Phenotypic impact of FXN gene splicing reprogramming in Friedreich Ataxia cells and mice
Salva questo lavoro e mantieni la tua ricerca organizzata
Crea un account gratuito per salvare lavori, creare avvisi e tornare a questa inserzione dalla tua dashboard.
Continuando accetti i nostri Termini & Informativa sulla privacy.
Organisation/Company Università di Trento Research Field Biological sciences Researcher Profile Recognised Researcher (R2) Leading Researcher (R4) First Stage Researcher (R1) Established Researcher (R3) Application Deadline 25 Nov 2026 - 12:00 (UTC) Country Italy Type of Contract To be defined Job Status Not Applicable Is the job funded through the EU Research Framework Programme? Not funded by a EU programme Is the Job related to staff position within a Research Infrastructure? No
Offer DescriptionFriedreich Ataxia (FRDA) is a rare, progressive neurodegenerative disorder caused by a GAA trinucleotide repeat expansion in the first intron of the FXN gene, resulting in reduced expression of frataxin, a mitochondrial protein essential for iron-sulfur cluster biogenesis and cellular energy metabolism. Frataxin deficiency leads to mitochondrial dysfunction and progressive neurological and cardiac manifestations, with cardiomyopathy representing a major cause of morbidity and mortality. The research program aims to investigate the molecular and functional consequences of a novel therapeutic strategy designed to increase endogenous frataxin expression through reprogramming of FXN pre-mRNA alternative splicing. [...]
- AFRICA
- EUROPE
- OCEANIA
- NORTH AMERICA
- SOUTH AMERICA
- ASIA
- OTHER
- E.U.
- CHINA (MAINLAND)
- CHINA (HONG KONG)
Eligibility of fellows: country/ies of residence:
- AFRICA
- EUROPE
- OCEANIA
- NORTH AMERICA
- SOUTH AMERICA
- ASIA
- OTHER
- E.U.
- CHINA (MAINLAND)
- CHINA (HONG KONG)
Eligibility of fellows: nationality/ies:
- Contact phone: +39 0461 281620 - 1157 - 1914 - 1969 - 3547