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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1989-2-7
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pubmed:abstractText |
Insulin and insulin-like growth factor I (IGF-I) are structurally related polypeptides that stimulate DNA synthesis and cellular proliferation, probably through a common pathway. Human arterial smooth muscle cells in culture demonstrated the presence of high-affinity receptors for both these hormones. Insulin and IGF-I both exhibited cross-reactivity to each other's receptors but with an affinity that is 100-fold less than for the homologous receptor. To examine more closely the receptor responsible for producing the growth effects, we used the polyclonal antibody against the insulin receptor, B2, and a monoclonal antibody to the IGF-I receptor, alpha IR3. We studied the growth effects of insulin and IGF-I as measured by stimulation of c-myc, DNA synthesis, and cellular proliferation in the presence and absence of these antibodies. F(ab') fragments of the anti-insulin-receptor antibody at a concentration of 10 micrograms/ml were capable of displacing greater than 90% of the bound insulin, thus establishing an effective insulin-receptor blockade. Under such blockade, insulin and IGF-I were both capable of doubling the amount of DNA synthesis and cell number in cultured human arterial smooth muscle cells. However, in the presence of a 1:2500 dilution of the monoclonal antibody alpha IR3, which caused a 90% displacement of IGF-I bound to its receptor, both the insulin and IGF-I effects on stimulating DNA synthesis or cellular proliferation were inhibited by greater than 90%. These findings demonstrate that the IGF-I receptor is the common pathway for the growth effects of both insulin and IGF-I.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Somatomedin,
http://linkedlifedata.com/resource/pubmed/chemical/Somatomedins
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0012-1797
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
123-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:2521209-Cell Division,
pubmed-meshheading:2521209-Cells, Cultured,
pubmed-meshheading:2521209-DNA,
pubmed-meshheading:2521209-Humans,
pubmed-meshheading:2521209-Insulin,
pubmed-meshheading:2521209-Insulin-Like Growth Factor I,
pubmed-meshheading:2521209-Muscle, Smooth, Vascular,
pubmed-meshheading:2521209-Proto-Oncogenes,
pubmed-meshheading:2521209-RNA, Messenger,
pubmed-meshheading:2521209-Receptor, Insulin,
pubmed-meshheading:2521209-Receptors, Somatomedin,
pubmed-meshheading:2521209-Somatomedins
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pubmed:year |
1989
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pubmed:articleTitle |
Characterization of induction of protooncogene c-myc and cellular growth in human vascular smooth muscle cells by insulin and IGF-I.
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pubmed:affiliation |
Research Division, Joslin Diabetes Center, Boston, Massachusetts 02215.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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