Beata Jastrzebska graduated from Warsaw University in Poland in 1994 with an MSc in Biology. In 1998, she enrolled in the PhD program at the Nencki Institute of Experimental Biology in Warsaw, Poland, in the Department of Molecular and Cellular Neurobiology. Her PhD thesis project focused on assessing the distribution and function of a novel protein called CacyBP, which was later discovered to be a component of a novel ubiquitination pathway and plays a role in cancer and neurodegeneration. Dr. Jastrzebska completed her PhD in 2003 in the field of Biochemistry and then moved to the US for her postdoctoral research training. Initially, she started at the University of Washington in the Departments of Ophthalmology and Structural Biology. Two years later, in 2005, she moved to Case Western Reserve University and was appointed as a Research Associate in the Department of Pharmacology. Her postdoctoral research focused on discerning the role of rhodopsin dimerization/oligomerization, and she provided compelling evidence that the oligomeric organization of this visual G protein-coupled receptor has important implications for signaling amplification and termination. The outcomes of this research were published in multiple, highly cited articles. Since 2016, Dr. Jastrzebska has continued her scientific career in the Department of Pharmacology at CWRU as an independent NIH-funded investigator. Her research interests include the development of pharmacological treatment strategies for retinal degenerative diseases associated with the dysfunction of rhodopsin and understanding the underlying mechanisms of these pathologies. Dr. Jastrzebska is also committed to undergraduate, graduate, and medical student teaching. In 2021, for her dedication to CWRU medical students' education and the Case Inquiry (IQ) program, she received the Edmond S. Ricanati, M.D. IQ Facilitator Award.
My areas of research include signaling complexes of rhodopsin, rhodopsin oligomeric organization in signal transduction, Molecular bases of light-induced retinal degeneration, and mouse models of retinal degenerative diseases.
Publications
Selected Publications
J. T. Ortega, T. Parmar and B. Jastrzebska* (2019). Flavonoids enhance rod opsin stability, folding, and self-association by directly binding to ligand-free opsin, and modulating its conformation. J. Biol. Chem., 294(20): 8101-8122. PMCID: PMC6527159
J. T. Ortega, T. Parmar, M. Golczak and B. Jastrzebska* (2021). Protective Effects of Flavonoids in Acute Models of Light-Induced Retinal Degeneration. Mol. Pharmacol., 99(1): 60-77. PMCID: PMC7736834
J. T. Ortega, T. Parmar, M. Carmena-Bargueño, H. Pérez-Sánchez and B. Jastrzebska* (2022). Flavonoids improve the stability and function of P23H rhodopsin slowing down the progression of retinitis pigmentosa in mice. J. Neurosci. Res. 100(4):1063-1083. PMCID: PMC9615108
J.T. Ortega, A.G. McKee, F.J. Rouchar, W.D. Penn, J.P. Schlebach and B. Jastrzebska* (2022). Chromenone derivatives as novel pharmacological chaperones for retinitis pigmentosa-linked rod opsin mutants. Hum. Mol. Genet. 10,31(20):3439-3457 PMCID: PMC9558842
5. J.T. Ortega, T. Parmar and B. Jastrzebska* (2023). Galanin receptor 3 - a new pharmacological target in retina degeneration. Pharmacol. Research. 188:106675. PMCID: PMC9918719