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TransSplicHD

Single-Cell Transcriptomics and Spliceosome analysis to uncover new mechanisms of neuronal vulnerability to Huntington’s Disease.

Total Cost €

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EC-Contrib. €

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Partnership

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 TransSplicHD project word cloud

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

striatal    transition    ultimately    hdh    consolidate    msn    cerebellar    biogenesis    neurodegenerative    postdoctoral    models    drd1    mainly    death    capture    disentangle    repeat    genetic    cag    positioned    direct    mutation    caused    connections    single    pis    believe    mutant    ri    independent    genome    rna    disorders    expertise    expertize    neuronal    truly    context    initial    regulation    woman    exchange    ki    disease    caudate    manner    striatum    transcriptional    academic    mouse    knock    accurate    hypothesis    career    dominant    neuroscience    rnaseq    htt    msca    leads    transcription    scientific    blend    benefit    investigator    neurons    hd    biological    prevailing    aberrant    molecular    cell    neurobiology    gene    deeper    area    am    perfectly    instrumental    putamen    implications    deregulation    allele    drd2    laser    global    expression    spiny    expansion    medium    copy    host    cellular    indirect    integration    huntingtin    supervisor    alterations    huntington    human    splicing    training    alternative    pathological    exposure    competitive    synthesis    behavioral    cortical    skills    optimally    dissection    vulnerability    events    cibio    neuroanatomical   

Project "TransSplicHD" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITA DEGLI STUDI DI TRENTO 

Organization address
address: VIA CALEPINA 14
city: TRENTO
postcode: 38122
website: www.unitn.it

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 Italy [IT]
 Project website https://www.cibio.unitn.it/184/neuroepigenetics-laboratory AND https
 Total cost 180˙277 €
 EC max contribution 180˙277 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2016
 Duration (year-month-day) from 2016-09-01   to  2018-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI TRENTO IT (TRENTO) coordinator 180˙277.00

Map

 Project objective

Huntington’s disease (HD) is neurodegenerative disease caused by a CAG repeat expansion mutation in the HTT gene. The pathological process, which ultimately leads to neuronal loss mainly in the caudate and putamen, is induced - in a truly dominant manner - by a single copy of the mutant allele. Transcriptional deregulation has becoming a prevailing feature in HD and changes at single-gene level in RNA biogenesis and aberrant alternative splicing (AS) events have been associated to neuronal vulnerability. Here, I propose to disentangle at genome-wide level the connections between mutant huntingtin expression and RNA processing, and its implications for neuronal vulnerability to death. Specifically, I propose to study alterations in RNA transcription and AS in: Aim 1. Striatal, cortical and cerebellar areas of Hdh knock-in (KI) HD accurate mouse models through global RNAseq; Aim 2. In specific medium spiny neurons (MSN) of the Drd1 or Drd2 direct and indirect pathways of Hdh KI striatum through laser capture dissection and single-cell RNAseq. The present research proposal represents a synthesis of my interest, expertise in RNA regulation, genome-wide approaches and single-cell analysis in the context of neurodegenerative disorders with my most recent exposure to human genetic. On the other hand, at the CIBIO host institution I will greatly benefit from the scientific exchange with the PIs of the neurobiology area, and my supervisor in particular, whose skills in neuroscience, neuroanatomical and behavioral analyses will perfectly blend and consolidate my cellular and molecular expertize. Thus, I believe I am optimally positioned to accomplish the aims of the current application: the MSCA-RI-IF will be instrumental to develop this initial hypothesis into deeper biological understanding of HD and represent a crucial support to my scientific integration as a competitive, woman investigator in the transition from postdoctoral training to an independent academic career.

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

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