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A Novel Dual Eigen-Analysis of Mouse Multi-Tissues' Expression Profiles Unveils New Perspectives into Type 2 Diabetes.The effect Akt2 deletion on tumor development in Pten(+/-) mice.Spontaneous Hepatocellular Carcinoma after the Combined Deletion of Akt Isoforms.Use of the metallothionein promoter-human growth hormone-releasing hormone (GHRH) mouse to identify regulatory pathways that suppress pituitary somatotrope hyperplasia and adenoma formation due to GHRH-receptor hyperactivation.Akt deficiency impairs normal cell proliferation and suppresses oncogenesis in a p53-independent and mTORC1-dependent manner.Akt1 promotes stimuli-induced endothelial-barrier protection through FoxO-mediated tight-junction protein turnover.Akt-dependent Skp2 mRNA translation is required for exiting contact inhibition, oncogenesis, and adipogenesis.Leptin deficiency and beta-cell dysfunction underlie type 2 diabetes in compound Akt knockout mice.Homologous and heterologous in vitro regulation of pig pituitary somatostatin receptor subtypes, sst1, sst2 and sst5 mRNA.Thyrotrophin-dependent desensitization by Chinese hamster ovary cells that express the recombinant human thyrotrophin receptorA phosphoinositide 3-kinase-AKT-nitric oxide-cGMP signaling pathway in stimulating platelet secretion and aggregationAdiponectin is expressed in the pancreas of high-fat-diet-fed mice and protects pancreatic endothelial function during the development of type 2 diabetes
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description
researcher ORCID ID = 0000-0002-9214-0136
@en
wetenschapper
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name
Xiao-ding Peng
@ast
Xiao-ding Peng
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Xiao-ding Peng
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Xiao-ding Peng
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type
label
Xiao-ding Peng
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Xiao-ding Peng
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Xiao-ding Peng
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Xiao-ding Peng
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Xiao-ding Peng
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Xiao-ding Peng
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Xiao-ding Peng
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Xiao-ding Peng
@nl
P106
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22954205500
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0000-0002-9214-0136