Linked Life Data

11057021

Source:http://linkedlifedata.com/resource/pubmed/id/11057021

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-12-8
pubmed:abstractText
Fibroblast growth factor 2 (FGF2) inhibits proliferation and hypertrophy of chondrocytes in the growth plate, synthesis of cartilage matrix, terminal differentiation of hypertrophic chondrocytes and matrix calcification. Recent studies have found that mutations in the receptor for fibroblast growth factor 3 (FGFR3) cause achondroplasia, hypochondroplasia and thanatophoric dysplasia. These mutations evoke uncontrolled stimulation of the receptor, leading to inhibition of bone growth. Inactivation of the receptor in experimental animals causes excessive chondrocyte proliferation and abnormal bone length. Chondrocyte stem cells proliferate in the ossification groove of Ranvier and contribute to both peripheral and longitudinal growth of the growth plate. They express FGFR3, have a potential to differentiate into chondrocytes and are therefore considered adequate for healing cartilage defects in the articular surface. It is at present unknown what happens to the chondrocyte precursor cells in the ossification groove of patients with FGFR3 mutation.
pubmed:language
pol
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0009-479X
pubmed:author
pubmed:issnType
Print
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
327-33
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
[Molecular basis of achondroplasia, hypochondroplasia, and thanatophoric dysplasia].
pubmed:affiliation
Zak?ad Histologii i Embriologii, Centrum Biostruktury Akademii Medycznej w Warszawie.
pubmed:publicationType
Journal Article, English Abstract, Review, Research Support, Non-U.S. Gov't