Denise R Cooper, 744096 40Th St S, Saint Petersburg, FL 33711

2018027, Sep 27, 2018

Mar 26, 2018

15/936326

Denise Ratzlaff Cooper - St. Petersburg FL, US
Ryan Adam Kirchoffer - Ocala FL, US
Robert Pleasants Sparks - Urbana IL, US
Wayne Charles Guida - Saint Pete Beach FL, US

A61K 31/517
A61K 31/473
A61P 3/04

Disclosed herein are compositions and methods for transitioning or converting a white adipocyte to a beige adipocyte. The compositions and methods may be used in the treatment of obesity. In some embodiments, the compositions include a compound selected from DC677 and DC761.

2013005, Mar 7, 2013

Aug 17, 2012

13/588345

Niketa A. Patel - Land O' Lakes FL, US
Denise R. Cooper - St. Petersburg FL, US

UNITED STATES DEPARTMENT OF VETERAN AFFAIRS - Washington DC
UNIVERSITY OF SOUTH FLORIDA - Tampa FL

A61K 38/17
A61P 25/28
C12N 5/071
C12Q 1/68
G01N 33/573
A61K 31/203
A61P 35/00

514 177, 514559, 435 612, 435 74, 435375

RA treatment can improve cognition; promote neurogenesis; and regulate alternative splicing of genes, particularly by mediating mechanisms of 5′ splice site selection and generation of PKCδ alternatively spliced variants. Expression of PKCδVIII is an indicator of the levels of on-going apoptosis in neurons. In the aging brain, switching the isoform expression to PKCδVIII by RA could shield the cells from neuronal death. The inventors discovered that human PKCδVIII expression is increased in neuronal cancer and decreased in Alzheimer's disease. The data shows that PKCδVIII promotes neuronal survival and increases neurogenesis via Bcl2 and Bcl-xL. In addition, the trans-factor SC35 was found to be crucial in mediating the effects of RA on alternative splicing of PKCδVIII mRNA in neurons. The data described herein indicate that PKCδVIII can be used as a biomarker for neurological diseases such as cancers and Alzheimer's disease and as a tool for monitoring and evaluating treatment.

2005019, Sep 8, 2005

Feb 8, 2005

11/054024

Denise Cooper - St. Petersburg FL, US
Niketa Patel - Wesley Chapel FL, US

A61K048/00
C12Q001/68
C07H021/04
C12N005/02

514044000, 435006000, 435456000, 536023200, 435325000

The subject invention pertains to nucleic acid constructs for post-transcriptional control of expression of a polynucleotide encoding a protein in a cell, wherein the constructs include a metabolite responsive instability element such as the glucose-regulated mRNA instability element. The subject invention further pertains to host cells and vectors comprising the nucleic acid constructs of the invention, as well as probes, methods, and kits for detecting metabolite responsive instability elements or mutations thereof. The present invention further concerns a reporter vector useful for detecting intracellular glucose and glucose-analogs, host cells genetically modified with the reporter vector, and methods for detecting intracellular glucose. The present invention utilizes an element that regulates messenger RNA (mRNA) stability in response to a metabolite such as glucose or a glucose analog. This glucose-regulated mRNA instability element has been mapped to the protein kinase C βII (PKCβII) mRNA that was found to decrease in the presence of elevated glucose levels. When cloned into a reporter vector, the region of PKCβII containing the mRNA instability element imparts glucose-sensitive instability to the mRNA that is transcribed, thereby down-regulating the expression of the reporter gene when glucose is elevated. The reporter vector of the present invention may be introduced into host cells, allowing detection of intracellular glucose and glucose analogs within intact, living cells in real-time and, optionally, in a high-throughput format.