Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-7-17
pubmed:abstractText
Nitric oxide (NO) has been reported to regulate NF-kappaB, one of the best-characterized transcription factors playing important roles in many cellular responses to a large variety of stimuli. NO has been suggested to induce or inhibit the activation of NF-kappaB, its effect depending, among others, on the cell type considered. In this review, the inhibitory effect of NO on NF-kappaB (and subsequent suppression of NF-kappaB-dependent gene expression) in glial cells is reported. In particular, exogenous and endogenous NO has been observed to keep NF-kappaB suppressed, thus preventing the expression of NF-kappaB-induced genes, such as inducible NO synthase itself or HIV-1 long terminal repeat. Furthermore, the possible molecular mechanisms of NO-mediated NF-kappaB inhibition are discussed. More specifically, NO has been reported to suppress NF-kappaB activation inducing and stabilizing the NF-kappaB inhibitor, IkappaB-alpha. On the other hand, NO may inhibit NF-kappaB DNA binding through S-nitrosylation of cysteine residue (i. e., Cys62) of the p50 subunit. As a whole, a novel concept that the balance of intracellular NO levels may control the induction of NF-kappaB in glial cells has been hypothesized.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0361-9230
pubmed:author
pubmed:issnType
Print
pubmed:volume
52
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
155-61
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Nitric oxide: an inhibitor of NF-kappaB/Rel system in glial cells.
pubmed:affiliation
Department of Biology, University of Roma Tre, Rome, Italy. colasant@uniroma3.it
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't