Evidence map›Paper›PMID 25178567›Full record

ArticleBrain pathology (Zurich, Switzerland)2015

The Differential Profiling of Ubiquitin-Proteasome and Autophagy Systems in Different Tissues before the Onset of Huntington's Disease Models.

Lu-Shiun Her, Jian-Yu Lin, Mu-Hui Fu, Yu-Fan Chang, Chia-Ling Li, Ting-Yu Tang, Yu-Ling Jhang, Chih-Yi Chang, Meng-Chi Shih, Pei-Hsun Cheng and 1 more

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 42% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Wild-type C9orf72 drives proteasomal dysfunction and mutant aggregates via a Stat1-Isg15 axis in Huntington's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Lu-Shiun HerDepartment of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
Jian-Yu LinDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Mu-Hui FuInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yu-Fan ChangDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Chia-Ling LiInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Ting-Yu TangDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Yu-Ling JhangDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Chih-Yi ChangDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Meng-Chi ShihDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Pei-Hsun ChengDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
Shang-Hsun YangDepartment of Physiology, National Cheng Kung University, Tainan, Taiwan.
National Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is a genetic and neurodegenerative disease, leading to motor and cognitive dysfunction in HD patients. At cellular level, this disease is caused by the accumulation of mutant huntingtin (HTT) in different cells, and finally results in the dysfunction of different cells. To clean these mutant proteins, ubiquitin-proteasome system (UPS) and autophagy system are two critical pathways in the brain; however, little is known in other peripheral tissues. As mutant HTT affects different tissues progressively and might influence the UPS and autophagy pathways at early stages, we attempted to examine two clearance systems in HD models before the onset. Here, in vitro results showed that the accumulation of UPS signals with time was observed obviously in neuroblastoma and kidney cells, not in other cells. In HD transgenic mice, we observed the impairment of UPS, but not autophagy, over time in the cortex and striatum. In heart and muscle tissues, disturbance of autophagy was observed, whereas dysfunction of UPS was displayed in liver and lung. These results suggest that two protein clearance pathways are disturbed differentially in different tissues before the onset of HD, and enhancement of protein clearance at early stages might provide a potential stratagem to alleviate the progression of HD.

Indexed as

AnimalsAutophagyBrainCell LineDisease Models, AnimalGreen Fluorescent ProteinsHumansHuntingtin ProteinHuntington DiseaseKidneyLiverLungMiceMice, TransgenicMusclesMutationGreen Fluorescent ProteinsHTT protein, humanHuntingtin ProteinNerve Tissue ProteinsProteasome Endopeptidase ComplexUbiquitinautophagyHuntington's disease (HD)protein clearancetransgenic miceubiquitin-proteasome system

Identifiers

PMID25178567
PMCPMC8029242
OpenAlexW1942205467

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.