Awesome
I've ever had the best professor! Dr. Wooten cares so much and is so helpful about her learners. If you're going to a medical sector, she's a excellent teacher to have and she makes her class fun and pleasant!
Awesome
Doctor Wooten is the definition of someone who truly loves her job. I can say that she loves her students. She puts a lot of care and love into them every day. Her classes are always fun because she loves jokes and laughs a lot. And I can't remember a time when I didn't leave the classroom ready for her class in a few days. I suggest you have to pay attention and study every week to succeed.
Tallahassee Community College - Biological Sciences
Postdoctoral scholar
The focus of my research was the effects of chemotherapies which target de novo synthesis of ceramide on neuroblastoma.
Assistant Professor of Biology
Leslie worked at Tallahassee Community College as a Assistant Professor of Biology
Assistant Professor
My position at Claflin included teaching undergraduate and graduate students in the classroom and in the laboratory. My research focused on chemotherapy sensitivity in breast and prostate cancers.
Biology, General
Doctor of Philosophy (PhD)
Cell/Cellular and Molecular Biology
Postdoctoral scholar
The focus of my research was the effects of chemotherapies which target de novo synthesis of ceramide on neuroblastoma.
FASEB J
In this study, distinct roles of de novo-generated endogenous ceramides and mechanisms by which deacetylated Sp3 regulates the hTERT promoter activity in response to ceramide signaling were explored. The generation of C18-ceramide via the expression of ceramide synthase 1 (CerS1), and not C16-ceramide by CerS5 or CerS6 expression, resulted in repression of the hTERT promoter via deacetylation of Sp3 by histone deacetylase 1 (HDAC1) in A549 human lung adenocarcinoma cells. Then roles and mechanisms of action of ceramide-mediated deacetylation of Sp3 in inhibiting the hTERT promoter were determined using constitutively deacetylated or acetylated Sp3 mutants at lysine (K) 551. Expression of the deacetylated Sp3 mutant resulted in repression, whereas its acetylated mutant induced basal hTERT promoter activity in Drosophila S2 cells, which do not express any endogenous Sp3, and in A549 cells. Remarkably, chromatin immunoprecipitation data revealed that acetylated Sp3 mutant (K551Q-Sp3) did not bind whereas deacetylated Sp3 (K551R-Sp3) mutant bound strongly to the promoter DNA, resulting in the recruitment of histone deacetylase 1 (HDAC1) and inhibition of the association of RNA polymerase II with the promoter. Mechanistically, increased generation of C18-ceramide by hCerS1 expression, but not by its catalytically inactive mutant, mediated the association and recruitment of the deacetylated Sp3/HDAC1 complex to the hTERT promoter DNA, resulting in the local histone H3 deacetylation and repression of the promoter.