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

Hexokinase I N-terminal based peptide prevents the VDAC1-SOD1 G93A interaction and re-establishes ALS cell viability.

Scientific reports - 10 Oct 2016

Magrì Andrea, Belfiore Ramona, Reina Simona, Tomasello Marianna Flora, Di Rosa Maria Carmela, Guarino Francesca, Leggio Loredana, De Pinto Vito, Messina Angela

Abstract excerpt

Superoxide Dismutase 1 mutants associate with 20-25% of familial Amyotrophic Lateral Sclerosis (ALS) cases, producing toxic aggregates on mitochondria, notably in spinal cord. The Voltage Dependent Anion Channel isoform 1 (VDAC1) in the outer mitochondrial membrane is a docking site for SOD1 G93A mutant in ALS mice and the physiological receptor of Hexokinase I (HK1), which is poorly expressed in mouse spinal...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis
Share to Binding, Competitive

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hexokinase

Share to Membrane Potential, Mitochondrial

Share to Molecular Targeted Therapy

Share to Motor Neurons

Share to Peptide Fragments

Share to Superoxide Dismutase-1

Source

Open in PubMed Open full text

Identifiers

PMID: 27721436
DOI: 10.1038/srep34802
PMCID: PMC5056396

Genes

SOD1
VDAC1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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

Hexokinase I N-terminal based peptide prevents the VDAC1-SOD1 G93A interaction and re-establishes ALS cell viability.PMID 27721436Read ↗

In vivo pathogenic role of mutant SOD1 localized in the mitochondrial intermembrane space.Semantic proximity Read ↗

Exposure of a cryptic Hsp70 binding site determines the cytotoxicity of the ALS-associated SOD1-mutant A4V.Semantic proximity Read ↗

Biochemical and biophysical properties of the novel ALS-linked hSOD1 mutants: an experimental study accompanied by in silico analysisSemantic proximity Read ↗

Hexokinase-I protection against apoptotic cell death is mediated via interaction with the voltage-dependent anion channel-1: mapping the site of binding.Semantic proximity Read ↗

Structural Properties and Interaction Partners of Familial ALS-Associated SOD1 MutantsSemantic proximity Read ↗

SOD1 Function and Its Implications for Amyotrophic Lateral Sclerosis Pathology: New and Renascent Themes.Semantic proximity Read ↗

Misfolded SOD1 forms high-density molecular complexes with synaptic molecules in mutant SOD1-linked familial amyotrophic lateral sclerosis cases.Semantic proximity Read ↗

ALS-linked mutant SOD1 induces ER stress- and ASK1-dependent motor neuron death by targeting Derlin-1.Semantic proximity Read ↗

A small-molecule inhibitor of SOD1-Derlin-1 interaction ameliorates pathology in an ALS mouse modelSemantic proximity Read ↗

Inhibition of SOD1 trimerization is a novel drug target for ALS diseaseSemantic proximity Read ↗

The Hexokinase 1 5'-UTR Mutation in Charcot-Marie-Tooth 4G Disease Alters Hexokinase 1 Binding to Voltage-Dependent Anion Channel-1 and Leads to Dysfunctional Mitochondrial Calcium Buffering.Semantic proximity Read ↗

Implications of fALS Mutations on Sod1 Function and Oligomerization in Cell Models.Semantic proximity Read ↗

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