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磷脂酰丝氨酸在脑组织中从微粒体向线粒体内膜的转运。

Transport of phosphatidylserine from microsomes to the inner mitochondrial membrane in brain tissue.

作者信息

Corazzi L, Pistolesi R, Carlini E, Arienti G

机构信息

Istituto di Biochimica e Chimica Medica, Facoltà di Medicina e Chirurgia, Perugia, Italy.

出版信息

J Neurochem. 1993 Jan;60(1):50-6. doi: 10.1111/j.1471-4159.1993.tb05821.x.

Abstract

Phosphatidylserine was labeled by incubating rat brain homogenates with [3-14C]serine in the presence of Ca2+ (base-exchange conditions). Some labeled phosphatidylethanolamine also forms, in spite of the inhibition of Ca2+ on phosphatidylserine decarboxylase. Phosphatidylserine labeling and decarboxylation also occur on incubating a mixture of purified mitochondria and microsomes, suggesting that no soluble factors are necessary for the synthesis and the decarboxylation of phosphatidylserine. Ca2+ favors the transfer of phosphatidylserine from microsomes (where it forms) to mitochondria (where it is decarboxylated). The specific radioactivity of the phosphatidylserine transferred to mitochondria is higher than that of microsomal phosphatidylserine. This finding supports the hypothesis that the lipid is compartmentalized in microsomes and that radioactive, newly synthesized phosphatidylserine is much better exported than the bulk of microsomal phospholipid.

摘要

通过在Ca2+存在的情况下(碱基交换条件),用[3-14C]丝氨酸孵育大鼠脑匀浆来标记磷脂酰丝氨酸。尽管Ca2+对磷脂酰丝氨酸脱羧酶有抑制作用,但仍会形成一些标记的磷脂酰乙醇胺。在孵育纯化的线粒体和微粒体混合物时,也会发生磷脂酰丝氨酸的标记和脱羧反应,这表明磷脂酰丝氨酸的合成和脱羧反应不需要可溶性因子。Ca2+有利于磷脂酰丝氨酸从微粒体(它在其中形成)转移到线粒体(它在其中脱羧)。转移到线粒体的磷脂酰丝氨酸的比放射性高于微粒体磷脂酰丝氨酸的比放射性。这一发现支持了这样的假设,即脂质在微粒体中被分隔,并且放射性的新合成的磷脂酰丝氨酸比大部分微粒体磷脂更容易输出。

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