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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
TÁMOP
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2.

001-es BibID:BIBFORM055861
Első szerző:Bácsi Attila (immunológus)
Cím:Plant pollens and molds directly induce oxidative stress in the airways / Bácsi Attila, Sur Sanjiv, Choudhury Barun, Hazra Tapas K., Boldogh István
Dátum:2002
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Free Radical Biology and Medicine. - 33 : Suppl. 2 (2002), p. 343. -
További szerzők:Sur, Sanjiv Choudhury, Barun K. Hazra, Tapas K. Boldogh István
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3.

001-es BibID:BIBFORM055871
Első szerző:Bácsi Attila (immunológus)
Cím:Antigen-independent mitochondria-driven release of biogenic amines from RBL-2H3 cells / Bácsi Attila, Chodaczek Grzegorz, Dharajiya Nilesh, Sur Sanjiv, Hazra Tapas K., Boldogh István
Dátum:2007
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Journal of Allergy and Clinical Immunology. - 123 (2007), p. S118. -
További szerzők:Chodaczek, Grzegorz Dharajiya, Nilesh G. Sur, Sanjiv Hazra, Tapas K. Boldogh István
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4.

001-es BibID:BIBFORM047646
035-os BibID:PMID:16298690
Első szerző:Bácsi Attila (immunológus)
Cím:Modulation of DNA-dependent protein kinase activity in chlorambucil-treated cells / Attila Bacsi, Subbaraj Kannan, Myung-Soog Lee, Tapas K. Hazra, Istvan Boldogh
Dátum:2005
ISSN:0891-5849
Megjegyzések:DNA-dependent protein kinase (DNA-PK) is activated in a two-step process whereby the Ku heterodimer first binds to the DNA double-strandbreaks (dsbs) and then the DNA-PK catalytic subunit (cs) is recruited to form a repair complex. Oxidative stress is simultaneously generated alongwith DNA damage by ionizing radiation or chemotherapeutic agents whose impact on the DNA-PK activity has not previously been investigated.Here we show that the DNA damage-induced kinase activity of DNA-PK was modulated by oxidative stress, which was induced along with DNAdsbs in chlorambucil (Cbl)-exposed cells. Pretreatment with the antioxidants, 2(3)-t-butyl-4-hydroxyanisole or N-acetyl-l-cysteine enhanced theamount of DNA-PKcs phosphorylated at threonine 2609 (DNA-PKpThr2609) at the DNA dsbs and DNA-PK activity. Conversely, oxidative stressinduced by l-buthionine (SR)-sulfoximine or glucose oxidase decreased the DNA-PK activity in Cbl-exposed cells. In addition, DNA-PKpThr2609was poorly detectable at the site of DNA dsbs, as shown by colocalization to DNA-end-binding pH2AX or p53BP1. There was no change in theprotein levels of DNA-PKcs, Ku70, or Ku86. Data from these studies provide the first evidence that oxidative stress effects posttranslationalmodification and assembly of DNA-PK complex at DNA dsbs, and thereby repair of DNA dsbs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Oxidative stress
DNA-PK
DNA dsbs repair
Free radicals
Megjelenés:Free Radical Biology and Medicine. - 39 : 12 (2005), p. 1650-1659. -
További szerzők:Kannan, Subbaraj Myung-Soog, Lee Hazra, Tapas K. Boldogh István
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5.

001-es BibID:BIBFORM041838
Első szerző:Bácsi Attila (immunológus)
Cím:Down-regulation of 8-oxoguanine DNA glycosylase 1 expression in the airway epithelium ameliorates allergic lung inflammation / Bacsi Attila, Aguilera-Aguirre Leopoldo, Szczesny Bartosz, Radak Zsolt, Hazra Tapas K., Sur Sanjiv, Ba Xueqing, Boldogh Istvan
Dátum:2013
ISSN:1568-7864
Megjegyzések:Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston
Allergic airway inflammation is characterized by increased expression of pro-inflammatory mediators, inflammatory cell infiltration, mucus hypersecretion, and airway hyperresponsiveness, in parallel with oxidative DNA base and strand damage, whose etiological role is not understood. Our goal was to establish the role of 8-oxoguanine (8-oxoG), a common oxidatively damaged base, and its repair by 8-oxoguanine DNA glycosylase 1 (Ogg1) in allergic airway inflammatory processes. Airway inflammation was induced by intranasally administered ragweed (Ambrosia artemisiifolia) pollen grain extract (RWPE) in sensitized BALB/c mice. We utilized siRNA technology to deplete Ogg1 from airway epithelium; 8-oxoG and DNA strand break levels were quantified by Comet assays. Inflammatory cell infiltration and epithelial methaplasia were determined histologically, mucus and cytokines levels biochemically and enhanced pause was used as the main index of airway hyperresponsiveness. Decreased Ogg1 expression and thereby 8-oxoG repair in the airway epithelium conveyed a lower inflammatory response after RWPE challenge of sensitized mice, as determined by expression of Th2 cytokines, eosinophilia, epithelial methaplasia, and airway hyperresponsiveness. In contrast, 8-oxoG repair in Ogg1-proficient airway epithelium was coupled to an increase in DNA single-strand break (SSB) levels and exacerbation of allergen challenge-dependent inflammation. Decreased expression of the Nei-like glycosylases Neil1 and Neil2 that preferentially excise ring-opened purines and 5-hydroxyuracil, respectively, did not alter the above parameters of allergic immune responses to RWPE. These results show that DNA SSBs formed during Ogg1-mediated repair of 8-oxoG augment antigen-driven allergic immune responses. A transient modulation of OGG1 expression/activity in airway epithelial cells could have clinical benefits.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Allergic inflammation
DNA repair
Oxidative DNA damage
Oxidative stress
8-Oxoguanine
8-Oxoguanine DNA glycosylase 1
Molekuláris Medicina
Megjelenés:Dna Repair. - 12 : 1 (2013), p. 18-26. -
További szerzők:Aguilera-Aguirre, Leopoldo Szczesny, Bartosz Radák Zsolt Hazra, Tapas K. Sur, Sanjiv Ba, Xueqing Boldogh István
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Az oxidatív DNS károsodások javítása és a gyulladás kialakulásának kapcsolata
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6.

001-es BibID:BIBFORM002003
Első szerző:Bácsi Attila (immunológus)
Cím:Increased ROS generation in subsets of OGG1 knockout fibroblast cells / Attila Bacsi, Grzegorz Chodaczek, Tapas K. Hazra, David Konkel, Istvan Boldogh
Dátum:2007
Megjegyzések:Oxoguanine DNA glycosylase (OGG1) is a major base excision repair protein responsible for excision of the mutagenic 8-oxoguanosine (8-oxoG) lesions from the genome. Despite OGG1's importance, the moderate phenotype of Ogg1-null (Ogg1_/_) mice is not well understood. This study addresses a mechanism by which Ogg1_/_ cells limit accumulation of 8-oxoG in their genome. Our data reveal that a subset of Ogg1_/_ cells shows higher ROS levels (HROS cells), while _85% of Ogg1_/_ cells exhibit physiological levels of ROS (LROS cells). Ogg1_/_ cells were sorted based on their DCF fluorescence intensity to obtain LROS and HROS cell cultures. LROS cultures proliferated at a rate comparable to Ogg1+/+ and gradually accumulated cells exhibiting increased ROS and 8-oxoG levels. LROS cells show a 2.8-fold increase in 8-oxoG level vs. HROS cells (7? 27-fold). Mitochondria of HROS cells released more H2O2 than LROS and Ogg1+/+ cells and were eliminated by apoptotic-like processes. These findings suggest that in the absence of OGG1, a surveillance system is activated that removes cells with extreme 8-oxoG levels from Ogg1_/_ cultures. Whether similar mechanisms exists in tissues of Ogg1_/_ mice is the focus of future investigations.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Ogg1 null fibroblast
ROS
8-oxoguanine
Mitochondria
Megjelenés:Mechanisms of ageing and development. - 128 : 11-12 (2007), p. 637-649. -
További szerzők:Chodaczek, Grzegorz Hazra, Tapas K. Konkel, David Boldogh István
Internet cím:elektronikus változat
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elektronikus változat
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7.

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
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8.

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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9.

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
Borító:

10.

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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11.

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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12.

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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