A5073596294- Mitochondrial Function and Pathology
- Muscle Physiology and Disorders
- Adipose Tissue and Metabolism
- ATP Synthase and ATPases Research
- Autophagy in Disease and Therapy
- Neuroscience and Neuropharmacology Research
- Genetic Neurodegenerative Diseases
- Ion channel regulation and function
- Cancer, Hypoxia, and Metabolism
- Cell death mechanisms and regulation
- Photoreceptor and optogenetics research
- Wnt/β-catenin signaling in development and cancer
- Genetics, Aging, and Longevity in Model Organisms
- Metabolism and Genetic Disorders
- Muscle metabolism and nutrition
- Parkinson's Disease Mechanisms and Treatments
- Cancer, Lipids, and Metabolism
- Cancer-related gene regulation
- Enzyme Catalysis and Immobilization
- GDF15 and Related Biomarkers
- Metabolism, Diabetes, and Cancer
- Neurogenetic and Muscular Disorders Research
- Sirtuins and Resveratrol in Medicine
- Calcium signaling and nucleotide metabolism
- Ferroptosis and cancer prognosis
University of Padua
2016-2025
Neuroscience Institute
2011-2014
Kyowa Kirin (France)
2013
National Research Council
2011
Veneto Institute of Molecular Medicine
2007-2010
University of Perugia
2008
Massachusetts General Hospital
2001-2005
University of Lausanne
2005
University of Pennsylvania
2005
Harvard University
2001-2002
A highly conserved signaling pathway involving insulin-like growth factor 1 (IGF1), and a cascade of intracellular components that mediate its effects, plays major role in the regulation skeletal muscle growth. central component this is kinase Akt, also called protein B (PKB), which controls both synthesis, via kinases mammalian target rapamycin (mTOR) glycogen synthase 3β (GSK3β), degradation, transcription factors FoxO family. In paper, we review composition function fibers, focusing on...
Loss of muscle mass occurs in a variety diseases, including cancer, chronic heart failure, aquired immunodeficiency syndrome, diabetes, and renal often aggravating pathological progression. Preventing wasting by promoting growth has been proposed as possible therapeutic approach. Myostatin is an important negative modulator during myogenesis, myostatin inhibitors are attractive drug targets. However, the role pathway adulthood transcription factors involved signaling unclear. Moreover,...
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...
The balance between synthesis and degradation of intracellular components determines the overall muscle fiber size. Muscle atrophy occurs when rate is higher than rate, for example during disuse, fasting or systemic diseases such as diabetes, cancer renal failure. two main catabolic systems that are activated ubiquitin-proteasome autophagy-lysosome pathways. FoxO3 transcription factor causes marked in adult skeletal induces muscle-specific ubiquitin ligase Atrogin-1/MAFbx.(1) In addition, we...
Triple-negative breast cancer (TNBC) represents the most aggressive tumor subtype. However, molecular determinants responsible for metastatic TNBC phenotype are only partially understood. We here show that expression of mitochondrial calcium uniporter (MCU), selective channel Ca(2+) uptake, correlates with size and lymph node infiltration, suggesting uptake might be instrumental growth formation. Accordingly, MCU downregulation hampered cell motility invasiveness reduced growth, lung...
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...
A better understanding of the signaling pathways that control muscle growth is required to identify appropriate countermeasures prevent or reverse loss mass and force induced by aging, disuse, neuromuscular diseases. However, two major issues in this field have not yet been fully addressed. The first concerns involved leading physiological changes size. Muscle hypertrophy based on perturbations specific either characterized impaired generation, e.g., myostatin knockout, incompletely studied...
In keratinocytes, the cyclin/CDK inhibitor p21 WAF1/Cip1 is a direct transcriptional target of Notch1 activation; loss either or genes expands stem cell populations and facilitates tumor development. The tumor-suppressor function was associated with down-regulation Wnt signaling. Here, we show that suppression signaling by activation mediated, at least in part, down-modulation Wnts gene expression. negative regulator transcription downstream activation, independently effects on cycle. More...
The mammalian genome contains three ancient sarcomeric myosin heavy chain (MYH) genes, MYH14/7b, MYH15 and MYH16, in addition to the two well characterized clusters of skeletal cardiac MYHs. MYH16 is expressed jaw muscles carnivores; however expression pattern MYH14 not known. orthologues are present frogs birds, coding for chicken slow 2 ventricular MYH, respectively, whereas only have been detected fish. In all species gene a microRNA, miR-499. Here we report that rat mouse, miR-499...
PSEN2 (presenilin 2) is one of the 3 proteins that, when mutated, causes early onset familial Alzheimer disease (FAD) cases. In addition to its well-known role within γ-secretase complex (the enzyme ultimately responsible for Aβ peptides formation), endowed with some γ-secretase-independent functions in distinct cell signaling pathways, such as modulation intracellular Ca
Mitochondrial Ca2+ uptake depends on the mitochondrial calcium uniporter (MCU) complex, a highly selective channel of inner membrane (IMM). Here, we screen library 44,000 non-proprietary compounds for their ability to modulate uptake. Two them, named MCU-i4 and MCU-i11, are confirmed reliably decrease influx. Docking simulations reveal that these molecules directly bind specific cleft in MICU1, key element MCU complex controls gating. Accordingly, MICU1-silenced or deleted cells, inhibitory...
The Rho GTPase and Fyn tyrosine kinase have been implicated previously in positive control of keratinocyte cell–cell adhesion. Here, we show that operate along the same signaling pathway. Endogenous activity increases differentiating keratinocytes is required for both activation increased phosphorylation β- γ-catenin, which associated with establishment Conversely, expression constitutive active sufficient to promote adhesion through a kinase- Fyn-dependent mechanism, trigger activation,...