10 A niversary of IIMCB
10 A niversary of IIMCB
10 A niversary of IIMCB
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Publications in 2008<br />
• Bojarski L, Pomorski P, Szybinska A, Drab M, Skibinska-<br />
Kijek A, Gruszczynska-Biegala J, Kuznicki J. Presenilindependent<br />
expressions <strong>of</strong> STIM proteins and dysregulation<br />
<strong>of</strong> capacitative Ca(2+) entry in familial Alzheimer’s disease.<br />
Biochim Biophys Acta MCR, 2008 Dec 6; [Epub ahead <strong>of</strong><br />
print]<br />
• Klejman ME, Gruszczynska-Biegala J, Skibinska-Kijek<br />
A, Wisniewska MB, Misztal K, Blazejczyk M, Bojarski L,<br />
Kuznicki J. Expression <strong>of</strong> STIM1 in brain and puncta-like<br />
colocalization <strong>of</strong> STIM1 and ORAI1 upon depletion <strong>of</strong> Ca 2+<br />
store in neurons. Neurochem Int, 2009; 54:49-55<br />
• Erickson RP, Larson-Thome K, Weberg L, Szybinska<br />
A, Mossakowska M, Styczynska M, Barcikowska M,<br />
Kuznicki J. Variation in NPC1, the gene encoding<br />
Niemann-Pick C1, a protein involved in intracellular<br />
cholesterol transport, is associated with Alzheimer disease<br />
and/or aging in the Polish population. Neurosci Lett, 2008;<br />
447:153–157<br />
• Winiarska M, Bil J, Wilczek E, Wilczynski GM, Lekka M,<br />
Engelberts PJ, Mackus WJ, Gorska E, Bojarski L, Stoklosa<br />
T, Nowis D, Kurzaj Z, Makowski M, Glodkowska E, Issat T,<br />
Mrowka P, Lasek W, Dabrowska-Iwanicka A, Basak GW,<br />
Wasik M, Warzocha K, Sinski M, Gaciong Z, Jakobisiak M,<br />
Parren PW, Golab J. Statins impair antitumor effects <strong>of</strong><br />
rituximab by inducing conformational changes <strong>of</strong> CD20.<br />
PLoS Med, 2008; 5:e64<br />
• Mossakowska M, Barcikowska M, Broczek K, Grodzicki<br />
T, Klich-Raczka A, Kupisz-Urbanska M, Podsiadly-<br />
Moczydlowska T, Sikora E, Szybinska A, Wieczorkowska-<br />
Tobis K, Zyczkowska J, Kuznicki J. Polish Centenarians<br />
Programme - Multidisciplinary studies <strong>of</strong> successful<br />
ageing: Aims, methods, and preliminary results. Exp<br />
Gerontol, 2008; 43:238-244<br />
• Bojarski L, Herms J, Kuznicki J. Calcium dysregulation in<br />
Alzheimer’s disease. Neurochem Int, 2008; 52:621-633<br />
• Wojda U, Salinska E, Kuznicki J. Calcium ions in neuronal<br />
degeneration. IUBMB Life, 2008; 60:575-590<br />
• Sbroggiò M, Ferretti R, Percivalle E, Gutkowska M,<br />
Zylicz A, Michowski W, Kuznicki J, Accornero F, Pacchioni<br />
B, Lanfranchi G, Hamm J, Turco E, Silengo L, Tarone G,<br />
Brancaccio M. The mammalian CHORD-containing protein<br />
melusin is a stress response protein interacting with Hsp90<br />
and Sgt1. FEBS Lett, 2008; 582:1788-94<br />
• Lanni C, Racchi M, Mazzini G, Ranzenigo A, Polotti R,<br />
Sinforiani E, Olivari L, Barcikowska M, Styczynska M,<br />
Kuznicki J, Szybinska A, Govoni S, Memo M, Uberti D.<br />
Conformationally altered p53: a novel Alzheimer’s disease<br />
marker? Mol Psychiatry, 2008; 13:641-647<br />
• Zabka M, Lesniak W, Prus W, Kuznicki J, Filipek A. Sgt1<br />
has co-chaperone properties and is up-regulated by heat<br />
shock. Biochem Biophys Res Commun, 2008; 370:179-183<br />
• Filipek A, Michowski W, Kuznicki J. Involvement <strong>of</strong><br />
S<strong>10</strong>0A6 (calcyclin) and its binding partners in intracellular<br />
signaling pathways. Advan Enzyme Regul, 2008;<br />
48:225-239<br />
• Blazejczyk M, Wojda U. Factfile: Calmyrin 1 (review).<br />
Calcium Binding Proteins, 2008; 3:1-3<br />
Current Projects<br />
We are interested in molecular mechanisms involved<br />
in learning and memory, as well as neurodegeneration;<br />
we study these processes at the genomic, proteomic and<br />
cellular levels.<br />
Our major projects are:<br />
1. Search for bio-markers and potential therapeutic targets<br />
for Alzheimer’s disease (AD).<br />
2. Analysis <strong>of</strong> proteins involved in Ca 2+ homeostasis in<br />
neurons and non-neuronal cells.<br />
3. Analysis <strong>of</strong> Ca 2+ -binding proteins calmyrin1 and calmyrin2<br />
in neurons.<br />
4. Regulation and role <strong>of</strong> β-catenin/Lef1 complex in mature<br />
neurons.<br />
5. Characterization <strong>of</strong> biological functions <strong>of</strong> CHORD<br />
containing proteins in the nervous system.<br />
6. Studies on the cyclin-dependent kinase 5 involvement in<br />
pathogenesis <strong>of</strong> Alzheimer’s disease.<br />
1. Search for functional bio-markers and potential<br />
therapeutic targets <strong>of</strong> Alzheimer’s disease (Emilia<br />
Białopiotrowicz, Łukasz Bojarski, Mirosław Drab, Aleksandra<br />
Szybińska, Bożena Kuźniewska, Urszula Wojda, in<br />
collaboration with other laboratories)<br />
In this area, several projects were carried out:<br />
1.1. In cooperation with Pr<strong>of</strong>. Maurizio Memo and Dr. Daniela<br />
Uberti (University <strong>of</strong> Brescia) the conformational mutant p53<br />
as a new putative marker to discriminate AD from non-AD<br />
patients was analyzed. Conformation <strong>of</strong> p53 protein was<br />
studied in cell lysates from our immortalized B lymphocytes<br />
from 13 sporadic AD (SAD) and <strong>10</strong> familial AD (FAD) patients<br />
and 12 control subjects by immunoprecipitation experiments.<br />
Cells from SAD and FAD patients specifically expressed<br />
an increased amount <strong>of</strong> conformationally altered p53 that<br />
makes them distinguishable from cells <strong>of</strong> age-matched<br />
non-AD subjects. This suggests a role for a dearrangement<br />
<strong>of</strong> protein controlling the cell cycle in AD pathogenesis<br />
(C. Lanni, et al., Mol Psych, 2008). Since p53 conformational<br />
tertiary structure is influenced by redox status <strong>of</strong> the cells,<br />
we also evaluated the oxidative pr<strong>of</strong>ile <strong>of</strong> these patients. We<br />
found that among the markers <strong>of</strong> oxidative stress, hydroxytransnonenal-modified<br />
proteins were significantly increased<br />
in FAD patients. Furthermore it is interested to note that,<br />
besides increased levels <strong>of</strong> oxidative markers, the antioxidant<br />
defence mechanisms were compromised in these patients.<br />
These results supported and enhanced the first evidences <strong>of</strong><br />
peripheral unfolded p53 associated with AD pathology and<br />
highlighted the identification <strong>of</strong> oxidative stress markers in<br />
peripheral, immortalised cells derived from FAD patients.<br />
1.2. It has been suggested that the aberrant expression<br />
<strong>of</strong> cell cycle molecules in the brain contributes to the<br />
development <strong>of</strong> Alzheimer’s disease (AD) and causes<br />
neuronal death. The aim <strong>of</strong> the current study was to<br />
determine whether the alterations in cell cycle progression<br />
can be observed in lymphocytes from SAD and FAD<br />
patients. Immortalized B-lymphocytes from 17 SAD and 6<br />
FAD patients (bearing distinct PS1 mutations) were studied<br />
in comparison to lymphocytes from 18 healthy individuals.<br />
Laboratory <strong>of</strong> Neurodegeneration 41