Laura Cassina

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Mutations in the PINK1 gene cause autosomal recessive Parkinson's disease. The PINK1 gene encodes a protein kinase that is mitochondrially cleaved to generate two mature isoforms. In addition to its protective role against mitochondrial dysfunction and apoptosis, PINK1 is also known to regulate mitochondrial dynamics acting upstream of the PD-related(More)
Mmutations in paraplegin, a putative mitochondrial metallopeptidase of the AAA family, cause an autosomal recessive form of hereditary spastic paraplegia (HSP). Here, we analyze the function of paraplegin at the cellular level and characterize the phenotypic defects of HSP patients' cells lacking this protein. We demonstrate that paraplegin coassembles with(More)
The time-dependent CP asymmetry in B(s)(0)→J/ψK+K- decays is measured using pp collision data, corresponding to an integrated luminosity of 3.0  fb-1, collected with the LHCb detector at center-of-mass energies of 7 and 8 TeV. In a sample of 96,000 B(s)(0)→J/ψK+K- decays, the CP-violating phase ϕs is measured, as well as the decay widths ΓL and ΓH of the(More)
The mitochondrial metalloprotease AFG3L2 assembles with the homologous protein paraplegin to form a supracomplex in charge of the essential protein quality control within mitochondria. Mutations of paraplegin cause a specific axonal degeneration of the upper motoneuron and, therefore, hereditary spastic paraplegia. Here we present two Afg3l2 murine models:(More)
A measurement of the ratio of the branching fractions of the B(+) → K(+)μ(+)μ(-) and B(+) → K(+)e(+)e(-) decays is presented using proton-proton collision data, corresponding to an integrated luminosity of 3.0 fb(-1), recorded with the LHCb experiment at center-of-mass energies of 7 and 8 TeV. The value of the ratio of branching fractions for the dilepton(More)
Mitochondria are eukaryotic intracellular organelles that still bear the signatures of their prokaryotic ancestor and require nuclear assistance. They generously dispense energy to cells, but are also involved in several biosynthetic processes, as well as in cell signalling pathways and programmed cell death. Mitochondria are partitioned into four(More)
Little is known about the association of endothelial nitric oxide synthase (NOS3) gene polymorphisms and the presence of insulin resistance and the early evolution of atherosclerosis in nondiabetic subjects with cardiovascular disease (CAD) and stent implantation. The present study was performed in an attempt to better understand whether metabolic,(More)
AIMS Nitric oxide (NO) plays a key role in vascular homeostasis and is produced by endothelial NO synthase (eNOS), encoded by NOS3 gene. We previously reported the genetic association between NOS3 rs753482-A>C polymorphism on intron 19 and coronary artery disease (CAD). In the attempt of conferring functional implication to the rs753482-A>C polymorphism, we(More)
The mitochondrial protein AFG3L2 forms homo-oligomeric and hetero-oligomeric complexes with paraplegin in the inner mitochondrial membrane, named m-AAA proteases. These complexes are in charge of quality control of misfolded proteins and participate in the regulation of OPA1 proteolytic cleavage, required for mitochondrial fusion. Mutations in AFG3L2 cause(More)
We report the results of a search for neutrinoless double-beta decay in a 9.8 kg yr exposure of (130)Te using a bolometric detector array, CUORE-0. The characteristic detector energy resolution and background level in the region of interest are 5.1±0.3  keV FWHM and 0.058±0.004(stat)±0.002(syst)counts/(keV kg yr), respectively. The median 90% C.L.(More)