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Shaodong Guo

Researcher at Texas A&M University

Publications -  83
Citations -  6944

Shaodong Guo is an academic researcher from Texas A&M University. The author has contributed to research in topics: FOXO1 & Insulin resistance. The author has an hindex of 34, co-authored 68 publications receiving 6012 citations. Previous affiliations of Shaodong Guo include Texas A&M Health Science Center & University of Illinois at Chicago.

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Phosphorylation of the transcription factor forkhead family member FKHR by protein kinase B

TL;DR: FKHR, a human homologue of the DAF16 transcription factor in Caenorhabditis elegans, is rapidly phosphorylated by human protein kinase Bα (PKBα) at Thr-24, Ser-256, and Ser-319 in vitro and at a much faster rate than BAD, which is thought to be a physiological substrate for PKB.
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Phosphorylation of serine 256 by protein kinase B disrupts transactivation by FKHR and mediates effects of insulin on insulin-like growth factor-binding protein-1 promoter activity through a conserved insulin response sequence.

TL;DR: These results provide the first report that FK HR stimulates promoter activity through an IRS and that phosphorylation of FKHR by PKB mediates effects of insulin on gene expression, and may provide an evolutionarily conserved mechanism by which insulin and related factors regulate gene expression.
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Inactivation of Hepatic Foxo1 by Insulin Signaling Is Required for Adaptive Nutrient Homeostasis and Endocrine Growth Regulation

TL;DR: It is demonstrated that constitutively active Foxo1 significantly contributes to hyperglycemia during severe hepatic insulin resistance, and that the Irs1/2 --> PI3K --> Akt --> Foxo 1 branch of insulin signaling is largely responsible for hepatic diabetes-regulated glucose homeostasis and somatic growth.

Insulin Signaling, Resistance, and the Metabolic Syndrome: Insights

Shaodong Guo
TL;DR: In this article, the authors discuss the basis of insulin signaling, insulin resistance in different mouse models, and how a deficiency of insulin signalling components in different organs contributes to the features of the metabolic syndrome.