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1.

001-es BibID:BIBFORM072833
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Pollen-induced oxidative DNA damage response regulates miRNAs controlling allergic inflammation / Aguilera-Aguirre Leopoldo, Hao Wenging, Pan Lang, Li Xiaoxue, Saavedra-Molina Alfredo, Bacsi Attila, Radak Zsolt, Sur Sanjiv, Brasier Allan R., Ba Xueqing, Boldogh Istvan
Dátum:2017
ISSN:1040-0605 1522-1504
Megjegyzések:A mucosal oxidative burst is a hallmark response to pollen exposure that promotes allergic inflammatory responses. Reactive species constituents of oxidative stress signal via the modification of cellular molecules including nucleic acids. One of the most abundant forms of oxidative genomic base damage is 8-oxo-7,8-dihydroguanine (8-oxoG), which is removed from DNA by 8-oxoguanine DNA glycosylase 1 (OGG1). OGG1 in complex with 8-oxoG acts as a GDP-GTP exchange factor and induces acute inflammation; however, the mechanism(s) by which OGG1 signaling regulates allergic airway inflammation is not known. Here, we postulate that the OGG1 signaling pathway differentially altered the levels of small regulatory RNAs and increased the expression of T helper 2 (Th2) cytokines in ragweed pollen extract (RWPE)-challenged lungs. To determine this, the lungs of sensitized mice expressing or lacking OGG1 were challenged with RWPE and/or with OGG1's excision product 8-oxoG. The responses in lungs were assessed by next-generation sequencing, as well as various molecular and histological approaches. The results showed that RWPE challenge induced oxidative burst and damage to DNA and activated OGG1 signaling, resulting in the differential expression of 84 micro-RNAs (miRNAs), which then exacerbated antigen-driven allergic inflammation and histological changes in the lungs. The exogenous administration of the downregulated let-7b-p3 mimetic or inhibitors of upregulated miR-23a or miR-27a decreased eosinophil recruitment and mucus and collagen production via controlling the expression of IL-4, IL-5, and IL-13. Together, these data demonstrate the roles of OGG1 signaling in the regulation of antigen-driven allergic immune responses via differential expression of miRNAs upstream of Th2 cytokines and eosinophils.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DNA repair
allergy
cell signaling
micro-RNAs
Megjelenés:American Journal Of Physiology-Lung Cellular And Molecular Physiology 313 : 6 (2017), p. L1058-L1068. -
További szerzők:Hao, Wenging Pan, Lang Li, Xiaoxue Saavedra-Molina, Alfredo Bácsi Attila (1967-) (immunológus) Radák Zsolt Sur, Sanjiv Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:OTKA-109595
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2.

001-es BibID:BIBFORM065564
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Whole transcriptome analysis reveals a role for OGG1-initiated DNA repair signaling in airway remodeling / Leopoldo Aguilera-Aguirre, Koa Hosoki, Attila Bacsi, Zsolt Radák, Sanjiv Sur, Muralidhar L. Hegde, Bing Tian, Alfredo Saavedra-Molina, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2015
ISSN:0891-5849
Megjegyzések:Reactive oxygen species (ROS) generated by environmental exposures, and endogenously as by-products of respiration, oxidatively modify biomolecules including DNA. Accumulation of ROS-induced DNA damage has been implicated in various diseases that involve inflammatory processes, and efficient DNA repair is considered critical in preventing such diseases. One of the most abundant DNA base lesions is 7,8-dihydro-8-oxoguanine (8-oxoG), which is repaired by the 8-oxoguanine DNA glycosylase 1 (OGG1)-initiated base-excision repair (OGG1-BER) pathway. Recent studies have shown that the OGG1-BER by-product 8-oxoG base forms a complex with cytosolic OGG1, activating small GTPases and downstream cell signaling in cultured cells and lungs. This implies that persistent OGG1-BER could result in signaling leading to histological changes in airways. To test this, we mimicked OGG1-BER by repeatedly challenging airways with its repair product 8-oxoG base. Gene expression was analyzed by RNA sequencing (RNA-Seq) and qRT-PCR, and datasets were evaluated by gene ontology and statistical tools. RNA-Seq analysis identified 3252 differentially expressed transcripts (2435 up- and 817 downregulated, ? 3-fold change). Among the upregulated transcripts, 2080 mRNAs were identified whose encoded protein products were involved in modulation of the actin family cytoskeleton, extracellular matrix, cell adhesion, cadherin, and cell junctions, affecting biological processes such as tissue development, cell-to-cell adhesion, cell communication, and the immune system. These data are supported by histological observations showing epithelial alterations, subepithelial fibrosis, and collagen deposits in the lungs. These data imply that continuous challenge by the environment and consequent OGG1-BER-driven signaling trigger gene expression consistent with airway remodeling.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
8-Oxoguanine
Airway remodeling
OGG1-BER
Megjelenés:Free Radical Biology And Medicine 89 (2015), p. 20-33. -
További szerzők:Hosoki, Koa Bácsi Attila (1967-) (immunológus) Radák Zsolt Sur, Sanjiv Hegde, Muralidhar L. Tian, Bing Saavedra-Molina, Alfredo Brasier, Allan R. Ba, Xueqing Boldogh István
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3.

001-es BibID:BIBFORM065605
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Whole transcriptome analysis reveals an 8-oxoguanine DNA glycosylase-1-driven DNA repair-dependent gene expression linked to essential biological processes / Leopoldo Aguilera-Aguirre, Koa Hosoki, Attila Bacsi, Zsolt Radák, Thomas G. Wood, Steven G. Widen, Sanjiv Sur, Bill T. Ameredes, Alfredo Saavedra-Molina, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2015
ISSN:0891-5849
Megjegyzések:Reactiveoxygenspeciesinflict oxidativemodifications onvariousbiologicalmolecules,includingDNA.One ofthemostabundantDNAbaselesions,8-oxo-7,8-dihydroguanine(8-oxoG)isrepairedby8-oxoguanineDNAglycosylase-1(OGG1)duringDNAbaseexcisionrepair(OGG1-BER).8-OxoGaccumula-tion inDNAhasbeenassociatedwithvariouspathologicalandagingprocesses,althoughitsroleisunclear.ThelackofOGG1-BERin Ogg1 / mice resultedindecreasedinflammatory responsesandincreased susceptibilitytoinfectionsandmetabolicdisorders.Therefore,weproposedthatOGG1and/or8-oxoGbasemayhavearoleinimmuneandhomeostaticprocesses.Totestourhypothesis,wechallenged mouselungswithOGG1-BERproduct8-oxoGbaseandchangesingeneexpressionweredetermined byRNAsequencinganddatawereanalyzedbyGeneOntologyandstatisticaltools.RNA-Seqanalysisidentified 1592differentiallyexpressed(Z 3-fold change)transcripts.TheupregulatedmRNAswererelatedtobiologicalprocesses,includinghomeostatic,immune-system,macrophageactivation,regulation ofliquid-surfacetension,andresponsetostimulus.Theseprocessesweremediatedbychemokines, cytokines,gonadotropin-releasinghormonereceptor,integrin,andinterleukinsignalingpathways.Takentogether,these findings pointtoanewparadigmshowingthatOGG1-BERplaysarolein variousbiologicalprocessesthatmaybenefit thehost,butwheninexcesscouldbeimplicatedindisease and/oragingprocesses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
OGG1-BER
8-Oxoguanine
Gene expression
Biological processes
Megjelenés:Free Radical Biology And Medicine. - 81 (2015), p. 107-118. -
További szerzők:Hosoki, Koa Bácsi Attila (1967-) (immunológus) Radák Zsolt Wood, Thomas G. Widen, Steven G. Sur, Sanjiv Ameredes, Bill T. Saavedra-Molina, Alfredo Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:TAMOP4.2.2.A-11/1/KONV- 2012?2023
Egyéb
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4.

001-es BibID:BIBFORM055870
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Oxidative damage to mitochondrial respiratory chain complexes increases allergic inflammation in mice / Aguilera-Aguirre Leopoldo, Saavedra-Molina Alfredo, Bácsi Attila, Sur Sanjiv, Boldogh István
Dátum:2007
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Journal of Allergy and Clinical Immunology. - 123 (2007), p. S122. -
További szerzők:Saavedra-Molina, Alfredo Bácsi Attila (1967-) (immunológus) Sur, Sanjiv Boldogh István
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5.

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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6.

001-es BibID:BIBFORM010166
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Mitochondrial dysfunction increases allergic airway inflammation / Leopoldo Aguilera-Aguirre, Attila Bácsi, Alfredo Saavedra-Molina, Alexander Kurosky, Sanjiv Sur, István Boldogh
Dátum:2009
Megjegyzések:The prevalence of allergies and asthma among the world's population has been steadily increasing due to environmental factors. It has been described that exposure to ozone, diesel exhaust particles, or tobacco smoke exacerbates allergic inflammation in the lungs. These environmental oxidants increase the levels of cellular reactive oxygen species (ROS) and induce mitochondrial dysfunction in the airway epithelium. In this study, we investigated the involvement of preexisting mitochondrial dysfunction in the exacerbation of allergic airway inflammation. After cellular oxidative insult induced by ragweed pollen extract (RWE) exposure, we have identified nine oxidatively damaged mitochondrial respiratory chain-complex and associated proteins. Out of these, the ubiquinol-cytochrome c reductase core II protein (UQCRC2) was found to be implicated in mitochondrial ROS generation from respiratory complex III. Mitochondrial dysfunction induced by deficiency of UQCRC2 in airway epithelium of sensitized BALB/c mice prior the RWE challenge increased the Ag-induced accumulation of eosinophils, mucin levels in the airways, and bronchial hyperresponsiveness. Deficiency of UQCRC1, another oxidative damage-sensitive complex III protein, did not significantly alter cellular ROS levels or the intensity of RWE-induced airway inflammation. These observations suggest that preexisting mitochondrial dysfunction induced by oxidant environmental pollutants is responsible for the severe symptoms in allergic airway inflammation. These data also imply that mitochondrial defects could be risk factors and may be responsible for severe allergic disorders in atopic individuals.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Immunology. - 183 : 8 (2009), p. 5379-5387. -
További szerzők:Bácsi Attila (1967-) (immunológus) Saavedra-Molina, Alfredo Kurosky, Alexander Sur, Sanjiv Boldogh István
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7.

001-es BibID:BIBFORM055556
035-os BibID:(scopus)84907867357 (wos)000343109700119
Első szerző:Ba, Xueqing
Cím:The Role of 8-Oxoguanine DNA Glycosylase-1 in Inflammation / Xueqing Ba, Leopoldo Aguilera-Aguirre, Qura Tul Ain Nmi Rashid, Attila Bacsi, Zsolt Radak, Sanjiv Sur, Koa Hosoki, Muralidhar L. Hegde, Istvan Boldogh
Dátum:2014
ISSN:1661-6596 1422-0067
Megjegyzések:Many, if not all, environmental pollutants/chemicals and infectious agents increase intracellular levels of reactive oxygen species (ROS) at the site of exposure. ROS not only function as intracellular signaling entities, but also induce damage to cellular molecules including DNA. Among the several dozen ROS-induced DNA base lesions generated in the genome, 8-oxo-7,8-dihydroguanine (8-oxoG) is one of the most abundant because of guanine's lowest redox potential among DNA bases. In mammalian cells, 8-oxoG is repaired by the 8-oxoguanine DNA glycosylase-1 (OGG1)-initiated DNA base excision repair pathway (OGG1-BER). Accumulation of 8-oxoG in DNA has traditionally been associated with mutagenesis, as well as various human diseases and aging processes, while the free 8-oxoG base in body fluids is one of the best biomarkers of ongoing pathophysiological processes. In this review, we discuss the biological significance of the 8-oxoG base and particularly the role of OGG1-BER in the activation of small GTPases and changes in gene expression, including those that regulate pro-inflammatory chemokines/cytokines and cause inflammation.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Journal of Molecular Sciences. - 15 : 9 (2014), p. 16975-16997. -
További szerzők:Aguilera-Aguirre, Leopoldo Rashid, Qura Tul Ain Nmi Bácsi Attila (1967-) (immunológus) Radák Zsolt Sur, Sanjiv Hosoki, Koa Hegde, Muralidhar L. Boldogh István
Pályázati támogatás:TAMOP 4.2.2.A-11/1/KONV-2012-2023
TÁMOP
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8.

001-es BibID:BIBFORM051534
035-os BibID: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
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
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9.

001-es BibID:BIBFORM047649
Első szerző:Bácsi Attila (immunológus)
Cím:Colostrinin decreases spontaneous and induced mutation frequencies at the hprt locus in Chinese hamster V79 cells / Attila Bacsi, Leopoldo Aguilera-Aguirre, Peter German, Marian L. Kruzel, Istvan Boldogh
Dátum:2006
Megjegyzések:ColostrininTM (CLN), a uniform mixture of lowmolecular weight, proline-rich polypeptides, induces neurite outgrowth of pheochromocytoma cells, extends the lifespan of diploid fibroblast cells, inhibits beta amyloid-induced apoptosis and resulted in improved cognitive function when administered to Alzheimer's patients. Here we investigated CLN's antimutagenic activity in cells stressed oxidatively or exposed to chemical or physical agents. Our data show that CLN did not alter cell cycle kinetics and cloning efficiency, while it inhibited the development of spontaneous mutations at the coding region of the hypoxanthine phosphoribosyl-transferase (hprt) gene in Chinese hamster V79 cells. In a dosedependent manner, CLN lowered reactive oxygen species (ROS)-induced frequency of cells resistant to 6-thioguanine (6-TG) to nearly background level. Likewise, CLN decreased the frequency of methyl methanesulfonate- or mitomycin C-induced mutations in V79 cells. Notably, CLN (at 100, 250, and 500 ng per ml concentrations) decreased UVAinduced mutation frequency, while only the highest dose of CLN also decreased significantly the number of UVB-induced 6-TG-resistant mutant cells. Similar results were obtained using cell cultures of human origin. Overall, our data show that CLN significantly lowers the mutation frequency that develops spontaneously or is induced by ROS, chemical and physical agents. CLN itself has no mutagenic activity. Therefore, CLN may be used in human therapies systemically and/or locally for the prevention of diseases associated with sequence alterations in genomic and mitochondrial DNA.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
colostrinin
mutation frequency
oxidative stress
genotoxic chemical and physical agents
Megjelenés:Journal of Experimental Therapeutics and Oncology 5 : 4 (2006), p. 249-259. -
További szerzők:Aguilera-Aguirre, Leopoldo Germán Péter (gyermekgyógyász) Kruzel, Marian L. Boldogh István
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10.

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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11.

001-es BibID:BIBFORM055868
Első szerző:Boldogh István
Cím:Colostrinin (TM) increases the lifespan and neurological performance of mice / Boldogh I., Bácsi A., Agulera-Aguirre L., Germán P., Kruzel M.
Dátum:2008
Tárgyszavak:Természettudományok Biológiai tudományok előadáskivonat
Megjelenés:New Trends in Alzheimer and Parkinson Related Disorders : ADPD 2007 / eds. Hanin I., Windisch M., Poewe W., Fisher A. - [1] p. -
További szerzők:Bácsi Attila (1967-) (immunológus) Aguilera-Aguirre, Leopoldo Germán Péter (gyermekgyógyász) Kruzel, Marian L.
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12.

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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