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Discovery Sciences Emerging Scholars Lectures

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This lecture series features young scientists making notable discoveries as postdoctoral fellows or early career faculty.


2018 Speakers

Thursday, December 6, Angelina Hernandez-Carretero, 9:30 am, 206 Preston Research Building: “Novel Regulators of Obesity-Induced Insulin Resistance and Diabetes.” Dr. Hernandez-Carretero is a Staff Scientist at the City of Hope Beckman Research Institute. “Further investigation is needed to understand the molecular players involved in obesity-induced insulin resistance. We have utilized a dietary switch mouse model to perform transcriptomics of the skeletal muscle, and compared these findings with RNA-seq of human obese- diabetic muscle. This multispecies approach identified key genes that tracked with the insulin resistant state in both mouse and human muscle, including Cysteine and glycine-rich protein 3 (Csrp3).  Csrp3 expression is decreased in obese-insulin resistant muscle and plays an important role in insulin-stimulated glucose uptake.” Flyer   Hernandez-Carretero CV

Tuesday, November 13, Luisa Escobar-Hoyos, 4:00 pm, 206 Preston Research Building: “Targeting RAS and mutant p53: Discovery of RNA splicing as a therapeutic vulnerability in pancreatic cancer.” Dr. Escobar-Hoyos is a Postdoctoral Research Fellow at Memorial Sloan Kettering Cancer Center and Research Assistant Professor at Stony Brook University. “We recently discovered a novel mechanism of cooperation between the two most common oncogenes in pancreatic cancer, oncogenic RAS and neomorphic mutant p53, uncovering a potential therapeutic opportunity to target tumors that bear these mutations. Specifically, we found that mutant p53 causes aberrant splicing of GAP proteins, the negative regulators of RAS, resulting in expression of inactive GAP proteins (polyC GAPs), and ultimately promoting oncogenic RAS signaling. In addition, we identified that pancreatic tumors in mouse models depend on expression of polyC GAPs and splicing machinery proteins, as genetic and chemical inhibition of these proteins caused decrease in tumor growth, number of metastases and tripled the survival time of animals. These studies identified these proteins as new targets for tumors with neomorphic p53 and oncogenic KRAS. We expect to identify novel and specific dependencies of PDAC cells by studying and targeting specific alternatively spliced products and/or manipulating the function of splicing factors in the background of multiple forms of mutated TP53, to provide the foundation for future research that will lead to the development of more effective approaches to treat PDAC patients, improving their survival and quality of life.” Flyer   Escobar-Hoyos CV

Wednesday, October 10, Leonard Alfredo Harris, Vanderbilt University, 4:00 pm, 512 Light Hall: “Bet Hedging as a Survival Strategy in Complex Biological Systems and Cancer.” Cells are complex, dynamic systems capable of initiating internal biochemical programs and adjusting their behavior in response to microenvironmental signals and stressors. Under the general term “phenotypic plasticity,” this phenomenon underlies important biological processes such as stem cell differentiation and epithelial-to-mesenchymal transitions. In bacteria, isogenic cell populations are known to exploit plasticity by phenotypically diversifying to increase their chances of survival to catastrophic external challenges, a strategy known as “bet hedging.” Recent evidence suggests that cancer cells may employ a similar strategy to survive the initial onslaught of anticancer therapeutics. Understanding the complex biochemical networks that underlie signal propagation and cell fate decisions is thus critical for improving treatments of various human diseases, including cancer. Here, I describe the biochemical basis for phenotypic plasticity within the framework of “Waddington landscapes,” present evidence for its role in anticancer drug resistance in non-small cell lung cancer and melanoma populations treated with targeted drugs, and discuss initial work toward constructing a detailed computational model of the biochemical machinery underlying cellular responses to external perturbations.  Flyer  CV

Abdus_Ishmail_web.jpgThursday, May 3: Ishmail Abdus-Saboor, University of Pennsylvania, 4:00 pm, 512 Light Hall: “Genetic Interrogation of Neural Circuit Mechanisms for Pain.” The nervous system is exquisitely tuned to mount the appropriate behavioral response to somatosensory stimuli ranging from a gentle caress to a harsh mechanical insult. How our nervous systems encode this information, from the level of sensory neuron activation in the skin up towards the central nervous system, in both normal and diseased states, remains enigmatic. We are working to uncover the mechanisms governing sensory encoding of touch, itch, and pain. Using optogenetics, quantitative analysis of animal behavior, and in vivo calcium imaging we have 1) determined how a population of pain-sensing neurons have unique morphological and physiological outputs depending upon body location, and 2) developed a new behavioral platform using high-speed videography, statistics, and machine learning to distinguish between innocuous versus painful behavior responses.  Flyer   CV   Abdus-Saboor Lab

 

Silva_2.pngThursday, March 1: Gustavo Silva, Duke University, 4:00 pm, 406 Preston Research Building: “K63 ubiquitin and the regulation of translation in response to oxidative stress.” Ubiquitin is a prominent post-translational modification, which signals extensively beyond protein degradation. In this talk, Dr. Silva will present his research on how ubiquitin modifies ribosomes and controls cell resistance to stress.  Flyer   CV

 

Dionna-Williams_colorbg_web.jpgThursday, February 1: Dionna Williams, Johns Hopkins University, 4:00 pm, 512 Light Hall: “Beyond GPCR Recycling: B-Arrestin as a Neuroprotective Modulator of Innate Immune Responses.” Dr. Williams’ talk will focus on the organ-specific, immunomodulatory roles of B-arrestin that serve to suppress chronic immune activation during viral infection of the brain.  Flyer   CV

 

2017 Speakers

Kennedy_Arion_web.jpgThursday, December 14: Arion Kennedy, Vanderbilt University, 4:00 pm, 206 Preston Research Building: “CD8+ T Cells Regulate Liver Injury In Obesity-Related Nonalcoholic Fatty Liver Disease.” The incidence of NAFLD has increased in Western countries due to the prevalence of obesity. Current interests are aimed at identifying the type and function of immune cells that infiltrate the liver and key factors responsible for mediating their recruitment and activation in obesity-associated NAFLD. Dr. Kennedy’s talk will focus on the role of CD8+ T cells in the development of obesity- associated NAFLD.  Flyer   CV

 

Posey_web.jpgThursday, November 16: Avery Posey, Jr., University of Pennsylvania, 12:00 pm, 898 Preston Research Building: “Accelerating CAR T Cells from the Model T to Driverless.” Dr. Posey will discuss engineered T cell therapies developed to treat cancer, including progress and imitations of translating the success of leukemia treatments to solid tumor treatments.  Flyer   CV

 

 

Spencer_Sade_webphoto.jpgOctober 5: Sade Spencer, Medical University of South Carolina, 4:00 pm, 206 Preston Research Building: “Dopaminergic Regulation of Relapse-Dependent Glutamatergic Plasticity.” Dr. Spencer will present her modified cue-cocaine relapse model and the alterations in transient synaptic plasticity associated with relapse observed in the nucleus accumbens. She will also present newer data pertaining to the relationship between dopamine and glutamate during relapse, and how this impacts synaptic function.  Flyer   CV

 

Correa.pngApril 13: Stephanie Correa, UCLA, 4:00 pm, 206 Preston Research Building: “Sex-Specific Neural Regulation of Energy Balance.” The focus of Dr. Correa’s lab is understanding how reproductive hormones affect metabolic health and disease. Flyer    Photos

 

 

Raphemot_Rene.jpgMarch 16: Rene Raphemot, Duke University, 4:00 pm, 206 Preston Research Building: “A Genomic Screen Reveals New Host Factors Critical to Liver-Stage Malaria.” Dr. Raphemot studies host-parasite interactions during the liver-stage of malaria infection. His goal is to understand host-related factors that are exploited by the parasite. Flyer    Reporter Article    Photos