Accept Cookies?
Provided by OpenGlobal E-commerce

Please wait while your page loads ...

Activation of a type I interferon response associated with acute frataxin knockdown in iPSC-derived cardiomyocytes

Frataxin functions in the biogenesis of iron-sulfur clusters, which are prosthetic groups that are found in proteins involved in many biological processes. To study the changes associated with decreased frataxin in human cardiomyocytes, the authors developed a novel isogenic model by acutely knocking down frataxin, post-differentiation, in cardiomyocytes derived from induced pluripotent stem cells. Transcriptome analysis of four biological replicates identified severe mitochondrial dysfunction and a type I interferon response as the pathways most affected by frataxin knockdown. In iPSC-derived cardiomyocytes, loss of frataxin leads to mitochondrial dysfunction. The type I interferon response was activated in multiple cell types following acute frataxin knockdown and was caused, at least in part, by release of mitochondrial DNA into the cytosol, activating the cGAS-STING sensor pathway.

Read the Full article here
 


SHARE
 

Scientific News Archives

Tagged in
Scientific News

Beaker

Privacy Policy      Service Terms      Contact      Charity Navigator