ReviewChemMedChem2020
Targeted Protein Degradation as a Promising Tool for Epigenetic Upregulation of Fetal Hemoglobin.
Review in ChemMedChem, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 12 citations in OpenAlex.
- Targeted protein degradation for fetal hemoglobin induction: a new paradigm in β-hemoglobinopathy therapy.Biomarker research · 2026Review
- Comprehensive regulation of γ-globin expression by epigenetic modifications and protein post-translational modifications.Clinical epigenetics · 2025Review
- A cellular reporter system to evaluate endogenous fetal hemoglobin induction and screen for therapeutic compounds.HemaSphere · 2024Article
- In Silico Molecular Docking and Dynamics Simulation Analysis of Potential Histone Lysine Methyl Transferase Inhibitors for Managing β-Thalassemia.Molecules (Basel, Switzerland) · 2023Article
- Effective therapies for sickle cell disease: are we there yet?Trends in genetics : TIG · 2022Review
- Novel PRMT5 Inhibitors for Treating Cancer.ACS medicinal chemistry letters · 2021Article
- Targeted protein degradation: A promise for undruggable proteins.Cell chemical biology · 2021Review
- Recent Approaches for Manipulating Globin Gene Expression in Treating Hemoglobinopathies.Frontiers in genome editing · 2021Review
- Targeted Protein Degradation as a Promising Tool for Epigenetic Upregulation of Fetal Hemoglobin.ChemMedChem · 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The level of fetal hemoglobin (HbF) is an important disease modifier for β-thalassemia and sickle cell disease patients. Indeed, genetic tinkering with the HbF repression machinery has demonstrated great potential for disease mitigation. Such genetic treatments are costly and the high incidence of β-hemoglobinopathies in low-income countries, therefore, calls for the development of affordable, off-the-shelf, oral treatments. The use of PROTAC (PRoteolysis TArgeting Chimeras) technology to influence the epigenetic mechanisms involved in HbF suppression may provide a solution. In this minireview, we briefly explain the HbF repression network highlighting the epigenetic factors that could be targeted for degradation by PROTACs. We hope that this review will inspire clinicians, molecular and chemical biologists to collaborate and contribute to this fascinating field, which should ultimately deliver drugs that reactivate HbF expression with high specificity and low toxicity.
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.