交互的酰coa结合蛋白(ACBP)过程的酰coa衬底,产品或抑制剂。
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拉斯穆森JT, Rosendal J,克努森J
交互的酰coa结合蛋白(ACBP)过程的酰coa衬底,产品或抑制剂。
j . 1993 6月15日,292 (Pt 3): 907 - 13所示。
- PubMed ID
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8318018 (在PubMed]
- 文摘
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结果表明,酰coa结合蛋白(ACBP),在与脂肪酸结合蛋白(FABP),刺激线粒体长链酰coa酯的合成。ACBP有效地反对产品反馈抑制的长链酰coa合成酶合成酰coa酯的封存。反馈抑制微粒体的长链酰coa合成不能观察到,由于小酰coa绑定囊泡的形成在准备和/或孵化。微粒体膜制剂因此不适合研究长链酰coa合成的反馈抑制。ACBP被发现有强烈的衰减影响长链酰coa抑制乙酰辅酶a羧化酶和线粒体腺嘌呤核苷酸移位酶。两个过程未受影响的长链酰coa酯时,长链酰coa ACBP比率低于1,独立的酰基辅酶集中使用。因此不像这样酰基辅酶浓度从监管的角度来看这是很重要的,但ACBP酰coa的比率。的胞质比长链酰coa ACBP证明是远低于1喂养老鼠的肝脏。ACBP可能与triacylglycerol-synthesizing通路竞争,而不是与phospholipid-synthesizing酶酰coa酯。此外,与FABP相比,ACBP能够防止长链酰coa酯水解的微粒体酰coa水解酶。 The results suggest that long-chain acyl-CoA esters synthesized for either triacylglycerol synthesis or beta-oxidation have to pass through the acyl-CoA/ACBP pool before utilization. This means that acyl-CoA synthesized by microsomal or mitochondrial synthetases is uniformly available in the cell. It is suggested that ACBP has a duel function in (1) creating a cytosolic pool of acyl-CoA protected against acyl-CoA hydrolases, and (2) protecting vital cellular processes from being affected by long-chain acyl-CoA esters.