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NUCDDR SIGNED

Nucleolar Responses to DNA Damage: rDNA, an emerging hub of genome instability

Total Cost €

0

EC-Contrib. €

0

Partnership

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 NUCDDR project word cloud

Explore the words cloud of the NUCDDR project. It provides you a very rough idea of what is the project "NUCDDR" about.

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Project "NUCDDR" data sheet

The following table provides information about the project.

Coordinator
PANEPISTIMIO PATRON 

Organization address
address: UNIVERSITY CAMPUS RIO PATRAS
city: RIO PATRAS
postcode: 265 04
website: www.upatras.gr

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Greece [EL]
 Total cost 1˙499˙525 €
 EC max contribution 1˙499˙525 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-STG
 Funding Scheme ERC-STG
 Starting year 2020
 Duration (year-month-day) from 2020-06-01   to  2025-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    PANEPISTIMIO PATRON EL (RIO PATRAS) coordinator 1˙499˙525.00

Map

 Project objective

DNA lesions can impose serious threats to genome integrity and cell viability. Whereas DNA damage may occur anywhere in the genome, it is increasingly recognized that certain genomic loci rich in repetitive sequences display increased susceptibility to damage and are linked to chromosomal rearrangements and malignancy. Clusters of ribosomal DNA gene (rDNA) repeats, present on five different chromosomes, constitute the most heavily transcribed area of the human genome and are organized in a nuclear membrane-less organelle, the nucleolus. So far, putative links between rDNA damage and malignant processes have not been rigorously assessed. We will address the hypothesis that rDNA repeats represent a major hub of genomic instability contributing to malignant transformation. Using state-of-the-art experimental systems that allow enrichment for nucleolar DNA damage, we will explore: (i) hypothesis-driven and mass spectrometry-based approaches to define regulators of the rDNA damage response; (ii) live imaging and advanced molecular biology tools to uncover how histone epigenetic changes and formation of RNA:DNA hybrids impact on nucleolar chromatin, nucleolar organization, rDNA transcription and repair ; (iii) cell models that recapitulate malignant transformation caused by inducible oncogene expression or epigenetic inactivation of tumour suppressors, to assess replication stress in rDNA repeats as a primary source of genomic instability and pertinent to hallmarks of cancer. The proposed research is expected to yield novel insights into the signaling networks and biological processes regulating rDNA damage and repair within the nuclear environment and define how these mechanisms are corrupted during neoplastic transformation. This knowledge could be directly applicable to the design of new diagnostic or therapeutic strategies for cancer.

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The information about "NUCDDR" are provided by the European Opendata Portal: CORDIS opendata.

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