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CaralinaMarin De Evsikova

Caralina Marin De Evsikova, PhD

  • The early developmental environment plays a pivotal role in susceptibility to adulthood metabolic disease, such as obesity and diabetes. The long-term goal of this project is to understand how the maternal and embryonic environment alters gene expression, which ultimately leads to disease, via epigenetics. Epigenome of each individual is established during the egg-to-embryo transition, which is sensitive to teratogens, such as alcohol, bisphenol A, or dietary exposures. To identify the role of epigenetics in metabolic disease, I am using a naturally occurring “epigenetic barometer” allele (viable yellow) of the Agouti gene in mice, whose expression is controlled by methylation levels. Nutrigenomics & Healthspan. My long-term goal is to develop new mouse models of adult-onset metabolic diseases by monitoring in vivo physiology coupled with quantitative molecular genetics to detect genes and pathways involved with weight gain. This approach has been successful in identifying changes in eating, activity, and loss of circadian rhythms underlying “normal” weight fluctuations from across the lifespan.

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Post Docs


Eric Lewandowski

  • Our lab focuses on structure based drug design through the use of X-ray crystallography and molecular docking.
  • My research is focused on discovering novel inhibitors of the protein monofunctional transglycosylase (MTG). MTG catalyzes the second to last step of bacterial cell wall formation and has only one known inhibitor, but unfortunately it is ineffective in humans. By combining fragment based molecular docking with protein X-ray crystallography I hope to discover novel inhibitors against MTG and other transglycosylases involved in bacterial cell wall formation. These novel inhibitors could lead to a new class of antibiotic that would ultimately be effective against bacteria that are resistant to many currently available drugs.

Ph.D. Students

  • My current research focuses on understanding the role of the Amyloid Precursor Protein (APP) in pancreatic cancer. It is well known that pancreatic cancer has a poor prognosis and very low 5-year survival rates. Early detection poses a challenge mainly owing to the location of this organ and a non-symptomatic progression. At the molecular level, the oncogene RAS is known to be mutated and overexpressed in this cancer and the signaling pathways are somewhat understood. Using several pancreatic cancer cells lines, our recent findings show that APP is overexpressed in most pancreatic cancer cells lines as well. Preliminary studies have shown that APP can regulate RAS transcription levels and knock down of APP can inhibit RAS protein expression. Using this information, my project aims to understand the mechanism of regulation of RAS by APP and to establish APP, its processed fragments, and associated signaling pathways as possible targets for drug development against pancreatic cancer.