## Abstract The rapid, non‐genomic actions of 1,25‐dihydroxyvitamin D~3~ [1,25(OH)~2~D~3~] have been well described, however, the role of the nuclear vitamin D receptor (VDR) in this pathway remains unclear. To address this question, we used VDR(+/+) and VDR(−/−) osteoblasts isolated from wild‐type
The effects of thyroparathyroidectomy and 1,25 dihydroxyvitamin D3 on changes in the activities of some cytoplasmic and nuclear protein kinases during liver regeneration
✍ Scribed by M. Sikorska; J. F. Whitfield; R. H. Rixon
- Publisher
- John Wiley and Sons
- Year
- 1983
- Tongue
- English
- Weight
- 911 KB
- Volume
- 115
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
Partial hepatectomy (HPX), which proliferatively activates the remaining liver cells, triggered two transient prereplicative surges in the total activities of cytoplasmic types I and II cyclic AMP‐dependent protein kinase holoenzymes, and of nuclear catalytic subunits from cyclic AMP‐dependent protein kinases. It also induced a transient prereplicative increase in the activities of a nuclear Ca^2+^‐calmodulin‐stimulable, protamine‐phosphorylating protein kinase, and a nuclear poly(L‐lysine)‐phosphorylating, 105 kDa protein kinase. Thyroparathyroidectomy (TPTX) delayed and reduced the first surge and completely eliminated the second surge of both of the cytoplasmic cyclic AMP‐dependent protein kinases, reduced the rises in the activity of nuclear catalytic subunits, and completely eliminated the surge of the Ca^2+^‐calmodulin‐stimulable protein kinase, but did not affect the surge of the nuclear 105 kDa protein kinase. The impairment of the responses of the two cyclic AMP‐dependent protein kinases to HPX in TPTX rats was not accompanied by a rise in the level of heat‐stable inhibitor of cyclic AMP‐dependent protein kinase activity. One intraperitoneal injection of 1,25‐dihydroxyvitamin D~3~ into TPTX rats immediately after HPX completely restored the post‐HPX surges in the activity of type I cyclic AMP‐dependent protein kinase, but the hormone, even in high doses, had little or no effect on the type II isoenzyme or the nuclear Ca^2+^‐calmodulin‐stimulable, protamine‐phosphorylating enzyme.
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