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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
1996-4-15
|
| pubmed:abstractText |
Nitric oxide (NO) is a pathophysiological mediator with unique signal transducing properties. Signaling mechanisms are categorized as cGMP-dependent or cGMP-independent. Multiple interactions of NO with oxygen, superoxide, and transition metals determine the biological activity. Cyclic GMP-independent responses of NO account for the antimicrobial, the cytostatic, and the cytotoxic capacity of NO. Cytotoxicity is not only directed to harmful cells but also affects the NO-producing cell in a self-destructing loop. For macrophages and pancreatic beta-cells (RINm5F), we established NO-mediated apoptotic cell death. Endogenously generated or exogenously applied NO causes DNA cleavage after endonuclease activation. NO-mediated accumulation of the tumor suppressor p53 precedes apoptotic cell death.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0378-4274
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
82-83
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
233-7
|
| pubmed:dateRevised |
2005-11-17
|
| pubmed:meshHeading | |
| pubmed:year |
1995
|
| pubmed:articleTitle |
The role of nitric oxide in cell injury.
|
| pubmed:affiliation |
University of Erlangen-Nürnberg, Faculty of Medicine, Department of Medicine, Germany.
|
| pubmed:publicationType |
Journal Article,
Review
|