Accept Cookies?
Provided by OpenGlobal E-commerce

Please wait while your page loads ...

Silencing of frataxin gene expression triggers p53-dependent apoptosis in human neuron-like cells

Friedreich's ataxia (FRDA) is an autosomal recessive disease caused by mutations that produce a deficiency in frataxin. Despite the importance of neurodegeneration in FRDA, little is known about the consequences of frataxin deficiency in neuronal cells. Here we describe a neuronal cell model for FRDA based on the use of lentiviral vectors that carry minigenes encoding frataxin-specific shRNAs that silence the expression of this gene. These lentivectors can knockdown frataxin expression in human neuroblastoma SH-SY5Y cells, which results in large-scale cell death in differentiated neuron-like cells but not in undifferentiated neuroblastoma cells.

Silencing of frataxin gene expression triggers p53-dependent apoptosis in human neuron-like cells

SHARE

FacebookTwitterLinkedInYoutube
Family B.jpg

 

Archived in
  Scientific News


 

 

Tagged in
FARA Scientific News


Site Map     Privacy Policy     Service Terms     Log-in     Contact     Charity Navigator