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膜容量测量结果表明,钙依赖性地将突触结合蛋白插入磷脂酰丝氨酸双层膜中。

Membrane capacity measurements suggest a calcium-dependent insertion of synexin into phosphatidylserine bilayers.

作者信息

Rojas E, Pollard H B

出版信息

FEBS Lett. 1987 Jun 8;217(1):25-31. doi: 10.1016/0014-5793(87)81235-8.

Abstract

The mechanism by which synexin mediates calcium-dependent aggregation of medullary cell chromaffin granules and fusion of granule ghosts involves specific interactions with the lipid component of the membrane. To study the details of these interactions we measured synexin-induced changes in capacitance of phosphatidylserine bilayers formed at the tip of a patch pipet using the double-dip method. Provided calcium was present in the solution filling the pipet (10-50 mM) stable phosphatidylserine bilayers were easily formed. Addition of synexin (0.1 microgram/ml) to an external medium lacking added calcium induced no measurable changes in either bilayer resistance (10-30 G omega) or displacement current across the membrane. However, addition of calcium (0.1-2.5 mM) in the presence of synexin in the external solution caused a marked increase in the size and time constant of decay of the displacement current. From the steady-state value of the current we calculated a 5-fold decrease in resistance and from the charge displaced during the voltage-clamp pulses we calculated a 10-fold increase in membrane capacitance (from 20 to 200 fF). The size of the synexin-specific charge displacement in one direction during a pulse was always equal to the charge returning to the original configuration after the pulse. The synexin-specific transfer of charge reached saturation when the pipet potential was taken to a sufficient positive or negative value. These properties of the extra charge movement support our view that in the presence of calcium the cytosolic protein synexin penetrates into the bilayer. It is possible that these properties may be related to the mechanism by which synexin promotes membrane fusion in natural membranes.

摘要

联会蛋白介导髓质细胞嗜铬粒蛋白颗粒钙依赖性聚集以及颗粒空壳融合的机制涉及与膜脂质成分的特异性相互作用。为了研究这些相互作用的细节,我们使用双浸法测量了联会蛋白诱导的在膜片吸管尖端形成的磷脂酰丝氨酸双层电容的变化。如果在填充吸管的溶液中存在钙(10 - 50 mM),则很容易形成稳定的磷脂酰丝氨酸双层。向缺乏额外添加钙的外部介质中添加联会蛋白(0.1微克/毫升),不会引起双层电阻(10 - 30 GΩ)或跨膜位移电流的可测量变化。然而,在外部溶液中存在联会蛋白的情况下添加钙(0.1 - 2.5 mM),会导致位移电流的大小和衰减时间常数显著增加。根据电流的稳态值,我们计算出电阻降低了5倍,根据电压钳制脉冲期间位移的电荷量,我们计算出膜电容增加了10倍(从20 fF增加到200 fF)。脉冲期间一个方向上联会蛋白特异性电荷位移的大小总是等于脉冲后回到原始构型的电荷量。当吸管电位达到足够的正值或负值时,联会蛋白特异性的电荷转移达到饱和。额外电荷移动的这些特性支持了我们的观点,即在有钙存在的情况下,胞质蛋白联会蛋白会穿透双层。这些特性可能与联会蛋白在天然膜中促进膜融合的机制有关。

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