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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
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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
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