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Jagiellonian University

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Jagiellonian University

9 Projects, page 1 of 2

  • Regulation of gene expression by Elk-1 activated by MAPK pathways.

    assignment_turned_inProject2002 - 2004Partners:Jagiellonian University, Jagiellonian university
    Funder: Wellcome Trust Project Code: 068832
    Funder Contribution: 107,277 GBP
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  • Central European Conference of Neurobiology, Krakow, Poland August 2001

    assignment_turned_inProject2001 - 2001Partners:Jagiellonian University, Jagiellonian university
    Funder: Wellcome Trust Project Code: 064601
    Funder Contribution: 3,000 GBP
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  • Condensation of chromatin in apoptosis and mitosis of normal human fibroblasts. A study of live and fixed cells by confocal microscopy with deconvolution.

    assignment_turned_inProject2001 - 2004Partners:Jagiellonian University, Jagiellonian university
    Funder: Wellcome Trust Project Code: 064550
    Funder Contribution: 76,360 GBP
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  • Consequences of faulty electron transfer induced by asymmetric cytochrome bc1 for mitochondrial respiratory disease and aging.

    assignment_turned_inProject2011 - 2017Partners:Jagiellonian university, Jagiellonian University
    Funder: Wellcome Trust Project Code: 095078
    Funder Contribution: 652,119 GBP

    Complex III (cytochrome bc1), one of key enzymes of mitochondrial respiration, reversibly exchanges electrons between two major redox pools, ubiquinone and cytochrome c. This makes it an important point of regulation of mitochondrial electron flow. The enzyme is a symmetric homodimer shown, by our recent studies, to embed a rather unique H-shaped electron transfer system with four branches and a bridge connecting the two monomers. This system rapidly distributes electrons between four quinone ox idation-reduction terminals at the corners of the dimer, acting like a molecular-scale bus bar. To elucidate molecular mechanisms underlying the operation of this symmetric design and understand their physiological meaning, we propose to exploit forms with broken symmetry to investigate the putative advantages of the bus bar in regulation of productive electron flow, in diminishing risks of generation of reactive oxygen species (ROS), and in protection against damage caused by mutations in mit ochondrial DNA. We propose to examine how the quinone exchange and oxidation/reduction at the four catalytic terminals integrates with the operation of the bus bar. As those processes occur in membrane, we also propose to analyze how membrane fluidity and some of its constituents affect physiological electron flow and generation of ROS by cytochrome bc1.

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  • Reversible energy coupling in ubiquinol-cytochrome c oxidoreductase engineering of cofactor chains for radical and short-circuit suppression, molecular basis of adaptation and disease.

    assignment_turned_inProject2006 - 2012Partners:Jagiellonian university, Jagiellonian University
    Funder: Wellcome Trust Project Code: 076488
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