GUANYLYL CYCLASE IS A HEAT-STABLE ENTEROTOXIN RECEPTOR
GUANYLYL CYCLASE IS A HEAT-STABLE ENTEROTOXIN RECEPTOR
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DOI：
10.1016/0092-8674(90)90497-3
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发表时间：
1990-11-30
期刊：
影响因子：
64.5
通讯作者：
GARBERS, DL
中科院分区：
文献类型：
--
作者：
SCHULZ, S;GREEN, CK;GARBERS, DL
质膜形式的鸟苷酸环化酶已被证明具有利钠肽受体的功能。我们描述了一个新的克隆（GC-C）编码鸟苷酸环化酶受体的热稳定肠毒素。GC-C编码的蛋白质含有细胞外氨基酸序列不同于以前克隆的鸟苷酸环化酶;然而，该蛋白质保留了细胞内蛋白激酶样和环化酶催化结构域。GC-C在COS-7细胞中的表达导致高鸟苷酸环化酶活性。此外，来自大肠杆菌的热稳定肠毒素，而不是利钠肽，引起环GMP的显著升高，并被GC-C转染的细胞特异性结合。肠毒素不能提高未转染细胞或用利钠肽/鸟苷酸环化酶受体转染的细胞中的环GMP。这些结果表明引起急性腹泻的热稳定肠毒素受体是鸟苷酸环化酶的质膜形式。
Plasma membrane forms of guanylyl cyclase have been shown to function as natriuretic peptide receptors. We describe a new clone (GC-C) encoding a guanylyl cyclase receptor for heat-stable enterotoxin. GC-C encodes a protein containing an extracellular amino acid sequence divergent from that of previously cloned guanylyl cyclases; however, the protein retains the intracellular protein kinase-like and cyclase catalytic domains. Expression of GC-C in COS-7 cells are results in high guanylyl cyclase activity. In addition, heat-stable enterotoxin from Escherichia coli, but not natriuretic peptides, causes marked elevations of cyclic GMP and is specifically bound by cells transfected with GC-C. The enterotoxin fails to elevate cyclic GMP in nontransfected cells or in cells transfected with the natriuretic peptide/guanylyl cyclase receptors. These results show that a heat-stable enterotoxin receptor responsible for acute diarrhea is a plasma membrane form of guanylyl cyclase.