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1.

001-es BibID:BIBFORM055555
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Innate Inflammation Induced by the 8-Oxoguanine DNA Glycosylase-1-KRAS-NF-kB Pathway / Leopoldo Aguilera-Aguirre, Attila Bacsi, Zsolt Radak, Tapas K. Hazra, Sankar Mitra, Sanjiv Sur, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2014
ISSN:0022-1767 1550-6606
Megjegyzések:8-Oxoguanine-DNA glycosylase-1 (OGG1) is the primary enzyme for repairing 7,8-dihydro-8-oxoguanine (8-oxoG) via the DNAbase excision repair pathway (OGG1-BER). Accumulation of 8-oxoG in the genomic DNA leads to genetic instability and carcinogenesis and is thought to contribute to the worsening of various inflammatory and disease processes. However, the disease mechanism is unknown. In this study, we proposed that the mechanistic link between OGG1-BER and proinflammatory gene expression is OGG1's guanine nucleotide exchange factor activity, acquired after interaction with the 8-oxoG base and consequent activationof the small GTPase RAS. To test this hypothesis, we used BALB/c mice expressing or deficient in OGG1 in their airwayepithelium and various molecular biological approaches, including active RAS pulldown, reporter and Comet assays, small interfering RNA?mediated depletion of gene expression, quantitative RT-PCR, and immunoblotting. We report that the OGG1-intiated repair of oxidatively damaged DNA is a prerequisite for GDP?GTP exchange, KRAS-GTP?driven signaling via MAP kinases and PI3 kinases and mitogen-stress?related kinase-1 for NF-kB activation, proinflammatory chemokine/cytokine expression, and inflammatory cell recruitment to the airways. Mice deficient in OGG1-BER showed significantly decreasedimmune responses, whereas a lack of other Nei-like DNA glycosylases (i.e., NEIL1 and NEIL2) had no significant effect. These data unveil a previously unidentified role of OGG1-driven DNA BER in the generation of endogenous signals for inflammation in the innate signaling pathway.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Immunology. - 193 : 9 (2014), p. 4643-4653. -
További szerzők:Bácsi Attila (1967-) (immunológus) Radák Zsolt Hazra, Tapas K. Mitra, Sankar Sur, Sanjiv Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:TAMOP 4.2.2.A-11/1/KONV-2012-2023
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2.

001-es BibID:BIBFORM038719
Első szerző:Bácsi Attila (immunológus)
Cím:Localization of superoxide anion production to mitochondrial electron transport chain in 3-NPA-treated cells / Bacsi Attila, Woodberry Mitchell, Widger William, Papaconstantinou John, Mitra Sankar, Peterson Johnny W., Boldogh Istvan
Dátum:2006
ISSN:1567-7249
Megjegyzések:3-Nitropropionic acid (3-NPA), an inhibitor of succinate dehydrogenase (SDH) at complex II of the mitochondrial electron transport chain induces cellular energy deficit and oxidative stress-related neurotoxicity. In the present study, we identified the site of reactive oxygen species production in mitochondria. 3-NPA increased O2- generation in mitochondria respiring on the complex I substrates pyruvate+malate, an effect fully inhibited by rotenone. Antimycin A increased O2- production in the presence of complex I and/or II substrates. Addition of 3-NPA markedly increased antimycin A-induced O2- production by mitochondria incubated with complex I substrates, but 3-NPA inhibited O2- formation driven with the complex II substrate succinate. At 0.6 microM, myxothiazol inhibits complex III, but only partially decreases complex I activity, and allowed 3-NPA-induced O2- formation; however, at 40 microM myxothiazol (which completely inhibits both complexes I and III) eliminated O2- production from mitochondria respiring via complex I substrates. These results indicate that in the presence of 3-NPA, mitochondria generate O2- from a site between the ubiquinol pool and the 3-NPA block in the respiratory complex II.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Mitochondrion. - 6 : 5 (2006), p. 235-244. -
További szerzők:Woodberry, Mitchell Widger, William Papaconstantinou, John Mitra, Sankar Peterson, Johnny W. Boldogh István
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3.

001-es BibID:BIBFORM055862
Első szerző:Boldogh István
Cím:Regulation of DNA-dependent protein kinase catalityc activity by ROS / Boldogh István, Subbaraj Kannan, Hazra Tapas K., Bácsi Attila, Liebenthal Daniel, Mitra Sankar
Dátum:2002
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Free Radical Biology and Medicine. - 33 : Suppl. 2 (2002), p. 439. -
További szerzők:Kannan, Subbaraj Hazra, Tapas K. Bácsi Attila (1967-) (immunológus) Liebenthal, Daniel Mitra, Sankar
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4.

001-es BibID:BIBFORM055875
Első szerző:Boldogh István
Cím:Role of 8-oxoG in Eliciting an Inflammatory Response / Boldogh István, Aguilera-Aguirre Leopoldo, Bácsi Attila, Germán Péter, Hajas György, Sur Sanjiv, Hazra Tapas K., Mitra Sankar
Dátum:2010
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Environmental And Molecular Mutagenesis. - 51 (2010), p. 697. -
További szerzők:Aguilera-Aguirre, Leopoldo Bácsi Attila (1967-) (immunológus) Germán Péter (gyermekgyógyász) Hajas György (1970-) (biológus) Sur, Sanjiv Hazra, Tapas K. Mitra, Sankar
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5.

001-es BibID:BIBFORM047643
035-os BibID:PMID:14599773
Első szerző:Boldogh István
Cím:Reduced DNA double strand breaks in chlorambucil resistant cells are related to high DNA-PKcs activity and low oxidative stress / Istvan Boldogh, Gargi Roy, Myung-Soog Lee, Attila Bacsi, Tapas K. Hazra, Kishor K. Bhakat, Gokul C. Das, Sankar Mitra
Dátum:2003
ISSN:0300-483X
Megjegyzések:Modulation of DNA repair represents a strategy to overcome acquired drug resistance of cells to genotoxic chemotherapeuticagents, including nitrogen mustards (NM). These agents induce DNA inter-strand cross-links, which in turn produce doublestrand breaks (dsbs). These breaks are primarily repaired via the nonhomologous end-joining (NHEJ) pathway.ADNA-dependentprotein kinase (DNA-PK) complex plays an important role in NHEJ, and its increased level/activity is associated with acquireddrug resistance of human tumors. We show in this report that the DNA-PK complex has comparable levels and kinase activityof DNA-PK catalytic subunit (DNA-PKcs) in a nearly isogenic pair of drug-sensitive (A2780) and resistant (A2780/100) cells;however, treatment with chlorambucil (Cbl), a NM-type of drug, induced differential effects in these cells. The kinase activityof DNA-PKcs was increased up to 2 h after Cbl treatment in both cell types; however, it subsequently decreased only in sensitivecells, which is consistent with increased levels of DNA dsbs. The decreased kinase activity of DNA-PKcs was not due to a changein its amount or the levels ofKu70 andKu86, their subcellular distribution, cell cycle progression or caspase-mediated degradationof DNA-PK. In addition to DNA cross-links, Cbl treatment of cells causes a 2.2-fold increase in the level of reactive oxygenspecies (ROS) in both cell types. However, the ROS in A2780/100 cells were reduced to the basal level after 3?4 h, while sensitivecells continued to produce ROS and undergo apoptosis. Pre-treatment of A2780 cells with the glutathione (GSH) precursor,N-acetyl-l-cysteine prevented Cbl-induced increase in ROS, augmented the kinase activity of DNA-PKcs, decreased the levelsof DNA dsbs and increased cell survival. Depletion in GSH from A2780/100 cells by l-buthionine sulfoximine (BSO) resulted insustained production of ROS, loweredDNA-PKcs kinase activity, enhanced levels ofDNAdsbs, and increased cell killing by Cbl.We propose that oxidative stress decreases repair of DNA dsbs via lowering kinase activity of DNA-PKcs and that induction ofROS could be the basis for adjuvant therapies for sensitizing tumor cells to nitrogen mustards and other DNA cross-linking drugs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Oxidative stress
DNA-PK
DNA double strand breaks
Megjelenés:Toxicology. - 193 : 1-2 (2003), p. 137-152. -
További szerzők:Roy, Gargi Myung-Soog, Lee Bácsi Attila (1967-) (immunológus) Hazra, Tapas K. Bhakat, Kishor K. Das, Gokul C. Mitra, Sankar
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6.

001-es BibID:BIBFORM047644
Első szerző:Boldogh István
Cím:ROS generated by pollen NADPH oxidase provide a signal that augments antigen-induced allergic airway inflammation / Istvan Boldogh, Attila Bacsi, Barun K. Choudhury, Nilesh Dharajiya, Rafeul Alam, Tapas K. Hazra, Sankar Mitra, Randall M. Goldblum, Sanjiv Sur
Dátum:2005
ISSN:0021-9738
Megjegyzések:Pollen exposure induces allergic airway inflammation in sensitized subjects. The role of antigenic pollen proteinsin the induction of allergic airway inflammation is well characterized, but the contribution of otherconstituents in pollen grains to this process is unknown. Here we show that pollen grains and their extractscontain intrinsic NADPH oxidases. The pollen NADPH oxidases rapidly increased the levels of ROS in lungepithelium as well as the amount of oxidized glutathione (GSSG) and 4-hydroxynonenal (4-HNE) in airwayliningfluid. These oxidases, as well as products of oxidative stress (such as GSSG and 4-HNE) generated bythese enzymes, induced neutrophil recruitment to the airways independent of the adaptive immune response.Removal of pollen NADPH oxidase activity from the challenge material reduced antigen-induced allergic airwayinflammation, the number of mucin-containing cells in airway epithelium, and antigen-specific IgE levelsin sensitized mice. Furthermore, challenge with Amb a 1, the major antigen in ragweed pollen extract that doesnot possess NADPH oxidase activity, induced low-grade allergic airway inflammation. Addition of GSSG or4-HNE to Amb a 1 challenge material boosted allergic airway inflammation. We propose that oxidative stressgenerated by pollen NADPH oxidases (signal 1) augments allergic airway inflammation induced by pollenantigen (signal 2).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DNA double strand breaks
Megjelenés:Journal of Clinical Investigation. - 115 : 8 (2005), p. 2169-2179. -
További szerzők:Bácsi Attila (1967-) (immunológus) Choudhury, Barun K. Dharajiya, Nilesh G. Alam, Rafeul Hazra, Tapas K. Mitra, Sankar Goldblum, Randall M. Sur, Sanjiv
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7.

001-es BibID:BIBFORM041839
Első szerző:Boldogh István
Cím:Activation of ras signaling pathway by 8-oxoguanine DNA glycosylase bound to its excision product, 8-oxoguanine / Istvan Boldogh, Gyorgy Hajas, Leopoldo Aguilera-Aguirre, Muralidhar L. Hegde, Zsolt Radak, Attila Bacsi, Sanjiv Sur, Tapas K. Hazra, Sankar Mitra
Dátum:2012
ISSN:0021-9258
Megjegyzések:8-Oxo-7,8-dihydroguanine (8-oxoG), arguably the most abundant base lesion induced in mammalian genomes by reactive oxygen species, is repaired via the base excision repair pathway that is initiated with the excision of 8-oxoG by OGG1. Here we show that OGG1 binds the 8-oxoG base with high affinity and that the complex then interacts with canonical Ras family GTPases to catalyze replacement of GDP with GTP, thus serving as a guanine nuclear exchange factor. OGG1-mediated activation of Ras leads to phosphorylation of the mitogen-activated kinases MEK1,2/ERK1,2 and increasing downstream gene expression. These studies document for the first time that in addition to its role in repairing oxidized purines, OGG1 has an independent guanine nuclear exchange factor activity when bound to 8-oxoG.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Biological Chemistry 287 : 25 (2012), p. 20769-20773. -
További szerzők:Hajas György (1970-) (biológus) Aguilera-Aguirre, Leopoldo Hegde, Muralidhar L. Radák Zsolt Bácsi Attila (1967-) (immunológus) Sur, Sanjiv Hazra, Tapas K. Mitra, Sankar
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8.

001-es BibID:BIBFORM065562
Első szerző:Germán Péter (gyermekgyógyász)
Cím:8-Oxoguanine DNA glycosylase1-driven DNA repair : a paradoxical role in lung aging / Peter German, David Saenz, Peter Szaniszlo, Leopoldo Aguilera-Aguirre, Lang Pan, Muralidhar L. Hegde, Attila Bacsi, Gyorgy Hajas, Zsolt Radak, Xueqing Ba, Sankar Mitra, John Papaconstantinou, Istvan Boldogh
Dátum:2017
ISSN:0047-6374
Megjegyzések:Age-associated changes in lung structure and function are some of the most important predictors of overall health, cognitive activities and longevity. Common to all aging cells is an increase in oxidatively modified DNA bases, primarily 8-oxo-7,8-dihydroguanine (8-oxoG). It is repaired via DNA base excision repair pathway driven by 8-oxoguanine DNA glycosylase-1 (OGG1-BER), whose role in aging has been the focus of many studies. This study hypothesizes that signaling and consequent gene expression during cellular response to OGG1-BER "wires" senescence/aging processes. To test OGG1-BER was mimicked by repeatedly exposing diploid lung fibroblasts cells and airways of mice to 8-oxoG base. Results showed that repeated exposures led to G1 cell cycle arrest and pre-matured senescence of cultured cells in which over 1000 genes were differentially expressed -86% of them been identical to those in naturally senesced cells. Gene ontology analysis of gene expression displayed biological processes driven by small GTPases, phosphoinositide 3-kinase and mitogen activated kinase cascades both in cultured cells and lungs. These results together, points to a new paradigm about the role of DNA damage and repair by OGG1 in aging and age-associated disease processes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
OGG1
8-oxoguanine
Senescence
Aging
Megjelenés:Mechanisms Of Ageing And Development 161 : Pt A (2017), p. 51-65. -
További szerzők:Saenz, David N. Szaniszló Péter Aguilera-Aguirre, Leopoldo Pan, Lang Hegde, Muralidhar L. Bácsi Attila (1967-) (immunológus) Hajas György (1970-) (biológus) Radák Zsolt Ba, Xueqing Mitra, Sankar Papaconstantinou, John Boldogh István
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