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钙调蛋白参与低渗应激后细胞体积恢复的证据。

Evidence of calmodulin involvement in cell volume recovery following hypo-osmotic stress.

作者信息

Pierce S K, Politis A D, Cronkite D H, Rowland L M, Smith L H

机构信息

Department of Zoology, University of Maryland.

出版信息

Cell Calcium. 1989 Apr;10(3):159-69. doi: 10.1016/0143-4160(89)90070-5.

DOI:10.1016/0143-4160(89)90070-5
PMID:2720760
Abstract

An influx of Ca2+ into red blood cells of the bivalve mollusc Noetia ponderosa occurs immediately following a hypo-osmotic stress. The volume recovery response to the stress is dependent upon [Ca2+]o and is inhibited by phenothiazines. The action of these drugs is on the amino acid regulation portion of the recovery rather than on the ionic portion. Since the phenothiazines are non-specific in action, we have conducted several experiments to decide the site of phenothiazine action on the volume recovery response. The sulfoxide derivatives of both chlorpromazine and trifluoperazine have no effect on volume regulation at the same dose where the parent compound inhibits. At 50-100 times the concentration of the parent compound, the derivatives block both volume regulation and taurine efflux. The phorbol ester, TPA, an activator of protein kinase C, alters the volume recovery, but does so by affecting K+ rather than amino acid regulation. The only phenothiazine target that we can not rule out is calmodulin, which we also demonstrate to be present in the clam red cells. Thus, the data presented suggest that calmodulin is involved in the amino acid regulatory portions of the volume recovery in response to hypo-osmotic swelling.

摘要

在双壳贝类软体动物诺氏重石鳖的红细胞中,低渗应激后会立即出现Ca2+内流。对该应激的体积恢复反应取决于细胞外Ca2+浓度([Ca2+]o),并受到吩噻嗪类药物的抑制。这些药物的作用是在恢复过程中的氨基酸调节部分,而不是离子部分。由于吩噻嗪类药物作用具有非特异性,我们进行了多项实验以确定吩噻嗪类药物对体积恢复反应的作用位点。氯丙嗪和三氟拉嗪的亚砜衍生物在母体化合物产生抑制作用的相同剂量下对体积调节没有影响。在母体化合物浓度的50 - 100倍时,这些衍生物会同时阻断体积调节和牛磺酸外流。佛波酯TPA(一种蛋白激酶C激活剂)会改变体积恢复,但它是通过影响钾离子(K+)而非氨基酸调节来实现的。我们唯一不能排除的吩噻嗪类药物作用靶点是钙调蛋白,我们也证明其存在于蛤类红细胞中。因此,所呈现的数据表明钙调蛋白参与了低渗肿胀后体积恢复过程中的氨基酸调节部分。

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Evidence of calmodulin involvement in cell volume recovery following hypo-osmotic stress.钙调蛋白参与低渗应激后细胞体积恢复的证据。
Cell Calcium. 1989 Apr;10(3):159-69. doi: 10.1016/0143-4160(89)90070-5.
2
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Calmodulin-binding peptide PEP-19 modulates activation of calmodulin kinase II In situ.钙调蛋白结合肽PEP-19在原位调节钙调蛋白激酶II的激活。
J Neurosci. 2000 Apr 15;20(8):2860-6. doi: 10.1523/JNEUROSCI.20-08-02860.2000.
2
Trifluoperazine enhancement of Ca2+-dependent inactivation of L-type Ca2+ currents in Helix aspersa neurons.三氟拉嗪增强蛞蝓神经元中L型钙电流的钙依赖性失活
Invert Neurosci. 1998 Mar;3(4):269-78. doi: 10.1007/BF02577687.
3
The role of swelling-induced anion channels during neuronal volume regulation.肿胀诱导的阴离子通道在神经元容积调节中的作用。
Mol Neurobiol. 1996 Oct;13(2):137-53. doi: 10.1007/BF02740638.
4
Specific protein phosphorylation occurs in molluscan red blood cell ghosts in response to hypoosmotic stress.特定的蛋白质磷酸化反应发生在软体动物红细胞血影中,以应对低渗应激。
J Membr Biol. 1991 Nov;124(2):169-77. doi: 10.1007/BF01870461.