Proteomics

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Overexpression of catalase delays age-related cardiac disease by preventing oxidative cysteine modifications


ABSTRACT: Reactive protein cysteine thiolates are instrumental in redox regulation. Aging associated to oxidative stress, can impair redox signaling by damaging essential cysteine thiolates. Our initial study found that cardiac-specific overexpression of catalase, can protect from oxidative stress and delay cardiac aging in mice. The Project aimed to investigate differential reversible cysteine thiol oxidation in cardiac proteome of wild type and Cat transgenic (Tg) mice, using “Tandem Mass Tag” (TMT) labeling strategy and mass spectrometry. Our results show globally decreased cysteine thiol occupancy in cardiac proteins in Cat Tg mice. The majority of proteins with differentially modified thiols may be involved in pathways of aging and cardiac disease including cellular stress response, proteostasis and apoptosis. Overexpressed catalase may modulate these protein cysteine thiol oxidations resulting in delayed cardiac aging and related pathologies.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Markus Bachschmid  

LAB HEAD: Richard A. Cohen

PROVIDER: PXD002479 | Pride | 2018-10-24

REPOSITORIES: Pride

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Reactive protein cysteine thiolates are instrumental in redox regulation. Oxidants, such as hydrogen peroxide (H2O2), react with thiolates to form oxidative post-translational modifications, enabling physiological redox signaling. Cardiac disease and aging are associated with oxidative stress which can impair redox signaling by altering essential cysteine thiolates. We previously found that cardiac-specific overexpression of catalase (Cat), an enzyme that detoxifies excess H2O2, protected from o  ...[more]

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