Linked Life Data

9220462

Source:http://linkedlifedata.com/resource/pubmed/id/9220462

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-9-2
pubmed:abstractText
When rat cultured neurons were incubated with unlabelled neurotensin (3 nM) for 1 or 24 h at 37 degrees C, the [3H]-neurotensin specific binding measured in cell homogenates was decreased to about 35 and 65% of control values, respectively. In these experiments, the decreases in binding corresponded to reductions of Bmax values without changes in the affinity. The slow neurotensin-induced receptor down-regulation is thought to result from receptor degradation since it was reduced by the lysosomotropic drugs chloroquine and methylamine and because no change in neurotensin mRNA level could be measured after the neurotensin stimulation. After their internalization, receptors slowly reappeared at the cell surface after further incubation in the absence of the peptide. Such receptor reappearance was prevented in the presence of the protein synthesis inhibitor cycloheximide and is therefore thought to result from new synthesis and not from recycling of internalized receptors. These results indicate that the neurotensin-induced receptor internalization in cultured neurons is irreversible and that it is followed by a down-regulation of the receptor through a degradative process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0197-0186
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
291-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Down-regulation of neurotensin receptors after ligand-induced internalization in rat primary cultured neurons.
pubmed:affiliation
Laboratory of Pharmacology, Catholic University of Louvain, Brussels, Belgium. hermans@nchm.ucl.ac.be
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't