J
Jordi Tamarit
Researcher at University of Lleida
Publications - 54
Citations - 4609
Jordi Tamarit is an academic researcher from University of Lleida. The author has contributed to research in topics: Frataxin & Oxidative stress. The author has an hindex of 31, co-authored 51 publications receiving 4265 citations. Previous affiliations of Jordi Tamarit include French Alternative Energies and Atomic Energy Commission.
Papers
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Oxidative stress in bacteria and protein damage by reactive oxygen species.
TL;DR: This paper reviews major key points in the generation of reactive oxygen species in bacteria, defense mechanisms and genetic responses to oxidative stress, with special attention to oxidative damage to proteins.
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Grx5 Is a Mitochondrial Glutaredoxin Required for the Activity of Iron/Sulfur Enzymes
TL;DR: Reduction of iron levels in grx5 null mutants does not restore the activity of iron/sulfur enzymes, and cell growth defects are not suppressed in anaerobiosis or in the presence of disulfide reductants.
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Identification of the major oxidatively damaged proteins in Escherichia coli cells exposed to oxidative stress.
TL;DR: Data is provided about the in vivo effects of oxidative stress on protein oxidation and insights are given into understanding how such modifications can affect cellular functions.
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Proteomic and oxidative stress analysis in human brain samples of Huntington disease.
Ma Alba Sorolla,Gemma Reverter-Branchat,Jordi Tamarit,Isidre Ferrer,Joaquim Ros,Elisa Cabiscol +5 more
TL;DR: In this paper, a proteomic analysis of human brain postmortem samples obtained from striatum and cortex of patients with Huntington disease compared to samples of age and sex-matched controls was performed.
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Oxidative damage to specific proteins in replicative and chronological-aged Saccharomyces cerevisiae: common targets and prevention by calorie restriction.
TL;DR: It is shown that replicative and chronological-aged yeast cells are affected by an oxidative stress situation demonstrated by increased protein carbonylation when compared with young cells, which may explain lengthening of the viability of chronological-aging cells and could have an important role in replicative life span extension by calorie restriction.