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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM047640
Első szerző:	Germán Péter (gyermekgyógyász)
Cím:	Activation of cellular signaling by 8-oxoguanine DNA glycosylase-1-initiated DNA base excision repair / Peter German, Peter Szaniszlo, Gyorgy Hajas, Zsolt Radak, Attila Bacsi, Tapas K. Hazra, Muralidhar L. Hegde, Xueqing Ba, Istvan Boldogh
Dátum:	2013
ISSN:	1568-7864
Megjegyzések:	Accumulation of 8-oxo-7,8-dihydroguanine (8-oxoG) in the DNA results in genetic instability and mutagenesis, and is believed to contribute to carcinogenesis, aging processes and various aging-related diseases. 8-OxoG is removed from the DNA via DNA base excision repair (BER), initiated by 8-oxoguanine DNA glycosylase-1 (OGG1). Our recent studies have shown that OGG1 binds its repair product 8-oxoG base with high affinity at a site independent from its DNA lesion-recognizing catalytic site and the OGG1?8-oxoG complex physically interacts with canonical Ras family members. Furthermore, exogenously added 8-oxoG base enters the cells and activates Ras GTPases; however, a link has not yet been established between cell signaling and DNA BER, which is the endogenous source of the 8-oxoG base. In this study, we utilized KG-1 cells expressing a temperature-sensitive mutant OGG1, siRNA ablation of gene expression, and a variety of molecular biological assays to define a link between OGG1-BER and cellular signaling. The results show that due to activation of OGG1-BER, 8-oxoG base is released from the genome in sufficient quantities for activation of Ras GTPase and resulting in phosphorylation of the downstream Ras targets Raf1, MEK1,2 and ERK1,2. These results demonstrate a previously unrecognized mechanism for cellular responses to OGG1-initiated DNA BER.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Ogg1 Base excision repair Cell signaling
Megjelenés:	Dna Repair. - 12 : 10 (2013), p. 856-863. -
További szerzők:	Szaniszló Péter Hajas György (1970-) (biológus) Radák Zsolt Bácsi Attila (1967-) (immunológus) Hazra, Tapas K. Hegde, Muralidhar L. Ba, Xueqing Boldogh István
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001-es BibID:	BIBFORM057878
Első szerző:	Szaniszló Péter
Cím:	Effects of Colostrinin on gene expression-transcriptomal network analysis / Peter Szaniszlo, Peter German, Gyorgy Hajas, David N. Saenz, Mitchell W. Woodberry, Marian L. Kruzel, Istvan Boldogh
Dátum:	2009
ISSN:	1567-5769
Megjegyzések:	Colostrinin (CLN) is a uniform mixture of low-molecular weight proline-rich polypeptides isolated from the mother's first milk, colostrum. Exposure of cells to CLN decreases intracellular levels of reactive oxygen species by regulating glutathione metabolism and modulating activities of antioxidant enzymes and mitochondrial function. It also inhibits beta amyloid-induced apoptosis and induces neurite outgrowth of pheochromocytoma cells. Administration of CLN to Alzheimer's disease patients has resulted in a stabilizing effect on cognitive function. We analyzed CLN-induced gene expression changes using high-density oligonucleotide arrays and transcriptomal network analysis. We found that CLN elicited highly complex and multiphasic changes in the gene expression profile of treated cells. CLN treatment affected a total of 58 molecular networks, 27 of which contained at least 10 differentially expressed genes. Here we present CLN-modulated gene networks as potential underlying molecular mechanisms leading to the reported effects of CLN on cellular oxidative state, chemokine and cytokine production, and cell differentiation, as well as on pathological processes like allergy, asthma, Alzheimer's, and other neurological diseases. Based on our results, we also predict possible modulatory effects of CLN on adipocytokine gene networks that play a crucial role in the pathobiology of diabetes, cardiovascular disorders, obesity, and inflammation. Taken together, CLN-altered gene expression networks presented here provide the molecular basis for previously described biological phenomena and predict potential fields of application for CLN in the prevention and treatment of diseases.
Tárgyszavak:	Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	International Immunopharmacology. - 9 : 2 (2009), p. 181-193. -
További szerzők:	Germán Péter (gyermekgyógyász) Hajas György (1970-) (biológus) Saenz, David N. Woodberry, Mitchell Kruzel, Marian L. Boldogh István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM057879
Első szerző:	Szaniszló Péter
Cím:	New insights into clinical trial for Colostrinin in Alzheimer's disease / P. Szaniszlo, P. German, G. Hajas, D. N. Saenz, M. Kruzel, I. Boldogh
Dátum:	2009
ISSN:	1279-7707
Megjegyzések:	BACKGROUND: The pathomechanism of Alzheimer's disease (AD) is multifactorial although the most popular hypotheses are centered on the effects of the misfolded, aggregated protein, amyloid beta (Abeta) and on Tau hyperphosphorylation.OBJECTIVES: Double blinded clinical trials were planned to demonstrate the effect of Colostrinin (CLN) on instrumental daily activities of AD patients. The potential molecular mechanisms by which CLN mediates its effects were investigated by gene expression profiling.METHODS: RNAs isolated from CLN-treated cells were analyzed by high-density oligonucleotide arrays. Network and pathway analyses were performed using the Ingenuity Pathway Analysis software.RESULTS: The Full Sample Analysis at week 15 showed a stabilizing effect of CLN on cognitive function in ADAS-cog (p = 0.02) and on daily function in IADL (p = 0.02). The overall patient response was also in favor of CLN (p = 0.03). Patients graded as mild on entry also showed a superior response of ADAS-cog compared to more advanced cases (p = 0.01). Data derived from microarray network analysis show that CLN elicits highly complex and multiphasic changes in the cells' transcriptome. Importantly, transcriptomal analysis showed that CLN alters gene expression of molecular networks implicated in Abeta precursor protein synthesis, Tau phosphorylation and increased levels of enzymes that proteolitically eliminate Abeta. In addition, CLN enhanced the defense against oxidative stress and decreased expression of inflammatory chemokines and cytokines, thereby attenuating inflammatory processes that precede Alzheimer's and other neurological diseases.CONCLUSION: Together these data suggest that CLN has promising potential for clinical use in prevention and therapy of Alzheimer's and other age-associated central nervous system diseases.
Tárgyszavak:	Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of Nutrition Health & Aging. - 13 : 3 (2009), p. 235-241. -
További szerzők:	Germán Péter (gyermekgyógyász) Hajas György (1970-) (biológus) Saenz, David N. Kruzel, Marian L. Boldogh István
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