EHA 2021 | MIR-451 function on ULK1-mediated autophagy of free alpha-globin in beta-thalassemia
Christophe Lechauve, PhD, St. Jude Children’s Research Hospital, Memphis, TN, shares an overview of the key points from his presentation on miR-144/451 function in ULK1-mediated autophagy of free alpha-globin in beta-thalassemia. Dr Lechauve talks on the rationale and results of the study. The study reported that genetic elimination of miR-451 alleviates beta-thalassemia and that loss of miR-144/451 decreased erythroid mTORC1 activity in beta-thalassemic erythroblasts by 33%. In mice with beta-thalassemia, elimination of miR-144/451 caused a 92% reduction of erythrocyte alpha-globin precipitates and a 27% increase in erythrocyte count, as well as a decrease in spleen weight. The benefits of miR-144-451 ablation were reduced by genetic ablation of Ulk1 or Cab39, indicating that miR-451 loss stimulates ULK1-mediated autophagy of free alpha-globin through the AMPK/mTORC1 pathway. This interview took place at the virtual European Hematology Association (EHA) Congress 2021.
