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nencki.gov.pl » Working Groups » Department of Biochemistry »
Laboratory of Cellular Metabolism

Head
Krzysztof ZABŁOCKI

Staff
Anna DYGAS, Wanda KŁOPOCKA, Wojciech BRUTKOWSKI (PhD student), Patryk KRZEMIŃSKI (PhD student), Marta ONOPIUK (PhD student), Katarzyna WIERZBICKA (PhD student)

Research profile

The laboratory is focused on intracellular calcium handling in the relation to cellular metabolism under normal and pathological conditions. In particular, we are interested in:

  • Calcium signalling and intracellular calcium homeostasis in Duchenne Muscular Dystrophy (DMD)
  • Mitochondria as a potential target for antidiabetic therapy.
  • Identification and regulation of store-operated calcium channels in electrically non-excitable cells
  • Role of Rho-associated kinase (ROCK) in the actin skeleton arrangement and its influence on mechanical properties of cell surface, adhesion and cell motility

Cell culture, spectrofluorimetry, confocal microscopy, molecular biology, polarography, flow and laser scanning cytometry, proteomic approach and many standard biochemical methods are in use.

Current research activity is focused on:

  • Investigation on mechanisms responsible for impaired calcium metabolism which is one of the hallmarks of Duchenne Muscular Dystrophy and suggested to be a cause of accelerated dystrophic cells death. The role of P2Y and P2X receptors as well as store-operated calcium channels in abnormal calcium homeostasis in dystrophic muscle cells is the current topic of our study. We are using immortalized cell lines (myoblasts and myotubes) derived from mdx mice.
  • Investigation of mitochondrial lipid metabolism in the relation to type 2 diabetes. Possible beneficial (as well as unwanted) effects of potential antidiabetic drugs on mitochondrial metabolism are also in the range of our interest.
  • Investigation of calcium entry controlled by the filling state of intracellular calcium stores that is the major mechanism, which allows Ca2+ influx to electrically non-excitable cells. Its impairment causes severe pathological symptoms. The aim of our study is to identify proteins which compose store-operated calcium channels. This may be helpful for understanding the regulation of Ca2+ entry into electrically non-excitable cells.
  • Investigation of  the influence of Rho-associated kinase (ROCK) on the actin cytoskeleton arrangement, myosin II and cofilin activity as well as on Ca2+ signals evoked by UTP in glioma C6 cells, glioblastoma LN18, neurons and astrocytes. Effects of ROCK inhibition on mechanical properties of the cell surface as well as cell adhesion and motility.

Selected publications

P. Krzemiński, D. Supłat, R. Czajkowski, P. Pomorski, J. Barańska (2007) Expression and functional characterization of P2Y1 and P2Y12 nucleotide receptors in long-term serum-eprived glioma C6 cells. FEBS J. 274, 1970-1982

Kozieł R., Zabłocki K ., Duszyński J. (2006) Calcium signals are affected by ciprofloxacin as a consequence of reduction of mitochondrial DNA content in Jurkat cells. Antimicrob. Agent Chemother. 50: 1664-1671

Yeung D., Zabłocki K. , Lien C-F., Jiang T., Arkle S., Brutkowski W., Brown J., Lochmuller H., Simon J., Barnard E.A., Górecki D.C. (2006) Increased susceptibility to ATP via alteration of P2X  receptor function in dystrophic mdx mouse muscle cells. FASEB J. 20: 610-620

Duszyński J., Kozieł R., Brutkowski W., Szczepanowska J., Zabłocki K. (2006) Regulatory role of mitochondria in capacitative calcium entry. Biochim. Biophys. Acta 1757: 380-387

Zabłocki, K., Szczepanowska, J., Duszyński, J. (2005) Extracellular pH modifies mitochondrial control of capacitative calcium entry in Jurkat cells. J. Biol. Chem. 280: 3615-3621



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Published at: 2007-11-19 11:03
 

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