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Article ; Online: NAADP-Evoked Ca

Pereira, Cássia Arruda de Souza / Medaglia, Natalia de Castro / Ureshino, Rodrigo Portes / Bincoletto, Claudia / Antonioli, Manuela / Fimia, Gian Maria / Piacentini, Mauro / Pereira, Gustavo José da Silva / Erustes, Adolfo Garcia / Smaili, Soraya Soubhi

International journal of molecular sciences

2023 Volume 24, Issue 6

Abstract: Huntington's disease (HD) is a progressive neurodegenerative disease characterized by mutations in the huntingtin gene (mHtt), causing an unstable repeat of the CAG trinucleotide, leading to abnormal long repeats of polyglutamine (poly-Q) in the N- ... ...

Abstract	Huntington's disease (HD) is a progressive neurodegenerative disease characterized by mutations in the huntingtin gene (mHtt), causing an unstable repeat of the CAG trinucleotide, leading to abnormal long repeats of polyglutamine (poly-Q) in the N-terminal region of the huntingtin, which form abnormal conformations and aggregates. Alterations in Ca
MeSH term(s)	Mice ; Animals ; Calcium Channels/metabolism ; Astrocytes/metabolism ; Neurodegenerative Diseases/metabolism ; NADP/metabolism ; Lysosomes/metabolism ; Autophagy ; Calcium/metabolism ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism
Chemical Substances	Calcium Channels ; NAADP (5502-96-5) ; NADP (53-59-8) ; Calcium (SY7Q814VUP) ; Huntingtin Protein
Language	English
Publishing date	2023-03-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24065593
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Regulation of Autophagy in Cells Infected With Oncogenic Human Viruses and Its Impact on Cancer Development.

Vescovo, Tiziana / Pagni, Benedetta / Piacentini, Mauro / Fimia, Gian Maria / Antonioli, Manuela

Frontiers in cell and developmental biology

2020 Volume 8, Page(s) 47

Abstract: About 20% of total cancer cases are associated to infections. To date, seven human viruses have been directly linked to cancer development: high-risk human papillomaviruses (hrHPVs), Merkel cell polyomavirus (MCPyV), hepatitis B virus (HBV), hepatitis C ... ...

Abstract	About 20% of total cancer cases are associated to infections. To date, seven human viruses have been directly linked to cancer development: high-risk human papillomaviruses (hrHPVs), Merkel cell polyomavirus (MCPyV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), and human T-lymphotropic virus 1 (HTLV-1). These viruses impact on several molecular mechanisms in the host cells, often resulting in chronic inflammation, uncontrolled proliferation, and cell death inhibition, and mechanisms, which favor viral life cycle but may indirectly promote tumorigenesis. Recently, the ability of oncogenic viruses to alter autophagy, a catabolic process activated during the innate immune response to infections, is emerging as a key event for the onset of human cancers. Here, we summarize the current understanding of the molecular mechanisms by which human oncogenic viruses regulate autophagy and how this negative regulation impacts on cancer development. Finally, we highlight novel autophagy-related candidates for the treatment of virus-related cancers.
Language	English
Publishing date	2020-02-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2020.00047
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Article ; Online: TRIM proteins in autophagy: selective sensors in cell damage and innate immune responses.

Di Rienzo, Martina / Romagnoli, Alessandra / Antonioli, Manuela / Piacentini, Mauro / Fimia, Gian Maria

Cell death and differentiation

2020 Volume 27, Issue 3, Page(s) 887–902

Abstract: Autophagy, a main intracellular catabolic process, is induced in response to a variety of cellular stresses to promptly degrade harmful agents and to coordinate the activity of prosurvival and prodeath processes in order to determine the fate of the ... ...

Abstract	Autophagy, a main intracellular catabolic process, is induced in response to a variety of cellular stresses to promptly degrade harmful agents and to coordinate the activity of prosurvival and prodeath processes in order to determine the fate of the injured cells. While the main components of the autophagy machinery are well characterized, the molecular mechanisms that confer selectivity to this process both in terms of stress detection and cargo engulfment have only been partly elucidated. Here, we discuss the emerging role played by the E3 ubiquitin ligases of the TRIM family in regulating autophagy in physiological and pathological conditions, such as inflammation, infection, tumorigenesis, and muscle atrophy. TRIM proteins employ different strategies to regulate the activity of the core autophagy machinery, acting either as scaffold proteins or via ubiquitin-mediated mechanisms. Moreover, they confer high selectivity to the autophagy-mediated degradation as described for the innate immune response, where TRIM proteins mediate both the engulfment of pathogens within autophagosomes and modulate the immune response by controlling the stability of signaling regulators. Importantly, the elucidation of the molecular mechanisms underlying the regulation of autophagy by TRIMs is providing important insights into how selective types of autophagy are altered under pathological conditions, as recently shown in cancer and muscular dystrophy.
MeSH term(s)	Animals ; Autophagy ; Cells/pathology ; Humans ; Immunity, Innate ; Models, Biological ; Signal Transduction ; Tripartite Motif Proteins/metabolism
Chemical Substances	Tripartite Motif Proteins
Language	English
Publishing date	2020-01-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-020-0495-2
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Article: Emerging Mechanisms in Initiating and Terminating Autophagy.

Antonioli, Manuela / Di Rienzo, Martina / Piacentini, Mauro / Fimia, Gian Maria

Trends in biochemical sciences

2017 Volume 42, Issue 1, Page(s) 28–41

Abstract: Autophagy is a major degradative process activated in a rapid and transient manner to cope with stress conditions. Whether autophagy is beneficial or detrimental depends upon the rate of induction and the appropriateness of the duration. Alterations in ... ...

Abstract	Autophagy is a major degradative process activated in a rapid and transient manner to cope with stress conditions. Whether autophagy is beneficial or detrimental depends upon the rate of induction and the appropriateness of the duration. Alterations in both autophagy initiation and termination predispose the cell to death, and affect the execution of other inducible processes such as inflammation. In this review we discuss how stress signaling pathways dynamically control the activity of the autophagy machinery by mediating post-translational modifications and regulatory protein interactions. In particular, we highlight the emerging role of TRIM and CULLIN families of ubiquitin ligases which play opposite roles in the autophagy response by promoting or inhibiting, respectively, the activity of the autophagy initiation complex.
MeSH term(s)	Animals ; Autophagy/physiology ; Humans ; Protein Processing, Post-Translational ; Signal Transduction ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	194216-5
ISSN	1362-4326 ; 0968-0004 ; 0376-5067
ISSN (online)	1362-4326
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/j.tibs.2016.09.008
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Article ; Online: The interplay between SARS-CoV-2 infected airway epithelium and immune cells modulates regulatory/inflammatory signals.

Bordoni, Veronica / Matusali, Giulia / Mariotti, Davide / Antonioli, Manuela / Cimini, Eleonora / Sacchi, Alessandra / Tartaglia, Eleonora / Casetti, Rita / Grassi, Germana / Notari, Stefania / Castilletti, Concetta / Fimia, Gian Maria / Capobianchi, Maria Rosaria / Ippolito, Giuseppe / Agrati, Chiara

iScience

2022 Volume 25, Issue 2, Page(s) 103854

Abstract: To assess the cross-talk between immune cells and respiratory tract during SARS-CoV-2 infection, we analyzed the relationships between the inflammatory response induced by SARS-CoV-2 replication and immune cells phenotype in a reconstituted organotypic ... ...

Abstract	To assess the cross-talk between immune cells and respiratory tract during SARS-CoV-2 infection, we analyzed the relationships between the inflammatory response induced by SARS-CoV-2 replication and immune cells phenotype in a reconstituted organotypic human airway epithelium (HAE). The results indicated that immune cells failed to inhibit SARS-CoV-2 replication in the HAE model. In contrast, immune cells strongly affected the inflammatory profile induced by SARS-CoV-2 infection, dampening the production of several immunoregulatory/inflammatory signals (e.g., IL-35, IL-27, and IL-34). Moreover, these mediators were found inversely correlated with innate immune cell frequency (NK and γδ T cells) and directly with CD8 T cells. The enriched signals associated with NK and CD8 T cells highlighted the modulation of pathways induced by SARS-CoV-2 infected HAE. These findings are useful to depict the cell-cell communication mechanisms necessary to develop novel therapeutic strategies aimed to promote an effective immune response.
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.103854
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Article: Emerging Mechanisms in Initiating and Terminating Autophagy

Antonioli, Manuela / Gian Maria Fimia / Martina Di Rienzo / Mauro Piacentini

Trends in biochemical sciences. 2017 Jan., v. 42, no. 1

2017

Abstract	Autophagy is a major degradative process activated in a rapid and transient manner to cope with stress conditions. Whether autophagy is beneficial or detrimental depends upon the rate of induction and the appropriateness of the duration. Alterations in both autophagy initiation and termination predispose the cell to death, and affect the execution of other inducible processes such as inflammation. In this review we discuss how stress signaling pathways dynamically control the activity of the autophagy machinery by mediating post-translational modifications and regulatory protein interactions. In particular, we highlight the emerging role of TRIM and CULLIN families of ubiquitin ligases which play opposite roles in the autophagy response by promoting or inhibiting, respectively, the activity of the autophagy initiation complex.
Keywords	autophagy ; inflammation ; post-translational modification ; regulatory proteins ; signal transduction ; ubiquitin-protein ligase
Language	English
Dates of publication	2017-01
Size	p. 28-41.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	194220-7
ISSN	0968-0004 ; 0376-5067
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/j.tibs.2016.09.008
Database	NAL-Catalogue (AGRICOLA)

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Article: Rationale and Criteria for a COVID-19 Model Framework

Messina, Francesco / Montaldo, Chiara / Abbate, Isabella / Antonioli, Manuela / Bordoni, Veronica / Matusali, Giulia / Sacchi, Alessandra / Giombini, Emanuela / Fimia, Gian Maria / Piacentini, Mauro / Capobianchi, Maria Rosaria / Lauria, Francesco Nicola / Ippolito, Giuseppe / on behalf of COVID-19 Scoping Review Working Group

Viruses. 2021 July 06, v. 13, no. 7

2021

Abstract: Complex systems are inherently multilevel and multiscale systems. The infectious disease system is considered a complex system resulting from the interaction between three sub-systems (host, pathogen, and environment) organized into a hierarchical ... ...

Abstract	Complex systems are inherently multilevel and multiscale systems. The infectious disease system is considered a complex system resulting from the interaction between three sub-systems (host, pathogen, and environment) organized into a hierarchical structure, ranging from the cellular to the macro-ecosystem level, with multiscales. Therefore, to describe infectious disease phenomena that change through time and space and at different scales, we built a model framework where infectious disease must be considered the set of biological responses of human hosts to pathogens, with biological pathways shared with other pathologies in an ecological interaction context. In this paper, we aimed to design a framework for building a disease model for COVID-19 based on current literature evidence. The model was set up by identifying the molecular pathophysiology related to the COVID-19 phenotypes, collecting the mechanistic knowledge scattered across scientific literature and bioinformatic databases, and integrating it using a logical/conceptual model systems biology. The model framework building process began from the results of a domain-based literature review regarding a multiomics approach to COVID-19. This evidence allowed us to define a framework of COVID-19 conceptual model and to report all concepts in a multilevel and multiscale structure. The same interdisciplinary working groups that carried out the scoping review were involved. The conclusive result is a conceptual method to design multiscale models of infectious diseases. The methodology, applied in this paper, is a set of partially ordered research and development activities that result in a COVID-19 multiscale model.
Keywords	COVID-19 infection ; disease models ; ecological competition ; humans ; multiomics ; pathogens ; pathophysiology ; research and development
Language	English
Dates of publication	2021-0706
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v13071309
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Article: Dataset exploited for the development and validation of automated cyanobacteria quantification algorithm, ACQUA

Gandola, Emanuele / Antonioli, Manuela / Traficante, Alessio / Franceschini, Simone / Scardi, Michele / Congestri, Roberta

Data in Brief. 2016 Sept., v. 8

2016

Abstract: The estimation and quantification of potentially toxic cyanobacteria in lakes and reservoirs are often used as a proxy of risk for water intended for human consumption and recreational activities. Here, we present data sets collected from three volcanic ... ...

Abstract	The estimation and quantification of potentially toxic cyanobacteria in lakes and reservoirs are often used as a proxy of risk for water intended for human consumption and recreational activities. Here, we present data sets collected from three volcanic Italian lakes (Albano, Vico, Nemi) that present filamentous cyanobacteria strains at different environments. Presented data sets were used to estimate abundance and morphometric characteristics of potentially toxic cyanobacteria comparing manual Vs. automated estimation performed by ACQUA (“ACQUA: Automated Cyanobacterial Quantification Algorithm for toxic filamentous genera using spline curves, pattern recognition and machine learning” (Gandola et al., 2016) [1]). This strategy was used to assess the algorithm performance and to set up the denoising algorithm. Abundance and total length estimations were used for software development, to this aim we evaluated the efficiency of statistical tools and mathematical algorithms, here described. The image convolution with the Sobel filter has been chosen to denoise input images from background signals, then spline curves and least square method were used to parameterize detected filaments and to recombine crossing and interrupted sections aimed at performing precise abundances estimations and morphometric measurements.
Keywords	Cyanobacteria ; algorithms ; automation ; computer software ; crossing ; data collection ; humans ; morphometry ; risk ; toxicity
Language	English
Dates of publication	2016-09
Size	p. 817-823.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2016.06.042
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Article ; Online: AMBRA1-regulated autophagy in vertebrate development.

Antonioli, Manuela / Albiero, Federica / Fimia, Gian María / Piacentini, Mauro

The International journal of developmental biology

2015 Volume 59, Issue 1-3, Page(s) 109–117

Abstract: Autophagy is a catabolic process that mediates the lysosomal turn over of organelles and macromolecules, and is strongly activated in stress conditions to ensure cell survival. Autophagy core genes are highly conserved from yeast to mammals, with an ... ...

Abstract	Autophagy is a catabolic process that mediates the lysosomal turn over of organelles and macromolecules, and is strongly activated in stress conditions to ensure cell survival. Autophagy core genes are highly conserved from yeast to mammals, with an increasing number of positive and negative regulators that have evolved in higher eukaryotes. Autophagy takes part in different stages of development, as revealed by alterations in cell proliferation, differentiation and survival during the embryogenesis of organisms carrying mutations in autophagy genes. These defects are ascribed to the ability of autophagy to provide elements for new synthesis or energy production in limiting conditions during embryogenesis, as well as to contribute to the profound cell remodeling that occurs during differentiation. However, many differences have been observed in the phenotypes of autophagy mutant organisms, indicating that these genes have acquired specific functions in particular tissues, which may reflect the ability of autophagy to crosstalk with the main developmental processes. In this review, we discuss the role of upstream regulators of autophagy in the development of different model systems, focusing, in particular, on AMBRA1 (autophagy/beclin-1 regulator-1) and its role in the central nervous system.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Apoptosis/physiology ; Apoptosis Regulatory Proteins/metabolism ; Autophagy/physiology ; Autophagy-Related Protein-1 Homolog ; Beclin-1 ; Central Nervous System/embryology ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/metabolism ; Microtubule-Associated Proteins/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Vertebrates/embryology
Chemical Substances	AMBRA1 protein, human ; Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; BECN1 protein, human ; Beclin-1 ; Intracellular Signaling Peptides and Proteins ; MAP1LC3A protein, human ; Membrane Proteins ; Microtubule-Associated Proteins ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; ULK1 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2015-09-29
Publishing country	Spain
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1036070-0
ISSN	1696-3547 ; 0214-6282
ISSN (online)	1696-3547
ISSN	0214-6282
DOI	10.1387/ijdb.150057mp
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Article: Temporal regulation of autophagy response by the CULLIN 4-AMBRA1-CULLIN 5 axis.

Antonioli, Manuela / Albiero, Federica / Piacentini, Mauro / Fimia, Gian Maria

Molecular & cellular oncology

2015 Volume 3, Issue 5, Page(s) e1008304

Abstract: Autophagy controls cell homeostasis and provides a rapid response to a variety of stresses. Although many steps of the autophagy process have been elucidated, how they are temporally regulated is less well characterized. Recently, we reported that ... ...

Abstract	Autophagy controls cell homeostasis and provides a rapid response to a variety of stresses. Although many steps of the autophagy process have been elucidated, how they are temporally regulated is less well characterized. Recently, we reported that dynamic interaction of the pro-autophagic factor AMBRA1 with CULLIN E3 ubiquitin ligases ensures the timely onset and termination of the autophagy response.
Language	English
Publishing date	2015-02-03
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2015.1008304
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