Evidence map›Paper›PMID 21357679›Full record

ArticleHuman molecular genetics2011

Growth arrest-specific 1 binds to and controls the maturation and processing of the amyloid-beta precursor protein.

Julien Chapuis, Valérie Vingtdeux, Fabien Campagne, Peter Davies, Philippe Marambaud

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

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  9. Growth arrest specific 1 (GAS1) is abundantly expressed in the adult mouse central nervous system.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013
    Article
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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 3 institutions in 1 country.

Julien ChapuisLitwin-Zucker Research Center for the Study of Alzheimer's Disease, The Feinstein Institute for Medical Research, North Shore-LIJ, Manhasset, NY 11030, USA.
Valérie Vingtdeux
Fabien Campagne
Peter Davies
Philippe Marambaud
Albert Einstein College of Medicine · USFeinstein Institute for Medical Research · USCornell University · US

Funding

A Mouse Model of Tau Pathology in AD &Other DementiasR37AG022102 · NIA · YESHIVA UNIVERSITY · PI DAVIES, PETER P · 2003 to 2012
$3.7M
A Mouse Model of Tau Pathology in AD and Other DementiasR01AG022102 · NIA · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DAVIES, PETER P · 2013 to 2017
$1.7M
NIA NIH HHS R01 AG022102NIA NIH HHS R37 AG022102
6 · The paper itself

Abstract

Alzheimer's disease (AD), the most common neurodegenerative disorder, is characterized by cerebral deposition of amyloid-β (Aβ), a series of peptides derived from the processing of the amyloid-β precursor protein (APP). To identify new candidate genes for AD, we recently performed a transcriptome analysis to screen for genes preferentially expressed in the hippocampus and located in AD linkage regions. This strategy identified CALHM1 (calcium homeostasis modulator 1), a gene modulating AD age at onset and Aβ metabolism. Here, we focused our attention on another candidate identified using this screen, growth arrest-specific 1 (Gas1), a gene involved in the central nervous system development. We found that Gas1 formed a complex with APP and controlled APP maturation and processing. Gas1 expression inhibited APP full glycosylation and routing to the cell surface by leading to a trafficking blockade of APP between the endoplasmic reticulum and the Golgi. Gas1 expression also resulted in a robust inhibition of APP transport into multivesicular bodies, further demonstrating that Gas1 negatively regulated APP intracellular trafficking. Consequently, Gas1 overexpression led to a reduction in Aβ production, and conversely, Gas1 silencing in cells expressing endogenously Gas1 increased Aβ levels. These results suggest that Gas1 is a novel APP-interacting protein involved in the control of APP maturation and processing.

Indexed as

Protein Processing, Post-TranslationalAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCell Cycle ProteinsCell LineEndoplasmic ReticulumFemaleGene OrderGenetic Predisposition to DiseaseGlycosylationGolgi ApparatusGPI-Linked ProteinsHEK293 CellsHumansMiceAmyloid beta-Protein PrecursorCell Cycle ProteinsGAS1 protein, humanGPI-Linked Proteins

Identifiers

PMID21357679
PMCPMC3279048
OpenAlexW2113476847

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.