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RENOPROTECT SIGNED

Targeting tubular reabsorption for kidney protection

Total Cost €

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EC-Contrib. €

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Partnership

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 RENOPROTECT project word cloud

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

featured    drosophila    treatment    exon    variants    cell    genetic    hypothesis    locus    cryptic    safe    mechanisms    gene    metabolic    ptcs    balancing    humans    shows    vulnerable    proximal    despite    encoded    variability    leads    mice    relevance    specialized    partial    chronic    dysfunction    combine    mechanism    functionally    applicable    paradigm    cells    many    mutations    expression    albuminuria    forms    proteinuria    kidney    downstream    lies    renal    integrative    prognosis    urine    beneficial    fitness    tolerated    human    nanoparticle    hypothesize    diabetic    protection    first    inclusion    evolutionary    ptc    protein    signatures    receptor    albumin    evolution    proteinuric    cubilin    cubn    overload    advantage    altogether    haplotypes    monoallelic    tubular    tissue    explore    diagnosis    translational    humanized    tubule    damage    glomerulus    validate    homeostasis    demand    reabsorption    genetics    tissues    resistance    model    experimental    repair    lumen    disease   

Project "RENOPROTECT" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITATSKLINIKUM HEIDELBERG 

Organization address
address: IM NEUENHEIMER FELD 672
city: HEIDELBERG
postcode: 69120
website: www.klinikum.uni-heidelberg.de

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 Germany [DE]
 Total cost 1˙945˙250 €
 EC max contribution 1˙945˙250 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-COG
 Funding Scheme ERC-COG
 Starting year 2020
 Duration (year-month-day) from 2020-08-01   to  2025-07-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITATSKLINIKUM HEIDELBERG DE (HEIDELBERG) coordinator 1˙945˙250.00

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 Project objective

Many forms of chronic kidney disease are featured by the loss of protein into the urine (proteinuria). When the cause of proteinuria lies within the glomerulus, such as in diabetic kidney disease, then the protein overload in the tubular lumen may lead to damage of the downstream tubular cells. Particularly vulnerable are proximal tubular cells (PTCs), because these cells are specialized in protein reabsorption and have a high metabolic demand. Dysfunction of the main albumin uptake receptor cubilin (encoded by the CUBN gene) leads to the reduction of albumin uptake and albuminuria. Here, we hypothesize that genetic variants in CUBN are key for providing a cell-to-cell variability that is beneficial for PTC homeostasis and resistance against proteinuric kidney disease. This hypothesis is based on our recent findings that 1.) CUBN mutations are well tolerated by humans despite their proteinuric effects and that 2.) the CUBN locus shows signatures of balancing selection during human evolution. To address this hypothesis, we will first functionally validate common CUBN variants and haplotypes in a humanized Drosophila model and test whether they provide protection against renal disease in mice. Second, we will explore monoallelic CUBN expression and partial cryptic exon inclusion as two possible genetic mechanisms by which CUBN variants could promote proximal tubule fitness and tissue repair. Finally, taking advantage of cubilin dysfunction as a “safe” means to avoid PTC overload, we will target PTC protein uptake in proteinuric mice with the help of a nanoparticle delivery method. Altogether, our integrative translational approach will combine human genetics and experimental studies to explore a new mechanism of proximal tubule homeostasis that may also be applicable to other tissues. Based on evolutionary genetics, we aim to establish a novel paradigm for kidney protection with high relevance for the diagnosis, prognosis and treatment of proteinuric kidney disease.

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