Linked Life Data

9126355

Source:http://linkedlifedata.com/resource/pubmed/id/9126355

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-5-19
pubmed:abstractText
Previous work showed that the availability of insulin to the embryonic chick retina at a critical developmental stage stimulated the activity of the acetylcholine synthetic enzyme, choline acetyltransferase (ChAT) (R. E. Hausman et al., 1991, Dev. Brain Res. 59, 31-37). Here we show that a 2- to 5-min exposure to insulin results in a greater than 24 hr elevation in ChAT protein. Immediately following exposure to insulin there is a transient increase in the level of jun protein followed by an increase in ChAT. The stimulation of ChAT protein is not the result of an overall stimulation of protein synthesis as other proteins are not affected. Exposure of the cells to antisense oligonucleotide to jun, but not to sense oligonucleotide, reduces the increase in both jun and ChAT. These and previous results suggest that insulin is necessary for the characteristic increase in ChAT protein during retina development and that this increase requires the transient synthesis of jun.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
232
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
788-93
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Causal role for jun protein in the stimulation of choline acetyltransferase by insulin in embryonic chick retina.
pubmed:affiliation
Department of Biology, Boston University, Massachusetts 02215, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't