rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
9
|
pubmed:dateCreated |
2006-8-30
|
pubmed:abstractText |
Increased levels of ePP(i) in mice deficient in TNALP (i.e., Akp2(-/-)) lead to elevated OPN concentrations. We examined the skeletal phenotype of mice lacking both OPN and TNALP and concluded that the increased OPN levels contribute to the hypophosphatasia phenotype characteristic of Akp2(-/-) mice. We also found that extracellular OPN regulates the PP(i) output by osteoblasts.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
0884-0431
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
21
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1377-86
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:16939396-Alkaline Phosphatase,
pubmed-meshheading:16939396-Animals,
pubmed-meshheading:16939396-Bone and Bones,
pubmed-meshheading:16939396-Calcification, Physiologic,
pubmed-meshheading:16939396-Hypophosphatasia,
pubmed-meshheading:16939396-Mice,
pubmed-meshheading:16939396-Mice, Inbred C57BL,
pubmed-meshheading:16939396-Mice, Knockout,
pubmed-meshheading:16939396-Osteopontin,
pubmed-meshheading:16939396-Phenotype,
pubmed-meshheading:16939396-Phosphates,
pubmed-meshheading:16939396-Sialoglycoproteins
|
pubmed:year |
2006
|
pubmed:articleTitle |
Elevated skeletal osteopontin levels contribute to the hypophosphatasia phenotype in Akp2(-/-) mice.
|
pubmed:affiliation |
Burnham Institute for Medical Research, La Jolla, California 92037, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
|