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甲状旁腺切除术和1,25-二羟维生素D3对肝脏再生过程中某些细胞质和核蛋白激酶活性变化的影响。

The effects of thyroparathyroidectomy and 1,25 dihydroxyvitamin D3 on changes in the activities of some cytoplasmic and nuclear protein kinases during liver regeneration.

作者信息

Sikorska M, Whitefield J F, Rixon R H

出版信息

J Cell Physiol. 1983 Jun;115(3):297-304. doi: 10.1002/jcp.1041150313.

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 Ca2+-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 Ca2+-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 D1 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 not effect on the type II isoenzyme or the nuclear Ca2+-calmodulin-stimulable, protamine-phosphorylating enzyme.

摘要

部分肝切除术(HPX)可增殖性激活剩余的肝细胞,引发细胞质I型和II型环磷酸腺苷依赖性蛋白激酶全酶以及环磷酸腺苷依赖性蛋白激酶的核催化亚基总活性出现两个短暂的复制前激增。它还诱导了一种核钙调蛋白刺激的、鱼精蛋白磷酸化蛋白激酶以及一种核聚(L-赖氨酸)磷酸化的105 kDa蛋白激酶的活性在复制前短暂增加。甲状腺甲状旁腺切除术(TPTX)延迟并降低了第一次激增,并完全消除了两种细胞质环磷酸腺苷依赖性蛋白激酶的第二次激增,降低了核催化亚基活性的升高,并完全消除了钙调蛋白刺激的蛋白激酶的激增,但不影响核105 kDa蛋白激酶的激增。TPTX大鼠中两种环磷酸腺苷依赖性蛋白激酶对HPX反应的损伤并未伴随着环磷酸腺苷依赖性蛋白激酶活性的热稳定抑制剂水平的升高。在HPX后立即向TPTX大鼠腹腔注射一次1,25-二羟基维生素D1可完全恢复I型环磷酸腺苷依赖性蛋白激酶活性的HPX后激增,但该激素即使高剂量对II型同工酶或核钙调蛋白刺激的、鱼精蛋白磷酸化酶几乎没有影响。

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