ArticleBlood advances2019
The E3 ligase adaptor molecule SPOP regulates fetal hemoglobin levels in adult erythroid cells.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Using Clustered Regularly Interspaced Short Palindromic Repeats gene editing to induce permanent expression of fetal hemoglobin in β-thalassemia and sickle cell disease: A comparative meta-analysis.Frontiers in medicine · 2022Pooled it
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Comprehensive Review of Genetic and Epigenetic Regulation of Fetal Hemoglobin in β-Hemoglobinopathies: From Molecular Mechanisms to Clinical Applications.Mediterranean journal of hematology and infectious diseases · 2026Review
- Cul3 substrate adaptor SPOP targets Nup153 for degradation.Molecular biology of the cell · 2025Article
- Review
- Article
- A Cell-Permeant Nanobody-Based Degrader That Induces Fetal Hemoglobin.ACS central science · 2022Article
- Identification and characterization of RBM12 as a novel regulator of fetal hemoglobin expression.Blood advances · 2022Article
- Article
- Dual function NFI factors control fetal hemoglobin silencing in adult erythroid cells.Nature genetics · 2022Article
- Multi-Omics Analysis in β-Thalassemia Using anInternational journal of molecular sciences · 2022Article
- SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia.Cancer discovery · 2022Article
- Heterogeneity of fetal hemoglobin production in adult red blood cells.Current opinion in hematology · 2021Review
- Manipulation of Developmental Gamma-Globin Gene Expression: an Approach for Healing Hemoglobinopathies.Molecular and cellular biology · 2020Review
- HRI depletion cooperates with pharmacologic inducers to elevate fetal hemoglobin and reduce sickle cell formation.Blood advances · 2020Article
- Article
- Article
- SPOP and cancer: a systematic review.American journal of cancer research · 2020Review
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 1 country.
Funding
Abstract
Reactivation of fetal hemoglobin (HbF) production benefits patients with sickle cell disease and β-thalassemia. To identify new HbF regulators that might be amenable to pharmacologic control, we screened a protein domain-focused CRISPR-Cas9 library targeting chromatin regulators, including BTB domain-containing proteins. Speckle-type POZ protein (SPOP), a substrate adaptor of the CUL3 ubiquitin ligase complex, emerged as a novel HbF repressor. Depletion of SPOP or overexpression of a dominant negative version significantly raised fetal globin messenger RNA and protein levels with minimal detrimental effects on normal erythroid maturation, as determined by transcriptome and proteome analyses. SPOP controls HbF expression independently of the major transcriptional HbF repressors BCL11A and LRF. Finally, pharmacologic HbF inducers cooperate with SPOP depletion during HbF upregulation. Our study implicates SPOP and the CUL3 ubiquitin ligase system in controlling HbF production in human erythroid cells and may offer new therapeutic strategies for the treatment of β-hemoglobinopathies.
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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.