Affiliation: University of Padova
- Brain-derived neurotrophic factor and nerve growth factor potentiate excitatory synaptic transmission in the rat visual cortexG Carmignoto
Department of Physiology and Biophysics, Georgetown University School of Medicine, Washington DC, USA
J Physiol 498:153-64. 1997..6. The probability of neurotransmitter release represents a rapidly modifiable synaptic feature by which neurotrophins can potentiate the efficacy of excitatory synaptic transmission in the visual cortex...
- Close contacts with the endoplasmic reticulum as determinants of mitochondrial Ca2+ responsesR Rizzuto
Department of Biomedical Sciences and the National Research Council Center for the Study of Biomembranes, University of Padova, Via Colombo 3, 35121 Padova, Italy
Science 280:1763-6. 1998..These results emphasize the importance of cell architecture and the distribution of organelles in regulation of Ca2+ signaling...
- Digital imaging microscopy of living cellsR Rizzuto
Dept of Biomedical Sciences, University of Padova, Italy
Trends Cell Biol 8:288-92. 1998....
- New light on mitochondrial calciumP Pinton
Department of Biomedical Sciences, University of Padova, Italy
Biofactors 8:243-53. 1998..By using an imaging system endowed with high speed and sensitivity, which allows to obtain high-resolution 3D images, we could demonstrate that close contacts (< 80 nm) occur in vivo between mitochondria and the ER...
- Effects of PMCA and SERCA pump overexpression on the kinetics of cell Ca(2+) signallingM Brini
Department of Biochemistry and Center for the Study of Biomembranes of the National Research Council CNR, University of Padova, Viale G Colombo, 3, 35121 Padova, Italy
EMBO J 19:4926-35. 2000....
- Targeted recombinant aequorins: tools for monitoring [Ca2+] in the various compartments of a living cellM Brini
Department of Biochemistry, University of Padova, 35121 Padova, Italy
Microsc Res Tech 46:380-9. 1999....
- The Ca2+ concentration of the endoplasmic reticulum is a key determinant of ceramide-induced apoptosis: significance for the molecular mechanism of Bcl-2 actionP Pinton
Department of Biomedical Sciences and CNR Center for the Study of Biomembranes, University of Padova, Via Colombo 3, I-35121 Padova, Italy
EMBO J 20:2690-701. 2001..It is therefore concluded that the Bcl-2-dependent reduction of [Ca2+]er is an important component of the anti-apoptotic program controlled by this oncogene...
- VDAC1 selectively transfers apoptotic Ca2+ signals to mitochondriaD De Stefani
Department of Biomedical Sciences, University of Padova and CNR Neuroscience Institute, Padua, Italy
Cell Death Differ 19:267-73. 2012..These data highlight a non-redundant molecular route for transferring Ca(2+) signals to mitochondria in apoptosis...
- Intracellular calcium store depletion and acrosome reaction in human spermatozoa: role of calcium and plasma membrane potentialM Rossato
University of Padova, Department of Medical and Surgical Sciences, Clinica Medica 3, Via Ospedale 105, 35128 Padova, Italy
Mol Hum Reprod 7:119-28. 2001....
- The renaissance of mitochondrial calcium transportT Pozzan
Department of Biomedical Sciences and CNR Center for the Study of Biomembranes, University of Padova, Italy
Eur J Biochem 267:5269-73. 2000....
- Mitochondria and calcium homeostasis: a tale of three luminescent proteinsP J Magalhães
Department of Biomedical Sciences, University of Padua, Viale G Colombo 3, 35121 Padua, Italy
Luminescence 16:67-71. 2001..A final note regarding clinical implications demonstrates the practical usefulness of the data obtained...
- The comeback of mitochondria to calcium signallingT Pozzan
Department of Biomedical Sciences and CNR Center for the Study of Biomembranes, University of Padova, Padova, Italy
Cell Calcium 28:279-83. 2000..Particular attention is paid to recent developments which have contributed to a renewed interest in calcium handling by this organelle...
- Reduced mitochondrial Ca(2+) transients stimulate autophagy in human fibroblasts carrying the 13514A>G mutation of the ND5 subunit of NADH dehydrogenaseV Granatiero
Department of Biomedical Sciences, University of Padova and CNR Neuroscience Institute, Padova, Italy
Cell Death Differ 23:231-41. 2016..This indicates that the higher mitochondrial turnover in complex I deficient cells with this specific mutation is a pro-survival compensatory mechanism that could contribute to the mild clinical phenotype of this patient. ..