New perspectives into the molecular pathogenesis and treatment of type 2 diabetes.
By Alan R. Saltiel. Cell, 2001
730 citations recorded by the source corpus.
Subfields: Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/fb5dc2f9e713c408007d9a01424bb70230219753
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Citations in the corpus
- Regulation of insulin action and pancreatic β-cell function by mutated alleles of the gene encoding forkhead transcription factor Foxo1 (2002, background): “An autoimmune process destroys β-cells in type 1 diabetes, whereas a combination of genetic and environmental factors brings about β-cell failure in type 2 diabete”
- The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins (2004, background): “The signal transduction mechanisms operating downstream of insulin receptor ligation have highlighted the importance both of the receptor tyrosine kinase substrates (insulin receptor substrates, IRS-1 and IRS-2) and the lipid kinase phosphoinositide 3-OH kinase (PI3K; Saltiel, 2001; Saltiel and Kahn”
- The forkhead transcription factor Foxo1 (Fkhr) confers insulin sensitivity onto glucose-6-phosphatase expression. (2001, background): “Differential expression and acid-base regulation of glutaminase mRNAs in gluconeogenic LLC-PK(1)-FBPase(+) cells.”
- FGF-21 as a novel metabolic regulator. (2005, background): “New treatments are required that will allow an efficacious regulation of glycemia and reduce the risk of the side effects associated with current therapies (27, 37, 38).”