Opendata, web and dolomites

Myel-IN-Crisis SIGNED

Myelin at the crossroads of Development and Disease

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 Myel-IN-Crisis project word cloud

Explore the words cloud of the Myel-IN-Crisis project. It provides you a very rough idea of what is the project "Myel-IN-Crisis" about.

risk    controls    strategies    roles    metamorphosis    questions    6500    human    plp1    termination    oligodendrocytes    preterm    myelinating    universal    leads    proteolipid    lack    nutrient    dysregulation    intensively    pelizaeus    rescue    leukodystrophy    lipid    generate    accomplished    machinery    diseases    undergo    transcription    mutation    death    indicate    mechanisms    central    nerve    translation    coordinates    transcriptional    mammalian    myelination    apoptotic    substance    oligodendrocyte    underlie    synthetic    preliminary    surface    sensor    cell    regulating    mtor    extrinsic    put    cns    either    upregulated    axons    initiation    extensions    nervous    feat    sclerosis    transient    translational    function    protein    myelin    energy    stroke    iron    biology    intrinsic    palsy    extraordinary    smart    myel    multiple    usr    infants    crisis    area    white    hypoxia    developmental    defects    metabolic    precisely    cerebral    fold    toxic    dramatic    oxygen    synthesis    differentiation    pmd    hif    single    stress    fatal    injury    mutant    matter    isp    merzbacher    day    disease    overloaded   

Project "Myel-IN-Crisis" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.ac.uk

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 United Kingdom [UK]
 Total cost 2˙500˙000 €
 EC max contribution 2˙500˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-ADG
 Funding Scheme ERC-ADG
 Starting year 2018
 Duration (year-month-day) from 2018-10-01   to  2023-09-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 2˙500˙000.00

Map

 Project objective

The oligodendrocyte, the largest cell in mammalian biology, greatly enables central nervous system (CNS) function through production of a single substance: myelin. Oligodendrocytes undergo a dramatic 1-2 day metamorphosis during myelination, increasing their cell surface area ~6500-fold with proteolipid extensions to nerve axons in the CNS white matter. How is this synthetic feat accomplished? We lack a comprehensive understanding of machinery that precisely coordinates transcription, translation, lipid synthesis and energy production. Moreover, how do these mechanisms become so intensively upregulated during myelination? Does this extraordinary transient state put the myelinating oligodendrocyte at risk of death in diseases of white matter? These questions underlie the Aims of the proposal “Myel-IN-crisis.” I propose (Aim 1) testing whether an “Integrated Synthetic Programme (ISP)” controls oligodendrocyte differentiation, metabolic and synthetic requirements of developmental myelination. In Aim 2, I will investigate roles for “smart sensor” oxygen (HIF) and nutrient (mTOR) pathways in regulating initiation and termination of the ISP. During development, extrinsic white matter injury in preterm infants leads to cerebral palsy, while intrinsic defects in myelin protein PLP1 cause the fatal human leukodystrophy, Pelizaeus-Merzbacher disease (PMD). Preliminary studies indicate transcriptional and translational dysregulation in human PLP1-mutant oligodendrocytes, which become iron overloaded leading to apoptotic cell death. In Aim 3, I propose that either extrinsic (e.g., hypoxia) or intrinsic (e.g., PLP1 mutation) factors promote a “Universal Stress Response (USR)” in the pre-myelinating oligodendrocyte that leads to toxic dysregulation of the ISP. Finally, in Aim 4 we will identify the key pathways of the USR to generate strategies for rescue of myelination with potential translational impact in cerebral palsy and leukodystrophy, multiple sclerosis and stroke.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "MYEL-IN-CRISIS" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

The information about "MYEL-IN-CRISIS" are provided by the European Opendata Portal: CORDIS opendata.

More projects from the same programme (H2020-EU.1.1.)

evolSingleCellGRN (2019)

Constraint, Adaptation, and Heterogeneity: Genomic and single-cell approaches to understanding the evolution of developmental gene regulatory networks

Read More  

HEIST (2020)

High-temperature Electrochemical Impedance Spectroscopy Transmission electron microscopy on energy materials

Read More  

IMMUNOTHROMBOSIS (2019)

Cross-talk between platelets and immunity - implications for host homeostasis and defense

Read More