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首页> 外文期刊>Molecular and Cellular Biology >Human pro-tumor necrosis factor: molecular determinants of membrane translocation, sorting, and maturation.
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Human pro-tumor necrosis factor: molecular determinants of membrane translocation, sorting, and maturation.

机译：人类肿瘤前坏死因子：膜易位，分选和成熟的分子决定因素。

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Human pro-tumor necrosis factor (pro-TNF) is a type II transmembrane protein with a highly conserved 76-residue leader sequence. We have analyzed the behavior, both in a microsomal translocational system and by transfection, of a series of mutants with deletions from the cytoplasmic, transmembrane, and linking domains. Cytoplasmic deletions included the Arg doublet at -49 and -48 and/or the Lys doublet at -58 and -57; additional mutants included deletion of residues -73 to -55 and -73 to -55, -49, and -48. The transmembrane and linking domain mutants included deletions in the -42 to -35 region, combined with the deletion of residues -32 to -1. Two hybrid mutants combined the cytoplasmic deletions with the deletion of residues -32 to -1. All of the cytoplasmic deletion mutants were properly translocated, as were the transmembrane deletion mutants with deletions up to residues -36, -35, -32 to -1, although the last one exhibited reduced efficiency; further incremental deletions, including deletions of residues -38 to -35 and -32 to -1, completely blocked translocation. Both hybrid mutants were effectively translocated; furthermore, transfection analysis revealed competent expression and maturation of both the cytoplasmic and hybrid mutants. Thus, proper expression and maturation of human pro-TNF can be accomplished with as few as approximately 12 of the 26 residues of the native transmembrane domain and with a net negative charge in the cytoplasmic domain flanking the transmembrane region.
机译：人肿瘤坏死因子（pro-TNF）是具有高度保守的76个残基前导序列的II型跨膜蛋白。我们已经分析了在微粒体易位系统中以及通过转染，从细胞质，跨膜和连接域中缺失的一系列突变体的行为。细胞质的缺失包括-49和-48的Arg双峰和/或-58和-57的Lys双峰。其他突变体包括-73至-55和-73至-55，-49和-48残基的缺失。跨膜和连接域突变体包括-42至-35区域的缺失，以及-32至-1的残基的缺失。两个杂种突变体将细胞质缺失与-32至-1残基缺失结合在一起。所有的胞质缺失突变体都被适当地转移，而跨膜缺失突变体的缺失高达-36，-35，-32至-1残基，尽管最后一个具有降低的效率。进一步的增量缺失，包括残基-38至-35和-32至-1的缺失，完全阻断了易位。两种杂种突变体均有效转移。此外，转染分析揭示了细胞质和杂种突变体的有效表达和成熟。因此，人促TNF的正确表达和成熟可以通过天然跨膜结构域的26个残基中的少至约12个以及在跨膜区域侧翼的细胞质结构域中具有净负电荷来实现。

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