RETROGRADE TRANSPORT

The role of Rab7 in axonal retrograde transport and human pathologies

 Coordinatore CANCER RESEARCH UK 

 Organization address address: ST JOHN STREET 407 ANGEL BUILDING
city: LONDON
postcode: EC1V 4AD

contact info
Titolo: Ms.
Nome: Holly
Cognome: Elphinstone
Email: send email
Telefono: +44 20 7269 3524
Fax: +44 20 7269 3585

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 173˙240 €
 EC contributo 173˙240 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2009-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-02-01   -   2013-01-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    CANCER RESEARCH UK

 Organization address address: ST JOHN STREET 407 ANGEL BUILDING
city: LONDON
postcode: EC1V 4AD

contact info
Titolo: Ms.
Nome: Holly
Cognome: Elphinstone
Email: send email
Telefono: +44 20 7269 3524
Fax: +44 20 7269 3585

UK (LONDON) coordinator 173˙240.80

Mappa


 Word cloud

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   generate    human    cells    mutant    cmt    neurons    retrograde    rab    axonal    transport    motor   

 Obiettivo del progetto (Objective)

'Neurons are highly polarized cells that depend on anterograde and retrograde transport for survival, differentiation and maintenance of their morphology. Recently, impairment of axonal trafficking has been implicated as a causative agent in a number of human neurodegenerative disorders, such as Charcot-Marie-Tooth type 2B (CMT2B) neuropathy. CMT2B is characterized by the selective loss of motor and sensory neurons due to mutations in the small GTPase Rab7. Rab7 is a key component of the endocytic pathway in all eukaryotic cells and plays a major role in regulating long-range retrograde transport in motor neurons. However, we know very little about the cargoes and signalling components that enter this route, and how their transport is regulated. Furthermore, no animal model for the in vivo study of Rab7 is currently available. Therefore, the initial focus of my research project will be to generate novel mouse models, in which the activity of Rab7 is impaired. I will generate and characterise these mutant strains together with experts in the field, who kindly agreed to collaborate to this project. Furthermore, these mutant animals represent an invaluable tool to characterize the molecular and cellular role of Rab7 in axonal retrograde transport and its involvement in human neurodegeneration.'

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