Linked Life Data

19576893

Source:http://linkedlifedata.com/resource/pubmed/id/19576893

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2009-7-20
pubmed:abstractText
NFATc1 is a master regulator of RANKL-induced osteoclast differentiation and herein we investigate the regulatory mechanism of NFATc1 in osteoclast activation. Inactivation of NFATc1 strongly attenuates RANKL-induced bone resorption and overexpression of a constitutively active form of NFATc1 in osteoclasts induces formation of actin rings and resorption pits on dentin slices. We demonstrate that NFATc1 binds directly to the promoter regions of its target genes and induces expression of various genes, including LTBP3, ClC7, cathepsin K, MMP9, and c-Src, which are key players in bone resorption. Thus, NFATc1 is essential for RANKL-induced osteoclast activation via up-regulation of osteoclast-activating genes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1873-3468
pubmed:author
pubmed:issnType
Electronic
pubmed:day
21
pubmed:volume
583
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2435-40
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Regulatory mechanism of NFATc1 in RANKL-induced osteoclast activation.
pubmed:affiliation
National Research Laboratory for Regulation of Bone Metabolism and Disease, Medical Research Center for Gene Regulation, Brain Korea 21, Chonnam National University Medical School, 5 Hak-Dong, Dong-Ku, Gwangju 501-746, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't