Effects of CoA and acyl-CoAs on GTP-dependent Ca2+ release and vesicle fusion in rat liver microsomal vesicles.
Effects of CoA and acyl-CoAs on GTP-dependent Ca2+ release and vesicle fusion in rat liver microsomal vesicles.
复制标题
CoA 和酰基 CoAs 对大鼠肝微粒体囊泡中 GTP 依赖性 Ca2 释放和囊泡融合的影响。
DOI：
10.1042/bj2890561
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
A. Dawson
中科院分区：
文献类型：
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作者：
J. G. Comerford;A. Dawson
(1)辅酶A(IC_(50)23微米)和酰基-辅酶A(IC_(50)值15~18微米)抑制大鼠肝微囊泡GTP依赖的囊泡融合。碳链长度为C8和C20的酰基-COA的作用远不如碳链长度为C14-C18的酰基-COA有效。脱磷辅酶A的效果与脱磷辅酶A相似，而脱磷辅酶A不能模拟脱磷辅酶A的作用。较高的酰基辅酶A浓度(50微米)似乎有利于形成小囊泡(发芽)，而50微米辅酶A则不利于形成。(2)低浓度的辅酶A(EC50 2微米)和棕榈酰辅酶A(10微米)可引起GTP反应释放的钙离子重新聚集。这种再积累进入对INS(1，4，5)P3敏感的隔室。通过研究辅酶A和棕榈酰辅酶A对thapsigarin诱导的钙被动漏出速率和囊泡甘露糖-6-磷酸酶潜伏期的影响，我们得出结论：辅酶A和棕榈酰辅酶A导致囊泡通透性降低，而不是刺激钙泵活性。(3)GTP诱导的大鼠肝微粒体膜融合涉及一种尚未确定的酰化-脱酰化反应，这是产生完全囊泡封闭所必需的。
(1) CoA (IC50 23 microM) and acyl-CoAs (IC50 values 15-18 microM) inhibit GTP-dependent vesicle fusion in rat liver microsomal vesicles. Acyl-CoAs of carbon chain length C8 and C20 are much less effective than acyl-CoAs of carbon chain length C14-C18. The effect of CoA is mimicked by dephospho-CoA, but not by desulpho-CoA. High acyl-CoA concentrations (50 microM) appear to favour formation of small vesicles (budding), while 50 microM CoA does not. (2) Low concentrations of CoA (EC50 2 microM) and palmitoyl-CoA (10 microM) cause re-accumulation of Ca2+ released in response to GTP. This re-accumulation is into an Ins(1,4,5)P3-sensitive compartment. By investigation of the effects of CoA and palmitoyl-CoA on the thapsigargin-induced passive leak rate of Ca2+, and on the latency of the mannose-6-phosphatase of the vesicles, we conclude that CoA and palmitoyl-CoA cause decreased vesicle permeability rather than stimulation of Ca2+ pumping activity. (3) It is suggested that GTP-induced membrane fusion in rat liver microsomes involves an as yet uncharacterized acylation-deacylation reaction which is required to produce complete vesicle sealing.