Explore the words cloud of the LYSOSOMICS project. It provides you a very rough idea of what is the project "LYSOSOMICS" about.
The following table provides information about the project.
|Coordinator Country||Italy [IT]|
|Total cost||2˙362˙562 €|
|EC max contribution||2˙362˙562 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2016-10-01 to 2021-09-30|
Take a look of project's partnership.
|1||FONDAZIONE TELETHON||IT (ROMA)||coordinator||2˙362˙562.00|
For a long time the lysosome has been viewed as a “static” organelle that performs “routine” work for the cell, mostly pertaining to degradation and recycling of cellular waste. My group has challenged this view and used a systems biology approach to discover that the lysosome is subject to a global transcriptional regulation, is able to adapt to environmental clues, and acts as a signalling hub to regulate cell homeostasis. Furthermore, an emerging role of the lysosome has been identified in many types of diseases, including the common neurodegenerative disorders Parkinson's and Alzheimer’s. These findings have opened entirely new fields of investigation on lysosomal biology, suggesting that there is a lot to be learned on the role of the lysosome in health and disease. The goal of LYSOSOMICS is to use “omics” approaches to study lysosomal function and its regulation in normal and pathological conditions. In this “organellar systems biology project” we plan to perform several types of genetic perturbations in three widely used cell lines and study their effects on lysosomal function using a set of newly developed cellular phenotypic assays. Moreover, we plan to identify lysosomal protein-protein interactions using a novel High Content FRET-based approach. Finally, we will use the CRISPR-Cas9 technology to generate a collection of cellular models for all lysosomal storage diseases, a group of severe inherited diseases often associated with early onset neurodegeneration. State-of-the-art computational approaches will be used to predict gene function and identify disease mechanisms potentially exploitable for therapeutic purposes. The physiological relevance of newly identified pathways will be validated by in vivo studies performed on selected genes by using medaka and mice as model systems. This study will allow us to gain a comprehensive understanding of lysosomal function and dysfunction and to use this knowledge to develop new therapeutic strategies.
|year||authors and title||journal||last update|
Rosa Puertollano, Shawn M Ferguson, James Brugarolas, Andrea Ballabio
The complex relationship between TFEB transcription factor phosphorylation and subcellular localization
published pages: e98804, ISSN: 0261-4189, DOI: 10.15252/embj.201798804
|The EMBO Journal||2019-06-13|
Chiara Di Malta, Diletta Siciliano, Alessia Calcagni, Jlenia Monfregola, Simona Punzi, Nunzia Pastore, Andrea N. Eastes, Oliver Davis, Rossella De Cegli, Angela Zampelli, Luca G. Di Giovannantonio, Edoardo Nusco, Nick Platt, Alessandro Guida, Margret Helga Ogmundsdottir, Luisa Lanfrancone, Rushika M. Perera, Roberto Zoncu, Pier Giuseppe Pelicci, Carmine Settembre, Andrea Ballabio
Transcriptional activation of RagD GTPase controls mTORC1 and promotes cancer growth
published pages: 1188-1192, ISSN: 0036-8075, DOI: 10.1126/science.aag2553
Gabriella Doronzo, Elena Astanina, Davide CorÃ , Giulia Chiabotto, Valentina Comunanza, Alessio Noghero, Francesco Neri, Alberto Puliafito, Luca Primo, Carmine Spampanato, Carmine Settembre, Andrea Ballabio, Giovanni Camussi, Salvatore Oliviero, Federico Bussolino
TFEB controls vascular development by regulating the proliferation of endothelial cells
published pages: e98250, ISSN: 0261-4189, DOI: 10.15252/embj.201798250
|The EMBO Journal 38/3||2019-08-05|
Gennaro Napolitano, Alessandra Esposito, Heejun Choi, Maria Matarese, Valerio Benedetti, Chiara Di Malta, Jlenia Monfregola, Diego Luis Medina, Jennifer Lippincott-Schwartz, Andrea Ballabio
mTOR-dependent phosphorylation controls TFEB nuclear export
published pages: , ISSN: 2041-1723, DOI: 10.1038/s41467-018-05862-6
|Nature Communications 9/1||2019-08-05|
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The information about "LYSOSOMICS" are provided by the European Opendata Portal: CORDIS opendata.
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