ArticleACS central science2022
A Cell-Permeant Nanobody-Based Degrader That Induces Fetal Hemoglobin.
Article in ACS central science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 41 citations in OpenAlex.
- Protein Modifications for Cellular Protein Delivery.Chemical reviews · 2026Review
- Intracellular Delivery of Peptides and Proteins with an Engineered Membrane Translocation Domain.ACS chemical biology · 2026Article
- No Time to Fold: Intrinsically Disordered Microproteins in Action.Biochemistry · 2026Review
- The NanoBridge system for targeted post-translational modification of challenging proteins.bioRxiv : the preprint server for biology · 2026Article
- Hypervariable loop profiling decodes sequence determinants of antibody stability.Nature structural & molecular biology · 2026Article
- Molecular engineering of lysosome-based degraders unveils a rapidly expanding therapeutic strategy.Autophagy · 2026Review
- Targeted protein degradation for fetal hemoglobin induction: a new paradigm in β-hemoglobinopathy therapy.Biomarker research · 2026Review
- Nanobody-based bioPROTAC for viral protein degradation provides an antiviral strategy for porcine arterivirus.Journal of nanobiotechnology · 2026Article
- Emerging biologic modalities for targeted protein degradation.The Journal of biological chemistry · 2026Review
- Intracellular Delivery of Peptides and Proteins with an Engineered Membrane Translocation Domain.bioRxiv : the preprint server for biology · 2026Article
- Evolution of proteolysis-targeting chimeras (PROTAC) technology to overcome challenges of antimicrobial resistance.npj antimicrobials and resistance · 2025Review
- Development of a p62 biodegrader for autophagy targeted degradation.Nature communications · 2025Article
- Targeted degradation of endogenous YAP by nanobody bioPROTAC inhibits tumor progression.Nature communications · 2025Article
- The biophysical requirements that govern the efficient endosomal escape of designed mini-proteins.Nature chemistry · 2025Article
- Hastened Fusion-Dependent Endosomal Escape Improves Activity of Delivered Enzyme Cargo.ACS central science · 2025Article
- Engineering Cell-Specific Protein Delivery Vehicles for Erythroid Lineage Cells.ACS bio & med chem Au · 2025Article
- Protein-Based Degraders: From Chemical Biology Tools to Neo-Therapeutics.Chemical reviews · 2025Review
- Article
- Hemoglobin Variants as Targets for Stabilizing Drugs.Molecules (Basel, Switzerland) · 2025Review
- A potent and selective anti-glutathione peroxidase 4 nanobody as a ferroptosis inducer.Chemical science · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Proximity-based strategies to degrade proteins have enormous therapeutic potential in medicine, but the technologies are limited to proteins for which small molecule ligands exist. The identification of such ligands for therapeutically relevant but "undruggable" proteins remains challenging. Herein, we employed yeast surface display of synthetic nanobodies to identify a protein ligand selective for BCL11A, a critical repressor of fetal globin gene transcription. Fusion of the nanobody to a cell-permeant miniature protein and an E3 adaptor creates a degrader that depletes cellular BCL11A in differentiated primary erythroid precursor cells, thereby inducing the expression of fetal hemoglobin, a modifier of clinical severity of sickle cell disease and β-thalassemia. Our strategy provides a means of fetal hemoglobin induction through reversible, temporal modulation of BCL11A. Additionally, it establishes a new paradigm for the targeted degradation of previously intractable proteins.
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.