Linked Life Data

2877866

Source:http://linkedlifedata.com/resource/pubmed/id/2877866

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1987-1-20
pubmed:abstractText
We have used H-35 rat hepatoma cells to test whether the type II insulin-like growth factor (IGF) receptor mediates metabolic responses to IGF-II. On the basis of both affinity cross-linking experiments and competition binding experiments, H-35 cells display insulin and type II IGF receptors, but not type I IGF receptors. IGF-II and multiplication-stimulating activity (MSA; the rat homolog of IGF-II) stimulate tyrosine aminotransferase, amino acid transport, and glycogen synthase activities to the same magnitude as insulin. However, MSA and IGF-II stimulate these metabolic responses only at high concentrations, indicating that these peptides are acting through the insulin receptor. Incubation of H-35 cells with MSA also induces a state of unresponsiveness to the further actions of both MSA and insulin. There is no associated loss of either insulin or IGF-II binding, indicating that desensitization occurs at a postbinding step in hormone action. The high concentration of MSA necessary to induce desensitization is also consistent with MSA acting through the insulin receptor. We conclude that in H-35 cells, the insulin receptor, rather than the type II IGF receptor, mediates the metabolic responses stimulated by MSA and IGF-II as well as the MSA-induced desensitization to insulin and MSA action.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
120
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
401-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Mediation of insulin-like growth factor actions by the insulin receptor in H-35 rat hepatoma cells.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.