Linked Life Data

20440000

Source:http://linkedlifedata.com/resource/pubmed/id/20440000

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-5-4
pubmed:abstractText
During skeletal development and regeneration, bone-forming osteoblasts respond to high metabolic demand by active expansion of their rough endoplasmic reticulum (rER) and increased synthesis of type I collagen, the predominant bone matrix protein. However, the molecular mechanisms that orchestrate this response are not well understood. We show that insertional mutagenesis of the previously uncharacterized osteopotentia (Opt) gene disrupts osteoblast function and causes catastrophic defects in postnatal skeletal development. Opt encodes a widely expressed rER-localized integral membrane protein containing a conserved SUN (Sad1/Unc-84 homology) domain. Mice lacking Opt develop acute onset skeletal defects that include impaired bone formation and spontaneous fractures. These defects result in part from a cell-autonomous failure of osteoblast maturation and a posttranscriptional decline in type I collagen synthesis, which is concordant with minimal rER expansion. By identifying Opt as a crucial regulator of bone formation in the mouse, our results uncover a novel rER-mediated control point in osteoblast function and implicate human Opt as a candidate gene for brittle bone disorders.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1540-8140
pubmed:author
pubmed:issnType
Electronic
pubmed:day
3
pubmed:volume
189
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
511-25
pubmed:dateRevised
2010-11-4
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Osteopotentia regulates osteoblast maturation, bone formation, and skeletal integrity in mice.
pubmed:affiliation
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA. sohaskey@berkeley.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural