Linked Life Data

9655872

Source:http://linkedlifedata.com/resource/pubmed/id/9655872

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-8-3
pubmed:abstractText
The addition of nitric oxide (NO), in the form of either donor compounds or nitric oxide gas, inhibits hormone-stimulated cAMP accumulation in N18TG2 cells. Hormone receptors and Gs are not targets of NO because forskolin-stimulated cAMP accumulation is also inhibited. The inhibitory effect of NO is not altered by pretreatment of cells with pertussis toxin, indicating that Gi is not mediating the effect of NO. cAMP accumulation in these cells is not altered by cell incubation with Ca++ ionophore or calmidazolium, indicating that calmodulin is not the target for NO. Experiments also rule out changes in phosphodiesterase or cGMP as mediators of the effect of NO. Cell incubation with superoxide dismutase in the presence or absence of catalase indicate that nitric oxide is the reactive species. The inhibitory action of nitric oxide is readily reversed, allowing full recovery of hormone and forskolin stimulation within 20 min of incubation in the absence of nitric oxide. The sum of the data indicate that NO targets either the adenylyl cyclase itself, or a regulatory component distinct from G proteins or calmodulin, to inhibit activation of the enzyme.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
286
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
298-304
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Effects of nitric oxide on adenylyl cyclase stimulation in N18TG2 neuroblastoma cells.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, St. Louis University School of Medicine, Missouri, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't