Beata Jastrzebska graduated from Warsaw University, Poland in 1994 with MSc in Biology. In 1998 she was enrolled in the PhD program at the Nencki Institute of Experimental Biology, 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 as discovered later, is 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 continue 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 retina degenerative diseases associated with the dysfunction of rhodopsin, and understanding the underlying mechanisms of these pathologies. Dr. Jastrzebska also is committed to undergraduate, graduate, and medical students 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.
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.
J. T. Ortega, T. Parmar, M. Golczak and B. Jastrzebska* (2021). Flavonoids protect the retina from light-induced degeneration by multiple mechanisms. Mol. Pharmacol., 99(1): 60-77.
J. T. Ortega and B. Jastrzebska* (2021). Rhodopsin as a molecular target to mitigate retinitis pigmentosa. Adv. Exp. Med. Biol. – Protein Reviews, 1371:61-77.
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. J. Neurosci. Res. 100(4):1063-1083.
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