A peptide derived from TID1S rescues frataxin deficiency and mitochondrial defects in FRDA cellular models

A peptide derived from TID1S rescues frataxin deficiency and mitochondrial defects in FRDA cellular models

Friedreich’s ataxia (FRDA), the most common recessive inherited ataxia, results from homozygous guanine–adenine–adenine (GAA) repeat expansions in intron 1 of the FXN gene, which leads to the deficiency of frataxin, a mitochondrial protein essential for iron-sulphur cluster synthesis. The study of f...

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Bibliographic Details
Main Authors: Yi Na Dong, Lucie Vanessa Ngaba, Jacob An, Miniat W. Adeshina, Nathan Warren, Johnathan Wong, David R. Lynch
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-03-01
Series:Frontiers in Pharmacology
Subjects:
Friedreich ataxia (FRDA)
frataxin
Tid1
mitochondrial fragmentation
ATP
Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2024.1352311/full

Internet

https://www.frontiersin.org/articles/10.3389/fphar.2024.1352311/full

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