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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2004-2-18
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pubmed:abstractText |
Morphological analyses in and around the epiphyseal cartilage of mice deficient in insulin receptor substrate-1 (IRS-1) showed IRS-1 signaling to be important for skeletal growth by preventing early closure of the epiphyseal cartilage and maintaining the subsequent bone turnover at the primary spongiosa. Introduction: IRS-1 is an essential molecule for intracellular signaling by IGF-I and insulin, both of which are potent anabolic regulators of cartilage and bone metabolism. To clarify the role of IRS-1 signaling in the skeletal growth, morphological analyses were performed in and around the epiphyseal cartilage of mice deficient in IRS-1 (IRS-1(-/-)), whose limbs and trunk were 20-30% shorter than wildtype (WT) mice.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0884-0431
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
19
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
214-23
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:14969391-Animals,
pubmed-meshheading:14969391-Bone Development,
pubmed-meshheading:14969391-Cartilage,
pubmed-meshheading:14969391-DNA Primers,
pubmed-meshheading:14969391-Epiphyses,
pubmed-meshheading:14969391-Immunohistochemistry,
pubmed-meshheading:14969391-Insulin Receptor Substrate Proteins,
pubmed-meshheading:14969391-Male,
pubmed-meshheading:14969391-Mice,
pubmed-meshheading:14969391-Mice, Inbred C57BL,
pubmed-meshheading:14969391-Mice, Inbred CBA,
pubmed-meshheading:14969391-Mice, Knockout,
pubmed-meshheading:14969391-Phosphoproteins,
pubmed-meshheading:14969391-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:14969391-Signal Transduction
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pubmed:year |
2004
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pubmed:articleTitle |
Deficiency of insulin receptor substrate-1 impairs skeletal growth through early closure of epiphyseal cartilage.
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pubmed:affiliation |
Department of MENICON Cartilage and Bone Regeneration, Faculty of Medicine, University of Tokyo, Bunkyo, Tokyo, Japan. pochi-tky@umin.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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