Linked Life Data

19822145

Source:http://linkedlifedata.com/resource/pubmed/id/19822145

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
2009-11-2
pubmed:abstractText
Reactive oxygen species not only serve as signaling molecules, they also contribute to oxidative stress and cell damage. The thioredoxin and glutaredoxin systems form along with peroxiredoxins a precisely regulated defense system to maintain the cellular redox homeostasis. There is evidence that nitric oxide (NO) protects cells from oxidative stress by preventing inactivation of peroxiredoxins by sulfinylation. Here we demonstrate that NO and hypoxia upregulate Sestrin2 by HIF-1-dependent and additional mechanisms and that Sestrin2 contributes to preventing peroxiredoxins from sulfinylation. We conclude that Sestrin2 plays a role in peroxide defense as a reductase for peroxiredoxins.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1873-3468
pubmed:author
pubmed:issnType
Electronic
pubmed:day
3
pubmed:volume
583
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3531-5
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Role of sestrin2 in peroxide signaling in macrophages.
pubmed:affiliation
Goethe-University Frankfurt, Faculty of Medicine, Biochemistry I, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
pubmed:publicationType
Journal Article