Simone Di Paola

ORCID: 0000-0003-3753-5722
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About
Contact & Profiles
Research Areas
  • Calcium signaling and nucleotide metabolism
  • Autophagy in Disease and Therapy
  • PARP inhibition in cancer therapy
  • Toxin Mechanisms and Immunotoxins
  • Lysosomal Storage Disorders Research
  • Cardiac Valve Diseases and Treatments
  • Cellular transport and secretion
  • Parkinson's Disease Mechanisms and Treatments
  • RNA Interference and Gene Delivery
  • Microtubule and mitosis dynamics
  • Lipid metabolism and biosynthesis
  • Metabolism, Diabetes, and Cancer
  • Genetic Neurodegenerative Diseases
  • Adipose Tissue and Metabolism
  • Photoreceptor and optogenetics research
  • Plant nutrient uptake and metabolism
  • Electrostatic Discharge in Electronics
  • Ion Channels and Receptors
  • Piperaceae Chemical and Biological Studies
  • Photosynthetic Processes and Mechanisms
  • Cardiac tumors and thrombi
  • Alzheimer's disease research and treatments
  • Cardiac and Coronary Surgery Techniques
  • Congenital Heart Disease Studies
  • Plant responses to water stress

Institute for Experimental Endocrinology and Oncology
2022-2024

University of Toronto
2024

Telethon Institute Of Genetics And Medicine
2015-2024

National Research Council
2022-2023

Harvard University
2021

Boston Children's Hospital
2021

Mario Negri Sud Foundation
2010-2014

Abstract The lysosomal calcium channel TRPML1, whose mutations cause the storage disorder (LSD) mucolipidosis type IV (MLIV), contributes to upregulate autophagic genes by inducing nuclear translocation of transcription factor EB (TFEB). Here we show that TRPML1 activation also induces vesicle (AV) biogenesis through generation phosphatidylinositol 3-phosphate (PI3P) and recruitment essential PI3P-binding proteins nascent phagophore in a TFEB-independent manner. Thus, formation requires...

10.1038/s41467-019-13572-w article EN cc-by Nature Communications 2019-12-10

Background Protein mono-ADP-ribosylation is a reversible post-translational modification that modulates the function of target proteins. The enzymes catalyze this reaction in mammalian cells are either bacterial pathogenic toxins or endogenous cellular ADP-ribosyltransferases. latter include members three different families proteins: well characterized arginine-specific ecto-enzymes ARTCs, two sirtuins and, more recently, novel poly(ADP-ribose) polymerase (PARP/ARTD) family have been...

10.1371/journal.pone.0037352 article EN cc-by PLoS ONE 2012-06-11

Abstract Selective removal of dysfunctional mitochondria via autophagy is crucial for the maintenance cellular homeostasis. This event initiated by translocation E3 ubiquitin ligase Parkin to damaged mitochondria, and it requires Serine/Threonine-protein kinase PINK1. In a coordinated set events, PINK1 operates upstream in linear pathway that leads phosphorylation Parkin, Ubiquitin, mitochondrial substrates, promote ubiquitination outer membrane proteins. Ubiquitin-decorated are selectively...

10.1038/s41418-023-01251-9 article EN cc-by Cell Death and Differentiation 2024-01-18

10.1007/978-1-4939-9018-4_12 article EN Methods in molecular biology 2019-01-01

Intracellular mono-ADP-ribosyltransferases (mono-ARTs) catalyze the covalent attachment of a single ADP-ribose molecule to protein substrates, thus regulating their functions. PARP10 is soluble mono-ART involved in modulation intracellular signaling, metabolism and apoptosis. also participates regulation G1- S-phase cell cycle. However, role this enzyme G2/M progression not defined. In study, we found that genetic ablation, depletion pharmacological inhibition cause delay transition...

10.3390/cancers14215210 article EN Cancers 2022-10-24

Mono-ADP-ribosylation is a reversible post-translational modification that can modulate the functions of target proteins. We have previously demonstrated β subunit heterotrimeric G proteins endogenously mono-ADP-ribosylated, and once modified, βγ dimer inactive toward its effector enzymes. To better understand physiological relevance this modification, we studied hormonal regulation. Here, report Gβ mono-ADP-ribosylation differentially modulated by protein-coupled receptors. In intact cells,...

10.1074/jbc.m110.112466 article EN cc-by Journal of Biological Chemistry 2010-12-10

An established hallmark of cancer cells is metabolic reprogramming, largely consisting in the exacerbated glucose uptake. Adipocytes tumor microenvironment contribute toward breast (BC) progression and are highly responsive to fluctuations. Metabolic conditions characterizing obesity and/or diabetes associate with increased BC incidence mortality. To explore BC-adipocytes interaction define impact such dialogue, Mammary Adipose-derived Mesenchymal Stem Cells (MAd-MSCs) were differentiated...

10.1038/s41598-024-76522-7 article EN cc-by-nc-nd Scientific Reports 2024-10-21

10.1007/978-1-4939-9018-4_13 article EN Methods in molecular biology 2019-01-01

Abstract The GTPase Rab14 is localized at the trans-Golgi network and intermediate compartment associated to sorting/recycling endosomes-like structures of transferrin-recycling pathway: as other Rab family members, it involved in regulation intracellular vesicle trafficking, though its role functional relationship with effector/endosomal proteins still incomplete. We have analysed whether post-translational modifications could affect activity: results obtained define mono-ADP-ribosylation...

10.1101/2022.11.26.517555 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2022-11-26

Abstract Selective removal of dysfunctional mitochondria via autophagy is crucial for the maintenance cellular homeostasis. This event initiated by translocation E3 ubiquitin ligase Parkin to damaged mitochondria, and it requires Serine/Threonine-protein kinase PINK1. In a coordinated set events, PINK1 operates upstream in linear pathway that leads phosphorylation Parkin, Ubiquitin, mitochondrial substrates, promote ubiquitination outer membrane proteins. Ubiquitin decorated are selectively...

10.1101/2023.01.31.526442 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-02-01
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