Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Identification of novel γ-globin inducers among all potential erythroid druggable targets

3 Mar 2022

Abstract excerpt

Human γ-globin is predominantly expressed in fetal liver erythroid cells during gestation from 2 nearly identical genes, HBG1 and HBG2, that are both perinatally silenced. Reactivation of these fetal genes in adult red blood cells can ameliorate many symptoms associated with the inherited β-globinopathies, sickle cell disease, and Cooley anemia. Although promising genetic strategies to reactivate the γ-globin...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Erythrocyte Function and Pathophysiology
Share to Hemoglobinopathies and Related Disorders
Share to Iron Metabolism and Disorders

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 35240686
DOI: 10.1182/bloodadvances.2021006802

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Identification of novel γ-globin inducers among all potential erythroid druggable targetsPMID 35240686Read ↗

CRISPR-Cas9 interrogation of a putative fetal globin repressor in human erythroid cellsSemantic proximity Read ↗

Identification of small molecule agonists of fetal hemoglobin expression for the treatment of sickle cell diseaseSemantic proximity Read ↗

CRISPR-Cas9 interrogation of a putative fetal globin repressor in human erythroid cellsSemantic proximity Read ↗

A Small Key for a Heavy Door: Genetic Therapies for the Treatment of HemoglobinopathiesSemantic proximity Read ↗

Natural regulatory mutations elevate the fetal globin gene via disruption of BCL11A or ZBTB7A binding.Semantic proximity Read ↗

EHMT1 and EHMT2 inhibition induces fetal hemoglobin expressionSemantic proximity Read ↗

Combined approaches for increasing fetal hemoglobin (HbF) and de novo production of adult hemoglobin (HbA) in erythroid cells from β-thalassemia patients: treatment with HbF inducers and CRISPR-Cas9 based genome editingSemantic proximity Read ↗

A Review of Gene Therapies for HemoglobinopathiesSemantic proximity Read ↗

A genome-editing strategy to treat β-hemoglobinopathies that recapitulates a mutation associated with a benign genetic condition.Semantic proximity Read ↗

Fetal globin gene repressors as drug targets for molecular therapies to treat the β-globinopathies.Semantic proximity Read ↗

Induction of fetal hemoglobin synthesis by CRISPR/Cas9-mediated editing of the human β-globin locusSemantic proximity Read ↗

Elevating fetal hemoglobin: recently discovered regulators and mechanismsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.