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

The Energy Status of Astrocytes Is the Achilles' Heel of eIF2B-Leukodystrophy.

Cells - 22 Jul 2021

Herrero Melisa, Daw Maron, Atzmon Andrea, Elroy-Stein Orna

Abstract excerpt

Translation initiation factor 2B (eIF2B) is a master regulator of global protein synthesis in all cell types. The mild genetic Eif2b5(R132H) mutation causes a slight reduction in eIF2B enzymatic activity which leads to abnormal composition of mitochondrial electron transfer chain complexes and impaired oxidative phosphorylation. Previous work using primary fibroblasts isolated from Eif2b5(R132H/R132H) mice...

Read the complete abstract on PubMed

Topics

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

Share to Adenosine Triphosphate
Share to AMP-Activated Protein Kinases
Share to Astrocytes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Energy Metabolism

Share to Eukaryotic Initiation Factor-2B

Share to Leukoencephalopathies

Share to Mechanistic Target of Rapamycin Complex 1

Share to Reactive Oxygen Species

Source

Open in PubMed Open full text

Identifiers

PMID: 34440627
DOI: 10.3390/cells10081858
PMCID: PMC8393801

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The Energy Status of Astrocytes Is the Achilles' Heel of eIF2B-Leukodystrophy.PMID 34440627Read ↗

Mutant eIF2B leads to impaired mitochondrial oxidative phosphorylation in vanishing white matter disease.Semantic proximity Read ↗

The Translational Landscape of Reactive Astrocytes Reveals the Impact of eIF2B-mediated Dysregulation in VWM DiseaseSemantic proximity Read ↗

eIF2B localisation and its regulation during the integrated stress response is cell type specificSemantic proximity Read ↗

Vanishing white matter: a leukodystrophy due to astrocytic dysfunction.Semantic proximity Read ↗

Adult mouse eIF2Bε Arg191His astrocytes display a normal integrated stress response in vitro.Semantic proximity Read ↗

EIF2B5 mutations compromise GFAP+ astrocyte generation in vanishing white matter leukodystrophy.Semantic proximity Read ↗

Stem cell derived astrocytes with <i>POLG</i> mutations and mitochondrial dysfunction including abnormal NAD+ metabolism is toxic for neuronsSemantic proximity Read ↗

EIF2B2 mutations in vanishing white matter disease hypersuppress translation and delay recovery during the integrated stress response.Semantic proximity Read ↗

MS-driven metabolic alterations are recapitulated in iPSC-derived astrocytesSemantic proximity Read ↗

eIF2B activator prevents neurological defects caused by a chronic Integrated Stress ResponseSemantic proximity Read ↗

Heightened stress response in primary fibroblasts expressing mutant eIF2B genes from CACH/VWM leukodystrophy patients.Semantic proximity Read ↗

APOE genotype-dependent differences in human astrocytic energy metabolismSemantic proximity Read ↗

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