Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-1-5
pubmed:abstractText
During long bone development, round proliferative chondrocytes (RPCs) differentiate into flat proliferative chondrocytes (FPCs), and then into hypertrophic chondrocytes (HCs). FPCs and HCs support longitudinal bone growth. Here we show that a putative protein kinase gene, Pkdcc (AW548124), is required for longitudinal bone growth. We originally found Pkdcc expressed in the head organizer, but it is also expressed throughout embryogenesis and in various adult tissues. Pkdcc-/- embryos had no head organizer-related defects, but showed various morphological abnormalities at birth, including short limbs, cleft palate, sternal dysraphia, and shortened intestine. In the long bones of the limbs, only the mineralized regions were shortened, and the cartilage length was normal. In the humerus, Pkdcc was strongly expressed in the early FPCs, and FPC and HC formation was delayed in Pkdcc-/- mutants. Together, these data indicate that Pkdcc encodes a protein kinase that is required for the appropriate timing of FPC differentiation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1058-8388
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2008 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
238
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
210-22
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Short limbs, cleft palate, and delayed formation of flat proliferative chondrocytes in mice with targeted disruption of a putative protein kinase gene, Pkdcc (AW548124).
pubmed:affiliation
Laboratory for Embryonic Induction, RIKEN Center for Developmental Biology, Hyogo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't