Janusz Tucholski, M.Sc., Ph.D.
- University of Gdañsk, Gdañsk, Poland – M.Sc., Biology – 1988
- University of Gdañsk, Gdañsk, Poland – Ph.D., with Honors in Biological Sciences – 1996
- 1995 Visiting Scientist, Max-Delbrück-Centrum for Molecular Medicine, Berlin, Germany
- 1996 Visiting Scientist, Biochemistry/Microbiology, Oxford University, Oxford, UK
- 1996-97 Postdoctoral Fellow, Neurobiology, Barrow Neurological Institute, Phoenix, AZ
- 1997-98 Postdoctoral Fellow, Pathology, School of Medicine, Wayne State University, Detroit, MI
- 1998-02 Postdoctoral Fellow, Psychiatry and Behavioral Neurobiology, UAB, Birmingham, AL
Academic Appointments with UAB:
- 2003-05 Research Instructor, Psychiatry and Behavioral Neurobiology, UAB
- 2005- Assistant Professor, Psychiatry and Behavioral Neurobiology, UAB
- 2005- Center for Aging, UAB (secondary)
- Role tissue transglutaminase (TG-2) in neuronal physiology and pathology.
- Retinoic acid-induced neurogenesis.
- The Ca2+ and cAMP-signaling interplay in determination of neuronal fate, outgrowth and in acute and persistent stress.
- Neuronal homeostasis and plasticity in response to acute injury (e.g. brain injury, stroke, epilepsy), and in neurodegeneration (e.g. HD, PD) and in psychiatric conditions (e.g. depression).
Primary in my research, I am interested in the role of TG-2 in determination of neuronal fate, neurogenesis, maturation and regeneration of neurons, and in theirs response to pathological conditions (e.g. excitotoxicity). Secondly, because Ca2+ and cAMP-signaling play a prominent role in above processes and TG-2 is known modulate or to be modulated by Ca2+ and cAMP-signaling, I am interested in a relationship between TG-2, and Ca2+/cAMP-signaling in neurons and cells destined to become neurons, especially during response of CNS neurons to acute and persistent stress. In my study, I use transgenic and knock-out mouse models, acute mouse brain slices, mouse neuronal cell culture and culture of neuronal-like human neuroblastoma SH-SY5Y cells.
In future, I intend, by using the mouse models, to investigate how RA, TG-2, Ca2+, cAMP-signaling molecules and signaling pathways are engaged in plasticity and in stress response of young and adult neurons in neurological (e.g. epilepsy) and psychiatric conditions such as major depression, bipolar disorder and schizophrenia.
- Tucholski, J., Kuret, J., Johnson, G.V.W. Tau is modified by tissue transglutaminase in situ: possible functional and metabolic effects of polyamination. J. Neurochem. 73 (1999), 1871-80.
- Zhang, J., Tucholski, J., Lesort, M., Jope, R.S., Johnson, G.V.W. Novel bimodal effects of the G-protein tissue transglutaminase on adrenoreceptor signalling. Biochemical J. 343 (1999), 541-549.
- Lesort, M., Tucholski, J., Zhang, J., Johnson, G.V.W. Impaired mitochondrial function in increased tissue transglutaminase activity in situ. J. Neurochem. 75 (2000), 1951-61.
- Tucholski, J., Lesort, M., Johnson, G.V.W. Tissue transglutaminase is essential for neurite outgrowth in human neuroblastoma SH-SY5Y cells. Neuroscience 102 (2) (2001), 481-491.
- Tucholski, J., Johnson, G.V.W. Tissue transglutaminase differentially modulates apoptosis in a stimuli-dependent manner. J. Neurochem. 81 (2002), 780-91.
- Tucholski, J., Johnson, G.V.W. Tissue transglutaminase modulates CREB transcriptional activity through the cAMP pathway. J. Biol. Chem. 278 (29) (2003), 26838-43.
- Milakovic, T., Tucholski, J., McCoy, E., Johnson, G.V.W. Intracellular localization and activity state of tissue transglutaminase differentially impacts cell death. J. Biol. Chem. 279 (10) (2004), 8715-22.
- Bailey, C. D.C., Tucholski, J. and Johnson, G. V.W. Transglutaminases in neurodegenerative disorders. Prog. Exp. Tumor Res. 38 (2005) 139-57.
- Tucholski, J., Roth, K.A. and Johnson, G. V.W. Tissue transglutaminase overexpression in the brain potentiates excitotoxicity-induced hippocampal damage. J. Neurochem. 97 (2006) 582-94.
- Kumar, A., Kneynsberg, A., Tucholski, Perry. G. van Groen, T., Detloff, p., Lesort, M. (2012) Tissue transglutaminase overexpression does not modify the disease phenotype of the R6/2 mouse model of Huntington’s disease (http://www.ncbi.nih.gov/pubmed/22698685). Experimental Neurology, 237 (1): 78-89.