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：2002
卷号：99
期号：1
页码：419-424
DOI：10.1073/pnas.012581799
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：On the basis of ex vivo studies using insulin-responsive cells, activation of a Class IA phosphoinositide 3-kinase (PI3K) seems to be required for a wide variety of cellular responses downstream of insulin. The Class IA PI3K enzymes are heterodimers of catalytic and regulatory subunits. In mammals, insulin-responsive tissues express both the p85 and p85{beta} isoforms of the regulatory subunit. Surprisingly, recent studies have revealed that disruption of the p85 gene in the mouse (p85-/- mice) results in hypoglycemia with decreased plasma insulin, and the p85+/- mice exhibit significantly increased insulin sensitivity. These results suggest either that p85 negatively regulates insulin signaling, or that p85{beta
