ArticleProceedings of the National Academy of Sciences of the United States of America2015
Reduced DOCK4 expression leads to erythroid dysplasia in myelodysplastic syndromes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
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- A glycan-based approach to cell characterization and isolation: Hematopoiesis as a paradigm.The Journal of experimental medicine · 2022Article
- Machine learning assisted real-time deformability cytometry of CD34+ cells allows to identify patients with myelodysplastic syndromes.Scientific reports · 2022Article
- Global Proteomics Analysis of Bone Marrow: Establishing Talin-1 and Centrosomal Protein of 55 kDa as Potential Molecular Signatures for Myelodysplastic Syndromes.Frontiers in oncology · 2022Article
- DOCK4 as a Potential Biomarker Associated with Immune Infiltration in Stomach Adenocarcinoma: A Database Analysis.International journal of general medicine · 2022Article
- Revertant somatic mosaicism as a cause of cancer.Cancer science · 2021Review
- Epigenetic modifiers in normal and aberrent erythropoeisis.Seminars in hematology · 2021Review
- Role of Plasma Gelsolin Protein in the Final Stage of Erythropoiesis and in Correction of Erythroid Dysplasia In Vitro.International journal of molecular sciences · 2020Article
- The Transcriptional Network That Controls Growth Arrest and Macrophage Differentiation in the Human Myeloid Leukemia Cell Line THP-1.Frontiers in cell and developmental biology · 2020Article
- Loss of Function of DOCK4 in Myelodysplastic Syndromes Stem Cells is Restored by Inhibitors of DOCK4 Signaling Networks.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis.Cancer discovery · 2019Article
- Disruption of erythroid nuclear opening and histone release in myelodysplastic syndromes.Cancer medicine · 2019Article
- Identification and Classification of Differentially Expressed Genes and Network Meta-Analysis Reveals Potential Molecular Signatures Associated With Tuberculosis.Frontiers in genetics · 2019Article
- The Selection of a Hepatocyte Cell Line Susceptible toFrontiers in microbiology · 2019Article
- Article
- High expression ofOncotarget · 2017Article
- Therapy-related myeloid neoplasms: when genetics and environment collide.Nature reviews. Cancer · 2017Review
- Erythropoietin Receptor Signaling and Lipid Rafts.Vitamins and hormones · 2017Review
- Perturbed hematopoietic stem and progenitor cell hierarchy in myelodysplastic syndromes patients with monosomy 7 as the sole cytogenetic abnormality.Oncotarget · 2016Article
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Authors and funding
24 authors at 6 institutions in 2 countries.
Funding
Abstract
Anemia is the predominant clinical manifestation of myelodysplastic syndromes (MDS). Loss or deletion of chromosome 7 is commonly seen in MDS and leads to a poor prognosis. However, the identity of functionally relevant, dysplasia-causing, genes on 7q remains unclear. Dedicator of cytokinesis 4 (DOCK4) is a GTPase exchange factor, and its gene maps to the commonly deleted 7q region. We demonstrate that DOCK4 is underexpressed in MDS bone marrow samples and that the reduced expression is associated with decreased overall survival in patients. We show that depletion of DOCK4 levels leads to erythroid cells with dysplastic morphology both in vivo and in vitro. We established a novel single-cell assay to quantify disrupted F-actin filament network in erythroblasts and demonstrate that reduced expression of DOCK4 leads to disruption of the actin filaments, resulting in erythroid dysplasia that phenocopies the red blood cell (RBC) defects seen in samples from MDS patients. Reexpression of DOCK4 in -7q MDS patient erythroblasts resulted in significant erythropoietic improvements. Mechanisms underlying F-actin disruption revealed that DOCK4 knockdown reduces ras-related C3 botulinum toxin substrate 1 (RAC1) GTPase activation, leading to increased phosphorylation of the actin-stabilizing protein ADDUCIN in MDS samples. These data identify DOCK4 as a putative 7q gene whose reduced expression can lead to erythroid dysplasia.
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Registered trials
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