修改的(apo)形式的大肠杆菌酰基载体蛋白是一种细胞生长的有效抑制剂。
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凯里先生,基廷DH Cronan我小
修改的(apo)形式的大肠杆菌酰基载体蛋白是一种细胞生长的有效抑制剂。
生物化学杂志。1995年9月22日;270 (38):22229 - 35。
- PubMed ID
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7673201 (在PubMed]
- 文摘
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酰基载体蛋白(ACP)是脂肪酸的载体在合成和利用率。运河管理局(或ACP-like蛋白质域)被发现在生物学和分享重要的氨基酸序列相似性。所有机场核心计划进行一个翻译修饰4“-phosphopantetheine从检验或转移到一个特定的apo-ACP丝氨酸。这个修改是必不可少的活动,因为脂肪酸绑定在辅基的巯基硫酯键。生产过剩multicopy质粒的大肠杆菌ACP强烈抑制大肠杆菌的生长。我们报告,超表达大肠杆菌翻译修饰ACP的低效和朊蛋白的积累和阻止细胞生长抑制脂质代谢。此外,ACP的突变形式的,无法进行翻译修饰是一个增长的有效抑制剂。最后,我们发现,增加修改过表达ACP导致效率降低毒性。累积apo-ACP作为有效的体外的抑制剂sn-glycerol-3-phosphate酰基转移酶导致无法完成的脂肪酸转移到sn-glycerol 3 -磷酸。抑制的程度取决于供体酰基链的物种。 Utilization of cis-vaccenoyl-ACP by the sn-glycerol-3-phosphate acyltransferase was inhibited to a much greater extent by apo-ACP than was utilization of palmitoyl-ACP. 1-Acyl glycerol-3-phosphate acyltransferase was also inhibited in vitro by apo-ACP, although not at physiologically relevant concentrations. These in vitro data are supported by in vivo labeling data, which showed a large decrease in cis-vaccenate incorporation into phospholipid during overproduction of ACP, but no decrease in the rate of synthesis of long chain acyl-ACPs. These data indicate that acylation of sn-glycerol 3-phosphate is the major site of inhibition by apo-ACP.