Evidence map›Paper›PMID 20304926›Full record

ArticleThe Journal of biological chemistry2010

Huntingtin-associated protein-1 deficiency in orexin-producing neurons impairs neuronal process extension and leads to abnormal behavior in mice.

Yung-Feng Lin, Xingshun Xu, Austin Cape, Shihua Li, Xiao-Jiang Li

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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  7. Loss of Hap1 selectively promotes striatal degeneration in Huntington disease mice.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

5 authors at 1 institution in 1 country.

Yung-Feng LinDepartment of Human Genetics, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Xingshun Xu
Austin Cape
Shihua Li
Xiao-Jiang Li
Emory University · US

Funding

Neuronal function of huntingtin-associated proteinR01NS036232 · NINDS · EMORY UNIVERSITY · PI ESCAYG, ANDREW P · 1998 to 2021
$6.7M
Polyglutamine expansion and neuropathologyR01NS045016 · NINDS · EMORY UNIVERSITY · PI LI, SHI-HUA · 2004 to 2013
$2.9M
Glial huntingtin and neuronal excitotoxicityR01AG031153 · NIA · EMORY UNIVERSITY · PI LI, SHI-HUA · 2009 to 2013
$1.5M
NIA NIH HHS R01 AG031153NINDS NIH HHS NS036232NINDS NIH HHS NS045016NINDS NIH HHS R01 NS036232NINDS NIH HHS R01 NS045016
6 · The paper itself

Abstract

Huntingtin-associated protein-1 (Hap1) is a neuronal protein that associates with huntingtin, the Huntington disease protein. Although Hap1 and huntingtin are known to be involved in intracellular trafficking, whether and how the impairment of Hap1-associated trafficking leads to neurological pathology and symptoms remain to be seen. As Hap1 is enriched in neuronal cells in the brain, addressing this issue is important in defining the role of defective intracellular trafficking in the selective neuropathology associated with Hap1 dysfunction. Here, we find that Hap1 is abundantly expressed in orexin (hypocretin)-producing neurons (orexin neurons), which are distinctly distributed in the hypothalamus and play an important role in the regulation of feeding and behavior. We created conditional Hap1 knock-out mice to selectively deplete Hap1 in orexin neurons via the Cre-loxP system. These mice show process fragmentation of orexin neurons and reductions in food intake, body weight, and locomotor activity. Sucrose density gradient fractionation reveals that loss of Hap1 in the mouse brain also reduces the distribution of trafficking protein complexes and cargo proteins in the fractions that are enriched in synaptosomes. These results suggest that Hap1 is critical for the transport of multiple proteins to the nerve terminals to maintain the integrity of neuronal processes and that selective disruption of the processes of orexin neurons can cause abnormal feeding and locomotor activity.

Indexed as

AnimalsBiological TransportEatingFeeding BehaviorHumansHuntingtin ProteinHuntington DiseaseHypothalamusIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMotor ActivityNerve Tissue ProteinsNeuronsNeuropeptidesNuclear ProteinsHap1 protein, mouseHtt protein, mouseHuntingtin ProteinIntracellular Signaling Peptides and ProteinsNerve Tissue ProteinsNeuropeptidesNuclear ProteinsOrexins

Identifiers

PMID20304926
PMCPMC2871462
OpenAlexW1988703154

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.