Resting zone chondrocyte differentiation is modulated by the vitamin D metabolite, 24,25-(OH) 2 D 3 , via activation of protein kinase C (PKC). In previous studies, inhibition of prostaglandin production with indomethacin caused an increase in PKC activity, suggesting that changes in prostaglandin l
Characterization of PGE2 receptors (EP) and their role as mediators of 1α,25-(OH)2D3 effects on growth zone chondrocytes
✍ Scribed by V.L Sylvia; F Del Toro Jr.; R.R Hardin; D.D Dean; B.D Boyan; Z Schwartz
- Book ID
- 117668209
- Publisher
- Elsevier Science
- Year
- 2001
- Tongue
- English
- Weight
- 495 KB
- Volume
- 78
- Category
- Article
- ISSN
- 0960-0760
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1a,25-(OH) 2 D 3 mediates its effects on growth zone chondrocytes via rapid membrane-associated events as well as through traditional nuclear receptor mechanisms. The membrane-associated signaling pathways include rapid production of diacylglycerol and activation of protein kinase C (PKC), as well a
Prior studies have shown that 24,25-(OH) 2 D 3 and 1,25-(OH) 2 D 3 regulate protein kinase C (PKC) in costochondral chondrocytes in a cell maturation-dependent manner, with 1,25-(OH) 2 D 3 affecting primarily growth zone (GC) cells and 24,25-(OH) 2 D 3 affecting primarily resting zone (RC) cells. In