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

Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington's model mice.

Human molecular genetics - 15 Feb 2015

Kurosawa Masaru, Matsumoto Gen, Kino Yoshihiro, Okuno Misako, Kurosawa-Yamada Mizuki, Washizu Chika, Taniguchi Harumi, Nakaso Kazuhiro, Yanagawa Toru, Warabi Eiji, Shimogori Tomomi, Sakurai Takashi, Hattori Nobutaka, Nukina Nobuyuki

Abstract excerpt

Huntington's disease (HD) is a dominantly inherited genetic disease caused by mutant huntingtin (htt) protein with expanded polyglutamine (polyQ) tracts. A neuropathological hallmark of HD is the presence of neuronal inclusions of mutant htt. p62 is an important regulatory protein in selective autophagy, a process by which aggregated proteins are degraded, and it is associated with several neurodegenerative...

Read the complete abstract on PubMed

Topics

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

Share to Autophagy
Share to Corpus Striatum

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hippocampus

Share to Huntington Disease

Share to Intracellular Space

Share to Intranuclear Inclusion Bodies

Share to Longevity

Share to Proteolysis

Source

Identifiers

PMID: 25305080
DOI: 10.1093/hmg/ddu522

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

Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington's model mice.PMID 25305080Read ↗

Mutant Huntingtin Disrupts the Nuclear Pore Complex.Semantic proximity Read ↗

Early autophagic response in a novel knock-in model of Huntington disease.Semantic proximity Read ↗

Transgenic models of Huntington'sdiseaseSemantic proximity Read ↗

Formation of polyglutamine inclusions in a wide range of non-CNS tissues in the HdhQ150 knock-in mouse model of Huntington's disease.Semantic proximity Read ↗

Role of TFEB in Huntington’s DiseaseSemantic proximity Read ↗

N-terminal Huntingtin Knock-In Mice: Implications of Removing the N-terminal Region of Huntingtin for Therapy.Semantic proximity Read ↗

Huntington's Disease Intranuclear Inclusions Contain Truncated, Ubiquitinated Huntingtin ProteinSemantic proximity Read ↗

p62/SQSTM1 differentially removes the toxic mutant androgen receptor via autophagy and inclusion formation in a spinal and bulbar muscular atrophy mouse model.Semantic proximity Read ↗

Progressive formation of inclusions in the striatum and hippocampus of mice transgenic for the human Huntington's disease mutation.Semantic proximity Read ↗

Mutant huntingtin interacts with the sterol regulatory element-binding proteins and impairs their nuclear import.Semantic proximity Read ↗

Subcellular Localization And Formation Of Huntingtin Aggregates Correlates With Symptom Onset And Progression In A Huntington’S Disease ModelSemantic proximity Read ↗

From neuronal inclusions to neurodegeneration: neuropathological investigation of a transgenic mouse model of Huntington'sdiseaseSemantic proximity Read ↗

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