reactive oxygen species. Arguably, the most abundant ROS-generated lesion in nuclear and mitochondrial DNA is 7, 8-dihydro-8-oxoguanine (8-oxoGua), which is repaired primarily by 8-oxoguanine DNA glycosylase 1, in the OGG1-initiated base excision repair pathway. Deficiency in OGG1 repair is believed to have role(s) in development and progression of various disease processes, including neurodegenerative, cardiovascular, metabolic diseases, and aging-associated pathologies. The common link among these diseases is acute/chronic inflammatory processes. Emerging data support the idea that OGG1-induced adjustments in DNA structure at genomic 8-oxoGua with or without excision, serve as a nucleation site for transcription factor binding allowing prompt expression of genes, essential for reestablishment of a homeostatic state via innate and adaptive immune responses after exposure to biological and/or cytotoxic agents. As part of the immune defenses, OGG1 in complex with a free 8-oxoGua base also exerts transcriptional control via small GTPase signaling pathways. These data are consistent with the limited immune responses of Ogg1 knockout mice. Thus, evolution integrated genome maintenance by OGG1-BER and control host homeostatic state via inflammation, which, if not controlled, can be one of the mechanistic explanations for OGG1's previously proposed link to diseases and aging processes.
ISBN:978-1-83916-251-0; 978-1-83916-254-1; 978-1-83916-256-5
Tárgyszavak:Természettudományok Biológiai tudományok könyvfejezet
könyvrészlet
OGG1
Megjelenés:DNA Damage, DNA Repair and Disease: Volume 2 / Eds. Miral Dizdaroglu, R. Stephen Lloyd. - p. 75-103. -
További szerzők:Pan, Lang Vlahopoulos, Spiros A. Zheng, Xiaoxiang Wang, K. Hazra, Tapas K. Hegde, Muralidhar L. Bácsi Attila (1967-) (immunológus) Radák Zsolt Brasier, Allan R. Ba, Xueqing
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM076050
035-os BibID:(WoS)000447820100006 (Scopus)85048764575
Első szerző:Hao, Wenjing
Cím:Effects of the stimuli-dependent enrichment of 8-oxoguanine DNA glycosylase1 on chromatinized DNA / Hao Wenjing, Qi Tianyang, Pan Lang, Wang Ruoxi, Zhu Bing, Aguilera-Aguirre Leopoldo, Radak Zsolt, Hazra Tapas K., Vlahopoulos Spiros A., Bacsi Attila, Brasier Allan R., Ba Xueqing, Boldogh Istvan
Dátum:2018
ISSN:2213-2317
Megjegyzések:8-Oxoguanine DNA glycosylase 1 (OGG1) initiates the base excision repair pathway by removing one of the most abundant DNA lesions, 8-oxo-7,8-dihydroguanine (8-oxoG). Recent data showed that 8-oxoG not only is a promutagenic genomic base lesion, but also functions as an epigenetic mark and that consequently OGG1 acquire distinct roles in modulation of gene expression. In support, lack of functional OGG1 in Ogg1(-/-) mice led to an altered expression of genes including those responsible for the aberrant innate and adaptive immune responses and susceptibility to metabolic disorders. Therefore, the present study examined stimulus-driven OGG1-DNA interactions at whole genome level using chromatin immunoprecipitation (ChIP)-coupled sequencing, and the roles of OGG1 enriched on the genome were validated by molecular and system-level approaches. Results showed that signaling levels of cellular ROS generated by TNF alpha, induced enrichment of OGG1 at specific sites of chromatinized DNA, primarily in the regulatory regions of genes. OGG1-ChIP-ed genes are associated with important cellular and biological processes and OGG1 enrichment was limited to a time scale required for immediate cellular responses. Prevention of OGG1-DNA interactions by siRNA depletion led to modulation of NF-kappa B's DNA occupancy and differential expression of genes. Taken together these data show TNF alpha-ROS-driven enrichment of OGG1 at gene regulatory regions in the chromatinized DNA, which is a prerequisite to modulation of gene expression for prompt cellular responses to oxidant stress.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Redox Biology. - 18 (2018), p. 43-53. -
További szerzők:Qi, Tianyang Pan, Lang Wang, Ruoxi Zhu, Bing Aguilera-Aguirre, Leopoldo Radák Zsolt Hazra, Tapas K. Vlahopoulos, Spiros A. Bácsi Attila (1967-) (immunológus) Brasier, Allan R. Ba, Xueqing Boldogh István
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM114252
035-os BibID:(cikkazonosító)1186369 (scopus)85168475682 (wos)001052448900001
Első szerző:Pan, Lang
Cím:Substrate-specific binding of 8-oxoguanine DNA glycosylase 1 (OGG1) reprograms mucosal adaptations to chronic airway injury / Pan Lang, Vlahopoulos Spiros, Tanner Lloyd, Bergwik Jesper, Bacsi Attila, Radak Zsolt, Egesten Arne, Ba Xueqing, Brasier Allan R., Boldogh Istvan
Dátum:2023
ISSN:1664-3224
Megjegyzések:Recent advances have uncovered the non-random distribution of 7, 8-dihydro-8-oxoguanine (8-oxoGua) induced by reactive oxygen species, which is believed to have epigenetic effects. Its cognate repair protein, 8-oxoguanine DNA glycosylase 1 (OGG1), reads oxidative substrates and participates in transcriptional initiation. When redox signaling is activated in small airway epithelial cells, the DNA repair function of OGG1 is repurposed to transmit acute inflammatory signals accompanied by cell state transitions and modification of the extracellular matrix. Epithelial-mesenchymal and epithelial-immune interactions act cooperatively to establish a local niche that instructs the mucosal immune landscape. If the transitional cell state governed by OGG1 remains responsive to inflammatory mediators instead of differentiation, the collateral damage provides positive feedback to inflammation, ascribing inflammatory remodeling to one of the drivers in chronic pathologies. In this review, we discuss the substrate-specific read through OGG1 has evolved in regulating the innate immune response, controlling adaptations of the airway to environmental and inflammatory injury, with a focus on the reader function of OGG1 in initiation and progression of epithelial to mesenchymal transitions in chronic pulmonary disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Immunology. - 14 (2023), p. 1-12. -
További szerzők:Vlahopoulos, Spiros A. Tanner, Lloyd Bergwik, Jesper Bácsi Attila (1967-) (immunológus) Radák Zsolt Egesten, Arne Ba, Xueqing Brasier, Allan R. Boldogh István
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

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
Borító:

5.

001-es BibID:BIBFORM114251
035-os BibID:(scopus)85168388624 (wos)001050570800001 (cikkazonosító)1161160
Első szerző:Xue, Yaoyao
Cím:Epigenetic control of type III interferon expression by 8-oxoguanine and its reader 8-oxoguanine DNA glycosylase1 / Xue Yaoyao, Pan Lang, Vlahopoulos Spiros, Wang Ke, Zheng Xu, Radak Zsolt, Bacsi Attila, Tanner Lloyd, Brasier Allan R., Ba Xueqing, Boldogh Istvan
Dátum:2023
ISSN:1664-3224
Megjegyzések:Interferons (IFNs) are secreted cytokines with the ability to activate expression of IFN stimulated genes that increase resistance of cells to virus infections. Activated transcription factors in conjunction with chromatin remodelers induce epigenetic changes that reprogram IFN responses. Unexpectedly, 8-oxoguanine DNA glycosylase1 (Ogg1) knockout mice show enhanced stimuli-driven IFN expression that confers increased resistance to viral and bacterial infections and allergen challenges. Here, we tested the hypothesis that the DNA repair protein OGG1 recognizes 8-oxoguanine (8-oxoGua) in promoters modulating IFN expression. We found that functional inhibition, genetic ablation, and inactivation by post-translational modification of OGG1 significantly augment IFN-? expression in epithelial cells infected by human respiratory syncytial virus (RSV). Mechanistically, OGG1 bound to 8-oxoGua in proximity to interferon response elements, which inhibits the IRF3/IRF7 and NF-?B/RelA DNA occupancy, while promoting the suppressor NF-?B1/p50-p50 homodimer binding to the IFN-?2/3 promoter. In a mouse model of bronchiolitis induced by RSV infection, functional ablation of OGG1 by a small molecule inhibitor (TH5487) enhances IFN-? production, decreases immunopathology, neutrophilia, and confers antiviral protection. These findings suggest that the ROS-generated epigenetic mark 8-oxoGua via its reader OGG1 serves as a homeostatic thresholding factor in IFN-? expression. Pharmaceutical targeting of OGG1 activity may have clinical utility in modulating antiviral response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Immunology. - 14 (2023), p. 1-19. -
További szerzők:Pan, Lang Vlahopoulos, Spiros A. Wang, Ke Zheng, Xu Radák Zsolt Bácsi Attila (1967-) (immunológus) Tanner, Lloyd Brasier, Allan R. Ba, Xueqing Boldogh István
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.