Discover Community Create You

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

ATF4 Regulates MYB to Increase γ-Globin in Response to Loss of β-Globin.

Cell reports - 4 Aug 2020

Boontanrart Mandy Y, Schröder Markus S, Stehli Gautier M, Banović Marija, Wyman Stacia K, Lew Rachel J, Bordi Matteo, Gowen Benjamin G, DeWitt Mark A, Corn Jacob E

Abstract excerpt

β-Hemoglobinopathies can trigger rapid production of red blood cells in a process known as stress erythropoiesis. Cellular stress prompts differentiating erythroid precursors to express high levels of fetal γ-globin. However, the mechanisms underlying γ-globin production during cellular stress are still poorly defined. Here, we use CRISPR-Cas genome editing to model the stress caused by reduced levels of adult...

Read the complete abstract on PubMed

Topics

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

Share to Activating Transcription Factor 4
Share to beta-Globins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA, Intergenic

Share to Enhancer Elements, Genetic

Share to Fetal Hemoglobin

Share to gamma-Globins

Share to Hematopoietic Stem Cells

Share to Proto-Oncogene Proteins c-myb

Source

Identifiers

PMID: 32755585
DOI: 10.1016/j.celrep.2020.107993

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

ATF4 Regulates MYB to Increase γ-Globin in Response to Loss of β-Globin.PMID 32755585Read ↗

ATF4 mediates fetal globin upregulation in response to reduced β-globinSemantic proximity Read ↗

The HRI-regulated transcription factor ATF4 activates BCL11A transcription to silence fetal hemoglobin expressionSemantic proximity Read ↗

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

Molecular basis of β thalassemia and potential therapeutic targets.Semantic proximity Read ↗

Blood Relatives: Splicing Mechanisms underlying Erythropoiesis in Health and DiseaseSemantic proximity Read ↗

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

Editing an α-globin enhancer in primary human hematopoietic stem cells as a treatment for β-thalassemiaSemantic proximity Read ↗

Fetal hemoglobin regulation in β-thalassemia: heterogeneity, modifiers and therapeutic approachesSemantic proximity Read ↗

Single-cell and bulk transcriptomic analyses identify HSP90AA1- associated oxidative stress adaptation during impaired erythroid differentiation in β-thalassemiaSemantic proximity Read ↗

Three fingers on the switchSemantic proximity Read ↗

Recent Approaches for Manipulating Globin Gene Expression in Treating HemoglobinopathiesSemantic proximity Read ↗

Development of pathophysiologically relevant models of sickle cell disease and β-thalassemia for therapeutic studies.Semantic proximity Read ↗

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