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2013 | 73 | Suppl.1 |

Tytuł artykułu

Dysfunction of store-operated calcium entry as an early event in the pathogenesis of neurodegenerative diseases

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EN

Abstrakty

EN
Store-operated calcium entry (SOCE) is a mechanism that regulates calcium influx from the extracellular space which affects calcium signalling in the cell and has been implicated with neuronal cell death. We hypothesized that SOCE might be altered at the early stages of Alzheimer’s (AD) and Huntington’s (HD) disease. We used PC12 cells with an inducible expression of mutated fulllength huntingtin as a cellular model of Huntington’s disease. Calcium measurements were performed by single cell imaging with the Fura-2. We found SOCE parameters were changed as a result of the expression of mutant huntingtin. We next investigated if these differences were caused by changes in the mRNA expression of genes involved in SOCE. Similar analyses are currently being conducted using mouse models of HD (YAC128) and AD (APP V717I) using custom-made TaqMan Low Density Arrays containing probes for genes involved in calcium homeostasis and signalling. Our preliminary results suggest that the expression of mutant proteins such as huntingtin or amyloid precursor protein affect the expression of selected components of calcium homeostasis and signalling pathways.

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-

Rocznik

Tom

73

Numer

Opis fizyczny

p.52-53

Twórcy

autor
  • Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Warsaw, Poland
  • Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Warsaw, Poland
autor
  • Department of Neurology, University Medical Center Mainz, Mainz, Germany
autor
  • Department of Neurology, University Medical Center Mainz, Mainz, Germany
autor
  • Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Warsaw, Poland
  • Nencki Institute of Experimental Biology, Polish academy of Sciences, Warsaw, Poland

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Bibliografia

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