Linked Life Data

16181808

Source:http://linkedlifedata.com/resource/pubmed/id/16181808

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-10-31
pubmed:abstractText
A key factor in the control of bone remodelling is parathyroid hormone (PTH), the principal regulator of calcium homeostasis. Elevated levels of PTH increase bone turnover, leading to either anabolic or catabolic effects on the skeleton depending upon the pattern and duration of elevation. New evidence indicating that downregulation of an osteocyte signal (sclerostin, the SOST gene product) occurs in response to intermittent PTH has rekindled interest in the key role played by osteocytes and bone-lining cells in co-ordinating surface anabolic activity. Microarray analysis has also delineated many genes and pathways regulated by intermittent and continuous PTH in osteoblasts and whole bones.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1471-4892
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
612-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Parathyroid hormone - a bone anabolic and catabolic agent.
pubmed:affiliation
Division of Bone Research, Department of Medicine, Level 5, University of Cambridge, Addenbrooke's Hospital (Box 157), Cambridge CB2 2QQ, UK.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't