A5014388603- Mitochondrial Function and Pathology
- ATP Synthase and ATPases Research
- Neuroscience and Neuropharmacology Research
- Adipose Tissue and Metabolism
- Metabolism and Genetic Disorders
- Cardiac Ischemia and Reperfusion
- Autophagy in Disease and Therapy
- Ion channel regulation and function
- Genetic Neurodegenerative Diseases
- Cell death mechanisms and regulation
- RNA and protein synthesis mechanisms
- Trace Elements in Health
- Fuel Cells and Related Materials
- Photosynthetic Processes and Mechanisms
- Calcium signaling and nucleotide metabolism
- Neurogenetic and Muscular Disorders Research
- Cannabis and Cannabinoid Research
- Protein Tyrosine Phosphatases
- Alzheimer's disease research and treatments
- MicroRNA in disease regulation
- Plant Stress Responses and Tolerance
- Muscle Physiology and Disorders
- Ion Channels and Receptors
- Amyotrophic Lateral Sclerosis Research
- Metabolism, Diabetes, and Cancer
University of Padua
2016-2025
Neuroscience Institute
2012-2016
Manchester Metropolitan University
2016
University of Ferrara
2006-2009
The voltage-dependent anion channel (VDAC) of the outer mitochondrial membrane mediates metabolic flow, Ca2+, and cell death signaling between endoplasmic reticulum (ER) networks. We demonstrate that VDAC1 is physically linked to Ca2+-release inositol 1,4,5-trisphosphate receptor (IP3R) through molecular chaperone glucose-regulated protein 75 (grp75). Functional interaction channels was shown by recombinant expression ligand-binding domain IP3R on ER or surface, which directly enhanced Ca2+...
Mitochondrial calcium accumulation was recently shown to depend on a complex composed of an inner-membrane channel (MCU and MCUb) regulatory subunits (MICU1, MCUR1, EMRE). A fundamental property MCU is low activity at resting cytosolic Ca(2+) concentrations, preventing deleterious cycling organelle overload. Here we demonstrate that these properties are ensured by heterodimer two proteins with opposite effects, MICU1 MICU2, which, both in purified lipid bilayers intact cells, stimulate...
The discovery of the multiple roles mitochondria-endoplasmic reticulum (ER) juxtaposition in cell biology often relied upon exploitation Mitofusin (Mfn) 2 as an ER-mitochondria tether. However, this established Mfn2 function was recently questioned, calling for a critical re-evaluation Mfn2's role cross-talk. Electron microscopy and fluorescence-based probes organelle proximity confirmed that reduced by constitutive or acute deletion. Functionally, mitochondrial uptake Ca2+ released from ER...
Mitochondrial quality control is essential in highly structured cells such as neurons and muscles. In skeletal muscle the mitochondrial fission proteins are reduced different physiopathological conditions including ageing sarcopenia, cancer cachexia chemotherapy-induced wasting. However, whether for homeostasis still unclear. Here we show that muscle-specific loss of pro-fission dynamin related protein (DRP) 1 induces wasting weakness. Constitutive Drp1 ablation muscles reduces growth causes...
Muscle atrophy contributes to the poor prognosis of many pathophysiological conditions, but pharmacological therapies are still limited. activity leads major swings in mitochondrial [Ca(2+)], which control aerobic metabolism, cell death, and survival pathways. We investigated vivo effects Ca(2+) homeostasis skeletal muscle function trophism by overexpressing or silencing calcium uniporter (MCU). The results demonstrate that both developing adult muscles, MCU-dependent uptake has a marked...
Mitochondrial ability of shaping Ca 2+ signals has been demonstrated in a large number cell types, but it is still debated heart cells. Here, we take advantage the molecular identification mitochondrial uniporter (MCU) and unique targeted probes to directly address this issue. We demonstrate that, during spontaneous pacing, peaks on outer membrane (OMM) are much greater than cytoplasm because hot spots generated OMM surface. Cytoplasmic reduced or enhanced by MCU overexpression siRNA...
Charcot–Marie–Tooth disease (CMT) type 2A is a form of peripheral neuropathy, due almost exclusively to dominant mutations in the nuclear gene encoding mitochondrial protein mitofusin-2 (MFN2). However, there no understanding relationship clinical phenotype genotype. MFN2 has two functions: it promotes inter-mitochondrial fusion and mediates endoplasmic reticulum (ER)–mitochondrial tethering at mitochondria-associated ER membranes (MAM). MAM regulates number key cellular functions, including...