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

Targeting the UPR transcription factor XBP1 protects against Huntington's disease through the regulation of FoxO1 and autophagy

14 Feb 2012

Abstract excerpt

Mutations leading to expansion of a poly-glutamine track in Huntingtin (Htt) cause Huntington's disease (HD). Signs of endoplasmic reticulum (ER) stress have been recently reported in animal models of HD, associated with the activation of the unfolded protein response (UPR). Here we have investigated the functional contribution of ER stress to HD by targeting the expression of two main UPR transcription factors,...

Read the complete abstract on PubMed

Topics

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

Share to Autophagy in Disease and Therapy
Share to Endoplasmic Reticulum Stress and Disease
Share to Genetic Neurodegenerative Diseases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 22337954
DOI: 10.1093/hmg/dds040

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Targeting the UPR transcription factor XBP1 protects against Huntington's disease through the regulation of FoxO1 and autophagyPMID 22337954Read ↗

Crosstalk between the UPR and autophagy pathway contributes to handling cellular stress in neurodegenerative diseaseSemantic proximity Read ↗

The unfolded protein response and its potential role in Huntington's disease elucidated by a systems biology approachSemantic proximity Read ↗

XBP-1 deficiency in the nervous system reveals a homeostatic switch to activate autophagySemantic proximity Read ↗

Enforced dimerization between XBP1s and ATF6f enhances the protective effects of the UPR in models of neurodegeneration.Semantic proximity Read ↗

The unfolded protein response transcription factor XBP1s ameliorates Alzheimer’s disease by improving synaptic function and proteostasisSemantic proximity Read ↗

Enforced dimerization between XBP1s and ATF6f enhances the protective effects of the unfolded protein response (UPR) in models of neurodegenerationSemantic proximity Read ↗

Insulin-like growth factor 2 (IGF2) protects against Huntington’s disease through the extracellular disposal of protein aggregatesSemantic proximity Read ↗

Induction of the Endoplasmic-Reticulum-Stress Response: MicroRNA-34a Targeting of the IRE1α-BranchSemantic proximity Read ↗

PGC-1α rescues Huntington's disease proteotoxicity by preventing oxidative stress and promoting TFEB function.Semantic proximity Read ↗

Amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease (AD) are characterised by differential activation of ER stress pathways: focus on UPR target genesSemantic proximity Read ↗

Optimized AAV to express the unfolded protein response transcription factor XBP1s ameliorates Alzheimer’s disease features in mouse modelsSemantic proximity Read ↗

Control of mammalian brain ageing by the unfolded protein response transcription factor XBP1Semantic proximity Read ↗

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