Supplementary Materials

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Ablation of Ulk1 in hematopoietic cells.
  • Fig. S2. Phenotyping of ablation of Ulk1 in hematopoietic cells.
  • Fig. S3. Developmental staging of erythroblasts in spleen and bone marrow of HbbTh3/+Ulk1+/+ and HbbTh3/+Ulk1−/− mice.
  • Fig. S4. Characteristics of autophagy in β-thalassemic RBC precursors.
  • Fig. S5. Ablation of Atg5 in erythroid cells.
  • Fig. S6. Elimination of insoluble α-globin by the proteasome and autophagy in β-thalassemic reticulocytes.
  • Fig. S7. Effects of systemic rapamycin on β-thalassemic erythropoiesis.
  • Fig. S8. Expression of Map1lc3bm (LC3) and Sqstm1 (p62) mRNAs in reticulocytes of HbbTh3/+Ulk1+/+ mice treated with rapamycin.
  • Fig. S9. Presence of free α-globin in CD34+ cell–derived erythroblasts from individuals with β-thalassemia.
  • Fig. S10. Rapamycin and MG132 treatment of CD34+ cells from normal donors or from individuals with β-thalassemia.
  • Fig. S11. Model for ULK1 kinase–dependent clearance of free α-globin in β-thalassemia.
  • Table S1. Effects of Ulk1 gene disruption on erythroid indices of β-thalassemic mice.
  • Table S2. Effects of Ulk1 loss on erythroid hyperplasia in β-thalassemic mice.
  • Table S3. Effects of Atg5 gene disruption on erythroid indices of β-thalassemic mice.
  • Table S4. Effects of systemic rapamycin on erythroid indices of β-thalassemic mice ± Ulk1 gene disruption.
  • Table S5. ULK1-dependent reduction of erythroid hyperplasia in β-thalassemic mice treated with rapamycin.
  • Table S6. Erythroid indices of individuals with β-thalassemia who provided CD34+ cells for this study.
  • Table S7. Genotypes of individuals with β-thalassemia who provided CD34+ cells for this study.
  • References (7276)

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