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炭疽毒素致死因子的1至254位氨基酸残基足以促使融合多肽被细胞摄取。

Residues 1-254 of anthrax toxin lethal factor are sufficient to cause cellular uptake of fused polypeptides.

作者信息

Arora N, Leppla S H

机构信息

Laboratory of Microbial Ecology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.

出版信息

J Biol Chem. 1993 Feb 15;268(5):3334-41.

PMID:8429009
Abstract

Anthrax lethal toxin is a complex of protective antigen (PA, 735 amino acids) and lethal factor (LF, 776 amino acids) that lyses certain eukaryotic cells. LF interacts with PA to gain access to the cytosol to assert its toxicity. The internalization of LF requires that PA bind to a specific membrane receptor and be cleaved by a cell-surface protease (probably furin), so as to expose a site on PA to which LF binds with high affinity. To localize LF functional domains, amino, carboxyl, and internal deletions of LF were made. Toxicity was eliminated by deletion of 40 and 47 residues from the amino and carboxyl termini, respectively. Similarly, deleting the first of the four imperfect repeats of 19 amino acids located at residues 308-383 made LF non-toxic, showing that this region is also essential for activity. To identify the minimum region of LF which is required for binding to PA, varying amino-terminal portions of LF were fused to the ADP-ribosylation domain of Pseudomonas exotoxin A. Fusion proteins containing residues 1-254 of LF were toxic when administered with PA, while those having only residues 1-198 of LF were inactive, showing that the PA-binding domain of LF lies within residues 1-254.

摘要

炭疽致死毒素是一种由保护性抗原(PA,735个氨基酸)和致死因子(LF,776个氨基酸)组成的复合物,可裂解某些真核细胞。LF与PA相互作用以进入细胞质发挥其毒性。LF的内化需要PA与特定的膜受体结合并被细胞表面蛋白酶(可能是弗林蛋白酶)切割,从而暴露出PA上一个LF能高亲和力结合的位点。为了定位LF的功能结构域,对LF进行了氨基端、羧基端和内部缺失。分别从氨基端和羧基端缺失40和47个残基可消除毒性。同样,缺失位于308 - 383位残基的四个19个氨基酸的不完全重复序列中的第一个,会使LF失去毒性,表明该区域对活性也至关重要。为了确定LF与PA结合所需的最小区域,将LF不同的氨基端部分与铜绿假单胞菌外毒素A的ADP - 核糖基化结构域融合。当与PA一起给药时,含有LF第1 - 254位残基的融合蛋白具有毒性,而仅含有LF第1 - 198位残基的融合蛋白无活性,表明LF的PA结合结构域位于第1 - 254位残基内。

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