ReviewBlood2014
Erythro-megakaryocytic transcription factors associated with hereditary anemia.
Review in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 60 citations in OpenAlex.
- Genetic variability in thrombopoietin receptor and GATA1 influences response to eltrombopag in dengue-induced thrombocytopenia.Scientific reports · 2026Trial
- Quantitative analysis of DNA-GATA1 binding alterations linked to hematopoietic disorders.The FEBS journal · 2026Article
- Prognostic Value of MicroRNA Profiles in Septic Patients with Rare Hereditary Anemias: Insights from a Longitudinal Cohort Study.International journal of general medicine · 2026Article
- Lineage-Specific Disruption of Hematopoiesis by Oxaliplatin: Mechanisms of Erythropoietin Resistance and Immune Suppression.Journal of hematology and oncology research · 2026Article
- Single-cell transcriptomic profiling reveals cell type heterogeneity between HFpEF and HFrEF.Communications biology · 2025Article
- Article
- GATA1 in Normal and Pathologic Megakaryopoiesis and Platelet Development.Advances in experimental medicine and biology · 2024Review
- Article
- Cytopenia: a report of haplo-cord transplantation in twin brothers caused by a novel germline GATA1 mutation and family survey.Annals of hematology · 2023Article
- SATB1 Chromatin Loops Regulate Megakaryocyte/Erythroid Progenitor Expansion by Facilitating HSP70 and GATA1 Induction.Stem cells (Dayton, Ohio) · 2023Article
- Preclinical studies on the use of a P-selectin-blocking monoclonal antibody to halt progression of myelofibrosis in the Gata1Experimental hematology · 2023Article
- Bioinformatic Tools for the Identification of MicroRNAs Regulating the Transcription Factors in Patients with β-Thalassemia.Bioinformatics and biology insights · 2022Review
- A Positive Regulatory Feedback Loop between EKLF/KLF1 and TAL1/SCL Sustaining the Erythropoiesis.International journal of molecular sciences · 2021Article
- Molecular Mechanisms of the Genetic Predisposition to Acute Megakaryoblastic Leukemia in Infants With Down Syndrome.Frontiers in oncology · 2021Review
- Article
- Sensitive and In Situ Hemoglobin Detection Based on a Graphene Oxide Functionalized Microfiber.Nanomaterials (Basel, Switzerland) · 2020Article
- Cellular and Molecular Mechanisms of Environmental Pollutants on Hematopoiesis.International journal of molecular sciences · 2020Review
- Stress erythropoiesis: definitions and models for its study.Experimental hematology · 2020Review
- Acute Megakaryocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2020Review
- Novel targets to cure primary myelofibrosis from studies on Gata1IUBMB life · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Most heritable anemias are caused by mutations in genes encoding globins, red blood cell (RBC) membrane proteins, or enzymes in the glycolytic and hexose monophosphate shunt pathways. A less common class of genetic anemia is caused by mutations that alter the functions of erythroid transcription factors (TFs). Many TF mutations associated with heritable anemia cause truncations or amino acid substitutions, resulting in the production of functionally altered proteins. Characterization of these mutant proteins has provided insights into mechanisms of gene expression, hematopoietic development, and human disease. Mutations within promoter or enhancer regions that disrupt TF binding to essential erythroid genes also cause anemia and heritable variations in RBC traits, such as fetal hemoglobin content. Defining the latter may have important clinical implications for de-repressing fetal hemoglobin synthesis to treat sickle cell anemia and β thalassemia. Functionally important alterations in genes encoding TFs or their cognate cis elements are likely to occur more frequently than currently appreciated, a hypothesis that will soon be tested through ongoing genome-wide association studies and the rapidly expanding use of global genome sequencing for human diagnostics. Findings obtained through such studies of RBCs and associated diseases are likely generalizable to many human diseases and quantitative traits.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.