The Non-Malignant Channel on VJHemOnc is an independent medical education platform, supported with funding from Agios (Gold). Supporters have no influence on the production of content. The levels of sponsorship listed are reflective of the amount of funding given.
The Thalassemia Channel on VJHemOnc is an independent medical education platform, supported with funding from Agios (Gold). Supporters have no influence on the production of content. The levels of sponsorship listed are reflective of the amount of funding given.
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.
