Linked Life Data

6989852

Source:http://linkedlifedata.com/resource/pubmed/id/6989852

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1980-7-26
pubmed:abstractText
We have studied insulin binding to cultured skin fibroblasts from a patient with the Type A syndrome of insulin resistance and acanthosis nigricans. Insulin binding was decreased aobut 50% at low insulin concentrations. This was due to a decrease in receptor affinity and in increase in the rate of dissociation of insulin from the receptor. In addition, there was a loss of negative cooperativity, as measured by the ability of unlabeled insulin to accelerate dissociation. This defect in the receptor was stable for up to 16 passages of the cells. By contrast, binding of epidermal growth factor did not differ from control. These data suggest that the Type A syndrome of insulin resistance is due to a primary, and possibly genetic, defect in the insulin receptor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-972X
pubmed:author
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1139-41
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Demonstration of a primary (? genetic) defect in insulin receptors in fibroblasts from a patient with the syndrome of insulin resistance and acanthosis nigricans type A.
pubmed:publicationType
Journal Article