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

Involvement of mitochondrial complex II defects in neuronal death produced by N-terminus fragment of mutated huntingtin.

Molecular biology of the cell - 1 Apr 2006

Benchoua Alexandra, Trioulier Yaël, Zala Diana, Gaillard Marie-Claude, Lefort Nathalie, Dufour Noelle, Saudou Frederic, Elalouf Jean-Marc, Hirsch Etienne, Hantraye Philippe, Déglon Nicole, Brouillet Emmanuel

Abstract excerpt

Alterations of mitochondrial function may play a central role in neuronal death in Huntington's disease (HD). However, the molecular mechanisms underlying such functional deficits of mitochondria are not elucidated yet. We herein showed that the expression of two important constituents of mitochondrial complex II, the 30-kDa iron-sulfur (Ip) subunit and the 70-kDa FAD (Fp) subunit, was preferentially decreased in...

Read the complete abstract on PubMed

Topics

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

Share to Corpus Striatum
Share to Electron Transport Complex II

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Huntingtin Protein

Share to Huntington Disease

Share to Iron-Sulfur Proteins

Share to Lentivirus

Share to Mitochondrial Proteins

Share to Succinate Dehydrogenase

Source

Open in PubMed Open full text

Identifiers

PMID: 16452635
DOI: 10.1091/mbc.e05-07-0607
PMCID: PMC1415305

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

Involvement of mitochondrial complex II defects in neuronal death produced by N-terminus fragment of mutated huntingtin.PMID 16452635Read ↗

A role of mitochondrial complex II defects in genetic models of Huntington's disease expressing N-terminal fragments of mutant huntingtin.Semantic proximity Read ↗

Mutant huntingtin induces iron overload via up-regulating IRP1 in Huntington’s diseaseSemantic proximity Read ↗

Dysregulation of gene expression in primary neuron models of Huntington's disease shows that polyglutamine-related effects on the striatal transcriptome may not be dependent on brain circuitry.Semantic proximity Read ↗

Dominant phenotypes produced by the HD mutation in STHdh(Q111) striatal cells.Semantic proximity Read ↗

Leucine 7 is a key residue for mutant huntingtin-induced mitochondrial pathology and neurotoxicity in Huntington's disease.Semantic proximity Read ↗

Mitochondria-targeted molecules MitoQ and SS31 reduce mutant huntingtin-induced mitochondrial toxicity and synaptic damage in Huntington's disease.Semantic proximity Read ↗

Reduced mitochondrial complex II activity enhances cell death via intracellular reactive oxygen species in STHdhQ111 striatal neurons with mutant huntingtin.Semantic proximity Read ↗

Extended polyglutamine repeats trigger a feedback loop involving the mitochondrial complex III, the proteasome and huntingtin aggregates.Semantic proximity Read ↗

The regulation of N-terminal Huntingtin (Htt552) accumulation by Beclin1.Semantic proximity Read ↗

Progressive and selective striatal degeneration in primary neuronal cultures using lentiviral vector coding for a mutant huntingtin fragment.Semantic proximity Read ↗

Heat shock protein 27 prevents cellular polyglutamine toxicity and suppresses the increase of reactive oxygen species caused by huntingtin.Semantic proximity Read ↗

MicroRNA-22 (miR-22) overexpression is neuroprotective via general anti-apoptotic effects and may also target specific Huntington's disease-related mechanisms.Semantic proximity Read ↗

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