scholarly journals Global transcriptome analyses of human and murine terminal erythroid differentiation

Blood ◽  
2014 ◽  
Vol 123 (22) ◽  
pp. 3466-3477 ◽  
Author(s):  
Xiuli An ◽  
Vincent P. Schulz ◽  
Jie Li ◽  
Kunlu Wu ◽  
Jing Liu ◽  
...  
Keyword(s):  
Erythroid Differentiation ◽  
Key Points ◽  
Global Transcriptome ◽  
Transcriptome Analyses ◽  
Significant Stage ◽  
Species Specific ◽  
Terminal Erythroid Differentiation

Key Points Transcriptome analyses of human and murine reveal significant stage and species-specific differences across stages of terminal erythroid differentiation. These transcriptomes provide a significant resource for understanding mechanisms of normal and perturbed erythropoiesis.

scholarly journals Quantitative analysis of murine terminal erythroid differentiation in vivo: novel method to study normal and disordered erythropoiesis

Blood ◽  
2013 ◽  
Vol 121 (8) ◽  
pp. e43-e49 ◽  
Author(s):  
Jing Liu ◽  
Jianhua Zhang ◽  
Yelena Ginzburg ◽  
Huihui Li ◽  
Fumin Xue ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Reliable Method ◽  
Erythroid Differentiation ◽  
Key Points ◽  
Novel Method ◽  
Terminal Erythroid Differentiation

Key Points The study establishes a reliable method to quantify differentiating mouse erythroblasts and to monitor terminal mouse erythropoiesis in vivo. Quantitative analysis of erythropoiesis of thalassemia mice revealed stage-specific changes in terminal erythroid differentiation.

scholarly journals Modified activin receptor IIB ligand trap mitigates ineffective erythropoiesis and disease complications in murine β-thalassemia

Blood ◽  
2014 ◽  
Vol 123 (25) ◽  
pp. 3864-3872 ◽  
Author(s):  
Rajasekhar N. V. S. Suragani ◽  
Sharon M. Cawley ◽  
Robert Li ◽  
Samantha Wallner ◽  
Mark J. Alexander ◽  
...  
Keyword(s):  
Iron Overload ◽  
Erythroid Differentiation ◽  
Bone Defects ◽  
Ineffective Erythropoiesis ◽  
Activin Receptor ◽  
Key Points ◽  
Terminal Erythroid Differentiation ◽  
Activin Receptor Iib

Key Points Modified ActRIIB ligand trap promotes terminal erythroid differentiation and mitigates ineffective erythropoiesis in murine β-thalassemia. This agent reduces anemia, α-globin aggregates, hemolysis, and disease complications such as iron overload, splenomegaly, and bone defects.

scholarly journals Widespread and dynamic translational control of red blood cell development

Blood ◽  
2017 ◽  
Vol 129 (5) ◽  
pp. 619-629 ◽  
Author(s):  
Juan R. Alvarez-Dominguez ◽  
Xu Zhang ◽  
Wenqian Hu
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Translational Control ◽  
Erythroid Differentiation ◽  
Cell Development ◽  
Key Points ◽  
Terminal Erythroid Differentiation

Key Points Critical roles for dynamic translational control during terminal erythroid differentiation. RBM38 can regulate translation during terminal erythropoiesis.

scholarly journals Severely impaired terminal erythroid differentiation as an independent prognostic marker in myelodysplastic syndromes

2018 ◽  
Vol 2 (12) ◽  
pp. 1393-1402 ◽  
Author(s):  
Abdullah Mahmood Ali ◽  
Yumin Huang ◽  
Ronald Feitosa Pinheiro ◽  
Fumin Xue ◽  
Jingping Hu ◽  
...  
Keyword(s):  
Prognostic Factor ◽  
Prognostic Marker ◽  
Myelodysplastic Syndromes ◽  
Erythroid Differentiation ◽  
Independent Prognostic Factor ◽  
Independent Prognostic Marker ◽  
Key Points ◽  
Terminal Erythroid Differentiation

Key Points TED is defective in patients with MDS. TED is an independent prognostic factor for survival in MDS.

scholarly journals Distinct roles for TET family proteins in regulating human erythropoiesis

Blood ◽  
2017 ◽  
Vol 129 (14) ◽  
pp. 2002-2012 ◽  
Author(s):  
Hongxia Yan ◽  
Yaomei Wang ◽  
Xiaoli Qu ◽  
Jie Li ◽  
John Hale ◽  
...  
Keyword(s):  
Erythroid Differentiation ◽  
Erythroid Progenitors ◽  
Key Points ◽  
Terminal Erythroid Differentiation

Key Points TET3 knockdown impairs terminal erythroid differentiation, whereas TET2 knockdown leads to accumulation of erythroid progenitors. Global levels of 5mC are not altered by knockdown of either TET2 or TET3.

scholarly journals The severe phenotype of Diamond-Blackfan anemia is modulated by heat shock protein 70

2017 ◽  
Vol 1 (22) ◽  
pp. 1959-1976 ◽  
Author(s):  
Marc Gastou ◽  
Sarah Rio ◽  
Michaël Dussiot ◽  
Narjesse Karboul ◽  
Hélène Moniz ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein 70 ◽  
Erythroid Differentiation ◽  
Severe Phenotype ◽  
Erythroid Progenitors ◽  
Erythroid Progenitor ◽  
Diamond Blackfan Anemia ◽  
Erythroid Progenitor Cells ◽  
Key Points ◽  
Terminal Erythroid Differentiation

Key Points Proteasomal HSP70 degradation results in cleavage of GATA1, decrease in erythroid progenitors, and apoptosis in severe DBA phenotype. HSP70 plays a role not only during terminal erythroid differentiation, but also in the earlier proliferation of erythroid progenitor cells.

scholarly journals Unexpected role for p19INK4d in posttranscriptional regulation of GATA1 and modulation of human terminal erythropoiesis

Blood ◽  
2017 ◽  
Vol 129 (2) ◽  
pp. 226-237 ◽  
Author(s):  
Xu Han ◽  
Jieying Zhang ◽  
Yuanliang Peng ◽  
Minyuan Peng ◽  
Xiao Chen ◽  
...  
Keyword(s):  
Protein Level ◽  
Posttranscriptional Regulation ◽  
Erythroid Differentiation ◽  
Protein Levels ◽  
Key Points ◽  
Terminal Erythroid Differentiation

Key Points Knockdown of CDKI p19INK4d impairs human terminal erythroid differentiation by decreasing GATA1 protein levels. GATA1 protein level is regulated by p19INK4d via the PEBP1-p-ERK-HSP70-GATA1 pathway.

Luspatercept in the treatment of lower-risk myelodysplastic syndromes

2021 ◽  
Author(s):  
Onyee Chan ◽  
Rami S Komrokji
Keyword(s):  
Clinical Trials ◽  
Myelodysplastic Syndromes ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Safety Data ◽  
Erythroid Differentiation ◽  
Fda Approval ◽  
The Us ◽  
Us Fda ◽  
Terminal Erythroid Differentiation

Transforming growth factor beta (TGF-β) signaling pathway is key to hematopoiesis regulation. Increased activation of this pathway contributes to ineffective terminal erythroid differentiation in myelodysplastic syndromes (MDS). Luspatercept is a novel fusion protein that traps TGF-β ligands preventing them from binding to Type II TGF-β receptors, thereby decreasing phosphorylated SMAD2/3 resulting in the downstream effect of promoting erythropoiesis. Seminal clinical trials using luspatercept, PACE-MD and MEDALIST, demonstrated impressive efficacy in the treatment of transfusion-dependent anemia in intermediate risk or lower MDS had led to the US FDA approval for this indication. This review summarizes luspatercept mechanisms of action, efficacy/safety data supporting its use and ongoing clinical trials in MDS.

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