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将1,2-(环)-4,5-三磷酸肌醇、1,3,4,5-四磷酸肌醇和1,4,5-三磷酸肌醇显微注射到完整的非洲爪蟾卵母细胞中,可诱导独立于细胞外钙的膜电流。

Microinjection of inositol 1,2-(cyclic)-4,5-trisphosphate, inositol 1,3,4,5-tetrakisphosphate, and inositol 1,4,5-trisphosphate into intact Xenopus oocytes can induce membrane currents independent of extracellular calcium.

作者信息

Stith B J, Proctor W R

机构信息

Biology Department, University of Colorado, Denver 80204.

出版信息

J Cell Biochem. 1989 Jul;40(3):321-30. doi: 10.1002/jcb.240400308.

Abstract

Inositol phosphate action in an intact cell has been investigated by intracellular microinjection of eight inositol phosphate derivatives into Xenopus laevis oocytes. These cells have calcium-regulated chloride channels but do not have a calcium-induced calcium release system. Microinjection of inositol 1,3,4,5-tetrakisphosphate (IP4), inositol 1,2-(cyclic)-4,5-trisphosphate (cIP3), inositol 1,4,5-trisphosphate (IP3), or inositol 4,5-bisphosphate [(4,5)IP2], open chloride channels to induce a membrane depolarization. However, inositol 1-phosphate (IP1), inositol 1,3,4,5,6-pentakisphosphate (IP5), inositol 1,4-bisphosphate, or inositol 3,4-bisphosphate are unable to induce this depolarization. The depolarization is mimicked by calcium microinjection, inhibited by EGTA coinjection, and is insensitive to removal of extracellular calcium. By means of the depolarization response, the efficacy of various inositol phosphate derivatives are compared. IP3 and cIP3 induce similar half-maximal, biphasic depolarization responses at an intracellular concentration of approximately 90 nM, whereas IP4 induces a mono- or biphasic depolarization at approximately 3400 nM. At concentrations similar to that required for IP3 and cIP3, (4,5)IP2 induces a long-term (greater than 40 min) depolarization. The efficacy (cIP3 = IP3 = (4,5)IP2 much greater than IP4) and action of the various inositol phosphates in an intact cell and their inability to induce meiotic cell division are discussed.

摘要

通过向非洲爪蟾卵母细胞内显微注射八种肌醇磷酸衍生物,研究了完整细胞中肌醇磷酸的作用。这些细胞具有钙调节氯离子通道,但没有钙诱导的钙释放系统。显微注射1,3,4,5-四磷酸肌醇(IP4)、1,2-环-4,5-三磷酸肌醇(cIP3)、1,4,5-三磷酸肌醇(IP3)或4,5-二磷酸肌醇[(4,5)IP2]可打开氯离子通道,诱导膜去极化。然而,1-磷酸肌醇(IP1)、1,3,4,5,6-五磷酸肌醇(IP5)、1,4-二磷酸肌醇或3,4-二磷酸肌醇无法诱导这种去极化。钙显微注射可模拟这种去极化,EGTA共注射可抑制这种去极化,且这种去极化对去除细胞外钙不敏感。通过去极化反应,比较了各种肌醇磷酸衍生物的效力。IP3和cIP3在细胞内浓度约为90 nM时诱导相似的半最大双相去极化反应,而IP4在约3400 nM时诱导单相或双相去极化。在与IP3和cIP3所需浓度相似的情况下,(4,5)IP2诱导长期(大于40分钟)去极化。讨论了各种肌醇磷酸在完整细胞中的效力(cIP3 = IP3 = (4,5)IP2远大于IP4)、作用及其诱导减数分裂细胞分裂的能力。

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