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268 results for “Erythropoiesis”
Data for: The ErythronDB Dataset of the cellular and molecular underpinnings of mammalian erythropoiesis
<p>The Erythron Database (ErythronDB) was a resource dedicated to facilitating better understanding of the cellular and molecular underpinnings of mammalian erythropoiesis. For more information about this project, please visit <a href="https://cstoeckert.github.io/past-projects/ErythronDB.html" rel="nofollow">https://cstoeckert.github.io/past-projects/ErythronDB.html</a>.</p>
Data for: The ErythronDB Dataset of the cellular and molecular underpinnings of mammalian erythropoiesis
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Efficient globin production during terminal erythropoiesis depends on the synergistic action of TENT5C poly(A) polymerase and LARP4/5
<p><span><span>Red blood cell development is a unique process </span><span>where</span> <span>reduced</span> <span>transcriptome and proteome complexity</span> <span>facilitate</span><span>s</span><span> vast</span> <span>hemoglobin</span><span> production</span><span>. Here, we describe the cooperative role of cytoplasmic poly(A) polymerase </span><span>TENT5C </span><span>and the poly(A) tail-protecting </span><span>LARP4</span><span>/5 RNA-binding proteins in ensuring proper </span><span>hemoglobin production</span><span>. </span><span>TENT5C </span><span>catalytic mutant </span><span>knock-in </span><span>mice</span><span> display microcytic hypochromic anemia </span><span>resembling</span><span> constitutive knockout</span><span>. </span><span>TENT5C </span><span>counteracts gradual globin mRNA </span><span>deadenylation</span> <span>during</span><span> erythropoiesis. </span><span>In the late stages, TENT5C</span><span> dysfunction leads to globin poly(A) tail shortening and a </span><span>drastic reduction of mRNA</span> <span>level</span><span>s</span> <span>in reticulocytes. </span><span>P</span><span>roteomic experiments revealed </span><span>transient </span><span>but</span><span> specific</span><span> association of TENT5C with </span><span>LARP4</span><span>/5</span><span>. </span><span>Indeed</span><span>,</span><span> LARP</span><span>4/</span><span>5</span> <span>depletion </span><span>leads to downregulation and poly(A) tail shortening of globin mRNAs</span><span>.</span><span> Furthermore</span><span>,</span> <span>lack of TENT5C catalytic activity </span><span>is accompanied by </span><span>compensatory </span><span>upregulation </span><span>of </span><span>LARP4</span><span>/</span><span>5. </span><span>F</span><span>i</span><span>nally</span><span>, the</span><span> importance of</span><span> precise regulation of globin poly(A) tails </span><span>by </span><span>deadenylation</span><span> and re-adenylation </span><span>is highlighted by the destabilization of TENT5C </span><span>by</span><span> CCR4-</span><span>NOT </span><span>deadenylase</span><span> complex-associated </span><span>E3 </span><span>ubiquitin ligase </span><span>C</span><span>NOT4.</span></span><span> <br><br>This repository contains supplementary data accompanying related publication. The uploaded files contain following data:<br><br></span></p> <div> <p><span><strong><span>Supplementary </span><span>Data </span></strong><span><strong>1</strong> </span></span><span><span>DRS of E14.5 fetal livers, </span><span>poly(A) </span><span>profiling </span><span>stat</span><span>istics.</span></span><span> </span></p> </div> <div> <p><span><strong><span>Supplementary </span><span>Data </span><span>2</span></strong> </span><span><span>(A) All </span><span>identified</span><span> proteins </span><span>in the</span> <span>TurboID</span><span> assay </span><span>(B) Overlap between 3 replicates (C) Statistically significant GO terms for overlapping proteins with average specificity > 0.</span></span><span> </span></p> </div> <div> <p><span><strong><span>Supplementary </span><span>Data</span> <span>3</span></strong> </span><span><span>(A) Overview of used input and method details used in </span><span>degronopedia</span><span> analysis (B) Identified degron motifs (C) Degron conservation (D) Evolutionary conservation of TENT5C aa sequence scored by </span><span>ConSurf</span><span> (The table shows the residue variety in % for each position in the query sequence, each column shows the % for that amino acid found in position in the MSA)</span><span>.</span></span><span> </span></p> </div> <div> <p><span><strong><span>Supplementary </span><span>Data </span></strong><span><strong>4</strong> </span></span><span><span>Key resources table</span><span>.</span></span><span> </span></p> </div> <div> <p><span><span><strong>Supplementary Data 5</strong> </span></span><span><span>Oligonucleotides </span><span>used</span><span> in the study</span><span>.</span></span><span> </span></p> </div> <div> <p><strong><span><span>Supplementary Resource</span><span> 1</span> </span></strong><span><span>TurboID</span><span> assay</span></span> <span><span>MS/MS raw data</span><span>, each file in the</span><span> archive</span><span> corresponds to a </span><span>biological replicate of either WT (control) or </span></span><span><span>Tent5c-EGFP</span><span>.</span></span><span> </span></p> </div> <p><span> </span></p>
Single-cell profiling of human bone marrow progenitors reveals mechanisms of failing erythropoiesis in Diamond-Blackfan anemia
<p>Ribosome dysfunction underlies the pathogenesis of many cancers and heritable ribosomopathies. Here we investigate how mutations in either ribosomal protein large (RPL) or ribosomal protein small (RPS) subunit genes selectively affect erythroid progenitor development and clinical phenotypes in Diamond-Blackfan anemia (DBA), a rare ribosomopathy with limited therapeutic options. Using single-cell assays of patient-derived bone marrow, we delineated two distinct cellular trajectories segregating with ribosomal protein genotypes: almost complete loss of erythroid specification were observed in <em>RPS</em>-DBA. In contrast, we observed relative preservation of qualitatively abnormal erythroid progenitors and precursors in <em>RPL</em>-DBA. Although both DBA genotypes exhibited a pro-inflammatory bone marrow milieu, <em>RPS</em>-DBA was characterized by erythroid differentiation arrest, whereas <em>RPL</em>-DBA was characterized by preserved GATA1 expression and activity. Compensatory stress erythropoiesis in <em>RPL</em>-DBA exhibited disordered differentiation underpinned by an altered glucocorticoid molecular signature, including reduced <em>ZFP36L2</em> expression<em>,</em> leading to milder anemia and improved corticosteroid response. This integrative analysis approach identified distinct pathways of erythroid failure and defined genotype-phenotype correlations in DBA. These findings may help facilitate therapeutic target discovery.</p> <p> </p>
Anemia Studies in Chronic Kidney Disease: Erythropoiesis Via a Novel Prolyl Hydroxylase Inhibitor Daprodustat-Non-Dialysis (ASCEND-ND)
ClinicalTrials.gov study NCT02876835. IPD Sharing: YES. Countries: 39. Publications: 5.
Anemia Studies in Chronic Kidney Disease (CKD): Erythropoiesis Via a Novel Prolyl Hydroxylase Inhibitor (PHI) Daprodustat-in Incident Dialysis (ASCEND-ID)
ClinicalTrials.gov study NCT03029208. IPD Sharing: YES. Countries: 15. Publications: 2.
Study of Roxadustat (FG-4592) to Correct Anemia in Newly Initiated Dialysis Participants Not on Erythropoiesis-Stimulating Agent Treatment
ClinicalTrials.gov study NCT01414075. IPD Sharing: Not stated. Countries: 4. Publications: 1.
Trial Evaluating the Efficacy and Safety of Oral Vadadustat Once Daily (QD) and Three Times Weekly (TIW) for the Maintenance Treatment of Anemia in Hemodialysis Subjects Converting From Erythropoiesis
ClinicalTrials.gov study NCT04313153. IPD Sharing: NO. Countries: 6. Publications: 2.
A Study of Intravenous Iron Isomaltoside 1000 (Monofer®) as Mono Therapy (Without Erythropoiesis Stimulating Agents) in Comparison With Oral Iron Sulfate in Subjects With Non-myeloid Malignancies Asso
ClinicalTrials.gov study NCT01145638. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Anemia Studies in CKD: Erythropoiesis Via a Novel Prolyl Hydroxylase Inhibitor (PHI) Daprodustat- Iron (ASCEND: Fe)
ClinicalTrials.gov study NCT03457701. IPD Sharing: YES. Countries: 1. Publications: 1.
Anemia Study in Chronic Kidney Disease (CKD): Erythropoiesis Via a Novel Prolyl Hydroxylase Inhibitor (PHI) Daprodustat-Blood Pressure (ASCEND-BP)
ClinicalTrials.gov study NCT03029247. IPD Sharing: YES. Countries: 1. Publications: 1.
Anemia Studies in Chronic Kidney Disease (CKD): Erythropoiesis Via a Novel Prolyl Hydroxylase Inhibitor (PHI) Daprodustat-Three-times Weekly Dosing in Dialysis (ASCEND-TD)
ClinicalTrials.gov study NCT03400033. IPD Sharing: YES. Countries: 13. Publications: 2.
Study Evaluating the Efficacy and Safety of Dose Conversion From a Long-acting Erythropoiesis-stimulating Agent (Mircera®) to Three Times Weekly Oral Vadadustat for the Maintenance Treatment of Anemia
ClinicalTrials.gov study NCT04707768. IPD Sharing: NO. Countries: 1. Publications: 2.
Anemia Studies in Chronic Kidney Disease: Erythropoiesis Via a Novel Prolyl Hydroxylase Inhibitor Daprodustat-Dialysis (ASCEND-D)
ClinicalTrials.gov study NCT02879305. IPD Sharing: Not stated. Countries: 35. Publications: 6.
Efficacy and Safety Study of GSK1278863 in Japanese Hemodialysis Subjects With Anemia Associated With Chronic Kidney Disease Who Are Not Taking Erythropoiesis Stimulating Agents
ClinicalTrials.gov study NCT02829320. IPD Sharing: YES. Countries: 1. Publications: 1.
Anemia Study in Chronic Kidney Disease (CKD) : Erythropoiesis Via a Novel Prolyl Hydroxylase Inhibitor (PHI) Daprodustat -Forearm Blood Flow (ASCEND-FBF)
ClinicalTrials.gov study NCT03446612. IPD Sharing: YES. Countries: 1. Publications: 1.
Anemia Studies in Chronic Kidney Disease (CKD): Erythropoiesis Via a Novel Prolyl Hydroxylase Inhibitor (PHI) Daprodustat in Non-Dialysis Subjects Evaluating Hemoglobin (Hgb) and Quality of Life (ASCE
ClinicalTrials.gov study NCT03409107. IPD Sharing: YES. Countries: 14. Publications: 2.
The transcriptomic landscape of normal and ineffective erythropoiesis at single cell resolution
<p><span>Ineffective erythropoiesis, the death of maturing erythroid cells, is a common cause of anemia. To better understand why this occurs, we studied the fates and adaptations of single erythroid marrow cells from individuals with Diamond Blackfan anemia (DBA), del(5q) myelodysplastic syndrome (del(5q) MDS), and normal controls, and defined an unhealthy (vs. healthy) differentiation trajectory, using velocity pseudotime and cell surface protein assessment. The pseudotime trajectories diverge immediately after the cells upregulate transferrin receptor (CD71), import iron, and initiate heme synthesis, although cell death occurs much later. Cells destined to die highly express heme-responsive genes, including ribosomal protein and globin genes. In contrast, surviving cells downregulate heme synthesis, while upregulating DNA damage response, hypoxia, and HIF1 pathways. Surprisingly, 24±12% of cells from controls follow the unhealthy trajectory, implying that heme also regulates cell fate decisions during normal red cell production. Del(5q) MDS (unlike DBA) results from somatic mutations, so many normal (unmutated) erythroid cells persist. By independently tracking their trajectory, we gained insight into why they cannot expand to prevent anemia. In addition, we show that intron retention is especially prominent during red cell differentiation. The additional information provided by messages with retained introns also allowed us to align data from multiple independent experiments and thus accurately query the transcriptomic changes that occur as single erythroid cells mature. </span></p>
Erythropoiesis Stimulating Agents for Anemia Management in Egyptian Hemodialysis Patients
ClinicalTrials.gov study NCT05699109. IPD Sharing: NO. Countries: 1. Publications: 5.
A Model of Computer-assisted Prescription of Erythropoiesis-stimulating Agents (ESA) in Patients Under Hemodialysis
ClinicalTrials.gov study NCT04185519. IPD Sharing: NO. Countries: 1. Publications: 1.
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International Brain Laboratory public data
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OpenNeuro
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