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Janusz Tucholski, Ph.D.
Assistant Professor of Psychiatry, University
of Alabama at Birmingham
I received my undergraduate degree in biology (M.Sc.)
and a graduate degree (Ph.D.) in molecular biology and
biochemistry from the
University of Gdańsk in Poland. I worked towards my graduate
degree at the Department of Microbiology in the
University of Gdańsk under the mentorship of Dr. Anna J.
Podhajska, purifying and characterizing proteins that
compose a MmeI restriction-modification system in
methylotrophic bacteria - Methylophilus methylotrophus.
During this time, I was awarded a fellowship from the
European’s Union TEMPUS program that allowed me to
broaden my knowledge by visiting the laboratory of Dr.
Brigitte Wittmann-Liebold at the Max-Delbrück-Center for
Molecular Medicine in Berlin,
and subsequently, the laboratory of Dr. Jane Mellor at
the Oxford
University in England.
After having completed my doctoral degree in
1996, I moved to the USA to pursue my
postdoctoral training. First, I studied the cell
singling events regulated by basic fibroblast growth
factor (bFGF) and its receptor -
FGF receptor-1
(FGFR-1) in human astroglia cells as a postdoctoral
fellow in the Barrow Neurological Institute in Phoenix
in the laboratory of Dr. Michal K. Stachowiak. Next, I
studied apoptosis and calcium signaling in the
laboratory of Dr. Tuan H. Kuo in the Department of
Pathology at Wayne State University in Detroit.
In 1998, I moved to Birmingham, were I started my work in the
laboratory of Dr. Gail Johnson at the UAB Department of
Psychiatry and Behavioral Neurobiology.
The major theme of my research, initially as a
postdoctoral fellow and subsequently as a research
instructor, was to understand the role of tissue
transglutaminase (TG2), a multifunctional member of
transglutaminase family of proteins, in physiological
and pathophysiological of neuroblastoma, neuronal cells,
and in neurodegenerative conditions, such as
Huntington’s Disease (HD) and
Alzheimer’s
Disease (AD).
In 2005 I was promoted to an Assistant Professor
position. I continued my previous line of research, now
in collaboration with Dr. Johnson’s group. I created a
transgenic mouse model, in which TG2 is overexpressed in
neurons of the CNS.
Using this model, we demonstrated that that TG2
plays a crucial role in regulation of neuronal injury in
response overactivation of ionotropic glutamate
receptors – excitotoxicity.
Furthermore, during this time, I was involved in
research describing a protective role of TG2 in response
of neuroblastoma and neuronal cells to
hypoxia/ischemia-induced stress.
I
joined Dr. James Meador-Woodruff's lab in the fall of
2008. Currently, I study abnormalities in biosynthesis,
posttranslational modifications (e.g. N-glycosylation,
S-palmitoylation) of glutamate receptors in
schizophrenia, assembly and trafficking in
schizophrenia. The assembly, trafficking and function at
the postsynaptic membrane of one class of ionotropic
glutamate receptors (AMPA receptors) has been documented
to be critically regulated by AMPA receptor auxiliary
proteins;
the transmembrane AMPA receptor regulatory
protein (TARPγ) family and recently discovered cornichon
(CNIH) protein family.
For this
reason, we study in collaboration with Dr. Daniel C.
Dahl a possible role of
TARPγ and CNIH proteins in observed abnormalities in
AMPAR function in schizophrenia.
E-Mail: jtuchol@uab.edu
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