IBRI RESEARCH PUBLISHED: The T1D-associated lncRNA Lnc13 modulates human pancreatic ß cell inflammation by allele-specific stabilization of STAT1 mRNA
The mechanisms by which autoimmunity is amplified in type 1 diabetes (T1D) remain to be clarified, and the lack of this understanding hampers efforts to prevent or arrest the disease.
The majority of T1D genetic association signals lie in noncoding regions of the human genome. Many have been predicted to affect the expression and secondary structure of long noncoding RNAs (lncRNAs), but the contribution of these lncRNAs to the pathogenesis of T1D remains to be clarified.
This paper describes a molecular mechanism by which the T1D-associated lncRNA Lnc13 regulates pancreatic β-cell inflammation via regulation of the key transcription factor STAT-1. These findings provide information on the molecular mechanisms by which disease-associated SNPs in lncRNAs influence disease pathogenesis and open the door for the development of novel diagnostic and therapeutic approaches based on lncRNA targeting.
To read the complete research article, go to Proceedings of the National Academy of Sciences of the United States of America.