Abstract:
:One G protein-coupled receptor (GPCR) can activate more than one G protein, but the physiologic importance of such activation has not been demonstrated in vivo. We have generated mice expressing exclusively a mutant form of the PTH/PTHrP receptor (DSEL) that activates adenylyl cyclase normally but not phospholipase C (PLC). DSEL mutant mice exhibit abnormalities in embryonic endochondral bone development, including delayed ossification and increased chondrocyte proliferation. Analysis of the differentiation of embryonic metatarsals in vitro shows that PTH(1-34) and forskolin inhibit, whereas active phorbol ester stimulates, hypertrophic differentiation. Thus, PLC signaling via the PTH/PTHrP receptor normally slows the proliferation and hastens the differentiation of chondrocytes, actions that oppose the dominant effects of PTH/PTHrP receptors and that involve cAMP-dependent signaling pathways.
journal_name
Dev Celljournal_title
Developmental cellauthors
Guo J,Chung UI,Kondo H,Bringhurst FR,Kronenberg HMdoi
10.1016/s1534-5807(02)00218-6keywords:
subject
Has Abstractpub_date
2002-08-01 00:00:00pages
183-94issue
2eissn
1534-5807issn
1878-1551pii
S1534-5807(02)00218-6journal_volume
3pub_type
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