Zobrazeno 1 - 10
of 28
pro vyhledávání: '"Tatyana V. Votyakova"'
Autor:
Dirk J. Van Der Windt, Marco Marigliano, Jing He, Tatyana V. Votyakova, Gabriel J. Echeverri, Burcin Ekser, David Ayares, Fadi G. Lakkis, David K. C. Cooper, Massimo Trucco, Rita Bottino
Publikováno v:
Cell Transplantation, Vol 21 (2012)
Currently, islet transplantation as a cell therapeutic option for type 1 diabetes occurs via islet injection into the portal vein. Direct contact between islets and blood is a pathophysiological “provocation” that results in the instant blood-med
Externí odkaz:
https://doaj.org/article/0cc2fd28e59c4d2db55c0f6187754de0
Autor:
Vitaly A Selivanov, Marta Cascante, Mark Friedman, Mark F Schumaker, Massimo Trucco, Tatyana V Votyakova
Publikováno v:
PLoS Computational Biology, Vol 8, Iss 9, p e1002700 (2012)
The mitochondrial electron transport chain transforms energy satisfying cellular demand and generates reactive oxygen species (ROS) that act as metabolic signals or destructive factors. Therefore, knowledge of the possible modes and bifurcations of e
Externí odkaz:
https://doaj.org/article/2e499935181f4a61919cc4248009c2d4
Autor:
Vitaly A Selivanov, Tatyana V Votyakova, Violetta N Pivtoraiko, Jennifer Zeak, Tatiana Sukhomlin, Massimo Trucco, Josep Roca, Marta Cascante
Publikováno v:
PLoS Computational Biology, Vol 7, Iss 3, p e1001115 (2011)
Reactive oxygen species (ROS) produced in the mitochondrial respiratory chain (RC) are primary signals that modulate cellular adaptation to environment, and are also destructive factors that damage cells under the conditions of hypoxia/reoxygenation
Externí odkaz:
https://doaj.org/article/e46d90fe41af4a36ab5ae3fbecd6f951
Autor:
Vitaly A Selivanov, Tatyana V Votyakova, Jennifer A Zeak, Massimo Trucco, Josep Roca, Marta Cascante
Publikováno v:
PLoS Computational Biology, Vol 5, Iss 12, p e1000619 (2009)
Increased production of reactive oxygen species (ROS) in mitochondria underlies major systemic diseases, and this clinical problem stimulates a great scientific interest in the mechanism of ROS generation. However, the mechanism of hypoxia-induced ch
Externí odkaz:
https://doaj.org/article/b353c157fd9a43da8d0e6b4696235dca
Autor:
Ines Batinic-Haberle, Meghan L. Marré, Eric Goetzman, Massimo Trucco, Jon D. Piganelli, Tatyana V. Votyakova, Dana M. Previte, Artak Tovmasyan, Meghan Delmastro-Greenwood
Publikováno v:
Antioxidants & Redox Signaling. 19:1902-1915
Aims: The immune system is critical for protection against infections and cancer, but requires scrupulous regulation to limit self-reactivity and autoimmunity. Our group has utilized a manganese porphyrin catalytic antioxidant (MnTE-2-PyP5+, MnP) as
Autor:
Tatyana V. Votyakova, Ian J. Reynolds
Publikováno v:
Journal of Neurochemistry. 79:266-277
Mitochondria are widely believed to be the source of reactive oxygen species (ROS) in a number of neurodegenerative disease states. However, conditions associated with neuronal injury are accompanied by other alterations in mitochondrial physiology,
Autor:
Jennifer A. Zeak, Massimo Trucco, Tatyana V. Votyakova, Marta Cascante, Vitaly A. Selivanov, Josep Roca
Publikováno v:
The Journal of Biological Chemistry
Reactive oxygen species (ROS) generation in mitochondria as a side product of electron and proton transport through the inner membrane is important for normal cell operation as well as development of pathology. Matrix and cytosol alkalization stabili
Publikováno v:
Journal of Biological Chemistry. 282:5171-5179
NADH dehydrogenase subunit 2, encoded by the mtDNA, has been associated with resistance to autoimmune type I diabetes (T1D) in a case control study. Recently, we confirmed a role for the mouse ortholog of the protective allele (mt-Nd2(a)) in resistan
Publikováno v:
Mitochondrion. 5:55-65
Emerging evidence suggests that Zn2+ may impair neuronal metabolism. We examined how Zn2+ affects the activity of isolated brain mitochondria fueled with glutamate + malate, succinate or glycerol 3-phosphate. Submicromolar levels of Zn2+ dissipated m
Publikováno v:
Journal of Neurochemistry. 85:563-570
An increasing body of evidence suggests that high intracellular free zinc promotes neuronal death by inhibiting cellular energy production. A number of targets have been postulated, including complexes of the mitochondrial electron transport chain, c