D
Denise R. Cooper
Researcher at University of South Florida
Publications - 111
Citations - 6370
Denise R. Cooper is an academic researcher from University of South Florida. The author has contributed to research in topics: Protein kinase C & Insulin. The author has an hindex of 39, co-authored 110 publications receiving 6076 citations. Previous affiliations of Denise R. Cooper include Veterans Health Administration & United States Department of Veterans Affairs.
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Journal ArticleDOI
Comparison of Markers and Functional Attributes of Human Adipose-Derived Stem Cells and Dedifferentiated Adipocyte Cells from Subcutaneous Fat of an Obese Diabetic Donor.
James E. Watson,Niketa A. Patel,Andrea N. Moor,Rekha Patel,Tomar Ghansah,Abhishek Mathur,Michel M. Murr,Paula C. Bickford,Lisa J. Gould,Denise R. Cooper +9 more
TL;DR: Compared with reports of ADSCs from a number of human depots, there have been no comparisons of the ability of dedifferentiated DFAT cells from the same donor and depot to differentiate or modulate migration of HDFs.
Journal ArticleDOI
Vitamin A Metabolite, All-trans-retinoic Acid, Mediates Alternative Splicing of Protein Kinase C δVIII (PKCδVIII) Isoform via Splicing Factor SC35
Hercules Apostolatos,Andre H. Apostolatos,Timothy A. Vickers,James E. Watson,Shijie Song,Fernando L. Vale,Denise R. Cooper,Juan Sanchez-Ramos,Niketa A. Patel +8 more
TL;DR: This study demonstrates how a nutrient, vitamin A, via its metabolite RA, regulates alternative splicing and thereby gene expression of the pro-survival protein PKCδVIII.
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Downregulation of Protein Kinase C and Insulin-Stimulated 2-Deoxyglucose Uptake in Rat Adipocytes by Phorbol Esters, Glucose, and Insulin
TL;DR: It is confirmed that protein kinase C is required during insulin-stimulated glucose uptake and raised the possibility that downregulation of protein Kinase C by continued translocative activation of the enzyme may contribute (along with other factors) to impaired responsiveness of the glucose transport system after prolonged insulin and/or glucose treatment.
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Insulin-like effects of epidermal growth factor and insulin-like growth factor-I on [3H]2-deoxyglucose uptake, diacylglycerol generation and protein kinase C activation in BC3H-1 myocytes.
TL;DR: The findings suggest that EGF and IGF-I, like insulin, increase DAG-protein kinase C signalling, apparently by activating co-ordinated lipid-synthesis and hydrolysis responses, which are distinctly different from the PIP2-hydrolysis response.
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Chronic effects of glucose on insulin signaling in A-10 vascular smooth muscle cells.
TL;DR: The down-regulation of protein kinase C beta and resultant inhibition of 2-[3H]DOG uptake by chronic glucose suggests a biochemical link between hyperglycemia and DAG-protein kinases C signaling in vascular smooth muscle cells.