Evidence map›Paper›PMID 24192129›Full record

ArticleNeuro-degenerative diseases2014

Regulation of autophagy by LRRK2 in Caenorhabditis elegans.

Shamol Saha, Liqun Liu-Yesucevitz, Benjamin Wolozin

Open access · greenAbstract read
In one paragraph

Article in Neuro-degenerative diseases, 2014. 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
1.0field-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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. The dopaminergic system ofRoyal Society open science · 2025
    Review
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  8. Models of LRRK2-Associated Parkinson's Disease.Advances in neurobiology · 2017
    Review
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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

3 authors at 1 institution in 1 country.

Shamol SahaDepartments of Pharmacology and Neurology, Boston University School of Medicine, Boston, Mass., USA.
Liqun Liu-Yesucevitz
Benjamin Wolozin
Boston University · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Stress Granules and the Biology of TDP-43R01ES020395 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2012 to 2016
$4.1M
LRRK2 and NeurodegenerationR01NS060872 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2009 to 2013
$1.9M
NIEHS NIH HHS R01 ES020395NIH HHS P40 OD010440NINDS NIH HHS NS06082NINDS NIH HHS R01 NS060872
6 · The paper itself

Abstract

backgroundMutations in LRRK2 (leucine-rich repeat kinase 2) are a common cause of familial Parkinson's disease. However, the mechanisms through which LRRK2 mutations contribute to neurodegeneration are poorly understood.

objectiveWe investigated the effects of WT, G2019S (GS), R1441C (RC) and kinase dead LRRK2 across multiple different cellular compartments in order to gain insight into the breadth of LRRK2 effects on cellular function.

methodsNematodes expressing lgg-1::RFP, hsp1::GFP, hsp4::GFP and hsp6::GFP were crossed to nematode lines expressing WT, GS, RC or kinase dead LRRK2.

resultsWe observed that GS and RC LRRK2 inhibited autophagy, while WT, GS and RC LRRK2 increased the response of the mitochondrial hsp6 reporter to stress. The response of the hsp reporters under basal conditions was more nuanced.

conclusionThese results support a putative role of LRRK2 in the autophagic and mitochondrial systems.

Indexed as

AnimalsAnimals, Genetically ModifiedAutophagyCaenorhabditis elegansLeucine-Rich Repeat ProteinsProteinsLeucine-Rich Repeat ProteinsProteins

Identifiers

PMID24192129
PMCPMC3946265
OpenAlexW1980236349

What OpenQuestion holds

Textmetadata
LicenceTDM
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.