期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：22
页码：8366-8371
DOI：10.1073/pnas.0308758101
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Because of the use of alternate exons 1, mammals express two distinct forms of Gs{alpha}-subunits: the canonical 394-aa Gs{alpha} present in all tissues and a 700+-aa extra-long {alpha}s (XL{alpha}s) expressed in a more restricted manner. Both subunits transduce receptor signals into stimulation of adenylyl cyclase. The XL exon encodes the XL domain of XL{alpha}s and, in a parallel ORF, a protein called Alex. Alex interacts with the XL domain of XL{alpha}s and inhibits its adenylyl cyclase-stimulating function. In mice, rats, and humans, the XL exon is thought to contribute 422.3, 367.3, and 551.3 codons and to encode Alex proteins of 390, 357, and 561 aa, respectively. We report here that the XL exon is longer than presumed and contributes in mice, rats, and humans, respectively, an additional 364, 430, and 139 codons to XL{alpha}s. We called the N-terminally extended XL{alpha}s extra-extra-long Gs{alpha
