Evidence for a functional cytoplasmic domain of phagocyte oxidase cytochrome b558.
Evidence for a functional cytoplasmic domain of phagocyte oxidase cytochrome b558.
复制标题
吞噬细胞氧化酶细胞色素 b558 功能性胞质结构域的证据。
DOI：
10.1016/s0021-9258(19)38951-3
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
H. Malech
中科院分区：
文献类型：
--
作者：
D. Rotrosen;Michael E. Kleinbergs;Hiroyuki Nunoi;T. Leto;J. Gallin;H. Malech
跨膜蛋白的细胞质结构域在涉及膜和细胞质成分之间相互作用的细胞过程中发挥着关键作用。吞噬细胞呼吸爆发氧化酶（负责产生超氧阴离子 (O2-) 的电子传递链）的激活需要膜成分，包括细胞色素 b558 和几种胞质蛋白；但人们对这些成分的生化相互作用知之甚少。细胞色素 b558 是氧化酶的电子传递成分。细胞色素 b558 在其他氧化酶成分的组织或整合中的作用也已被假设。结合细胞色素 b558 跨膜 91-kDa 亚基的细胞质羧基末端尾部的抗体特异性抑制需要中性粒细胞膜和胞质的两亲激活的无细胞 O2-.-生成系统。 91-kDa 亚基同一区域内包含 7 个氨基酸羧基末端序列 (RGVHFIF) 的合成肽可阻断花生四烯酸对氧化酶的激活，但在花生四烯酸后添加到无细胞 O2-生成系统中时，不会影响组装氧化酶的活性。当相同的肽在用甲酰基-甲硫氨酰-亮氨酰-苯丙氨酸或佛波醇肉豆蔻酸酯乙酸酯刺激之前扩散到电透化的中性粒细胞中时，会抑制呼吸爆发的激活。这些研究定义了细胞色素 b558 跨膜 91-kDa 亚基的功能性细胞质结构域，该结构域可能介导与吞噬细胞呼吸爆发激活所必需的其他细胞蛋白的相互作用。
Cytoplasmic domains of transmembrane proteins play a critical role in cellular processes involving interactions between membrane and cytosolic components. Activation of the phagocytic cell respiratory burst oxidase, the electron transport chain responsible for superoxide anion (O2-.) production, requires membrane components including cytochrome b558 and several cytosolic proteins; but the biochemical interactions of these components are poorly understood. Cytochrome b558 is an electron transport component of the oxidase. A role for cytochrome b558 in the organization or integration of other oxidase components has also been hypothesized. Antibodies binding the cytoplasmic carboxyl-terminal tail of the transmembrane 91-kDa subunit of cytochrome b558 specifically inhibited an amphiphile-activated cell-free O2-.-generating system that requires neutrophil membranes and cytosol. Synthetic peptides encompassing a 7-amino acid carboxyl-terminal sequence (RGVHFIF) within the same region of the 91-kDa subunit blocked activation of the oxidase by arachidonate, but did not affect activity of the assembled oxidase when added after arachidonate to the cell-free O2-.-generating system. The same peptides inhibited activation of the respiratory burst when allowed to diffuse into electrically permeabilized neutrophils before stimulation with formyl-methionyl-leucyl-phenylalanine or phorbol myristate acetate. These studies define a functional cytoplasmic domain of the transmembrane 91-kDa subunit of cytochrome b558 which may mediate interactions with other cellular proteins essential to activation of the phagocyte respiratory burst.