Evidence map›Paper›PMID 25071441›Full record

ReviewFrontiers in molecular neuroscience2014

Interaction of LRRK2 with kinase and GTPase signaling cascades.

Joon Y Boon, Julien Dusonchet, Chelsea Trengrove, Benjamin Wolozin

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Affective phenotypes in heterozygousFrontiers in genetics · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Exploring the focal role of LRRK2 kinase in Parkinson's disease.Environmental science and pollution research international · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. The Drosophila hep pathway mediates Lrrk2-induced neurodegeneration.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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

4 authors at 1 institution in 1 country.

Joon Y BoonDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine Boston, MA, USA.
Julien DusonchetDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine Boston, MA, USA.
Chelsea TrengroveDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine Boston, MA, USA.
Benjamin WolozinDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine Boston, MA, USA ; Neurology, Boston University School of Medicine Boston, MA, USA.
Boston University · US

Funding

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
Identification of compounds that inhibit aggregation and toxicity of TDP-43R21NS073679 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2011 to 2012
$486k
The Role of Stress Granules in the Pathophysiology of TDP-43R21NS066108 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2010 to 2011
$436k
NIEHS NIH HHS R01 ES020395NINDS NIH HHS R01 NS060872NINDS NIH HHS R21 NS066108NINDS NIH HHS R21 NS073679
6 · The paper itself

Abstract

LRRK2 is a protein that interacts with a plethora of signaling molecules, but the complexity of LRRK2 function presents a challenge for understanding the role of LRRK2 in the pathophysiology of Parkinson's disease (PD). Studies of LRRK2 using over-expression in transgenic mice have been disappointing, however, studies using invertebrate systems have yielded a much clearer picture, with clear effects of LRRK2 expression, knockdown or deletion in Caenorhabditis elegans and Drosophila on modulation of survival of dopaminergic neurons. Recent studies have begun to focus attention on particular signaling cascades that are a target of LRRK2 function. LRRK2 interacts with members of the mitogen activated protein kinase (MAPK) pathway and might regulate the pathway action by acting as a scaffold that directs the location of MAPK pathway activity, without strongly affecting the amount of MAPK pathway activity. Binding to GTPases, GTPase-activating proteins and GTPase exchange factors are another strong theme in LRRK2 biology, with LRRK2 binding to rac1, cdc42, rab5, rab7L1, endoA, RGS2, ArfGAP1, and ArhGEF7. All of these molecules appear to feed into a function output for LRRK2 that modulates cytoskeletal outgrowth and vesicular dynamics, including autophagy. These functions likely impact modulation of α-synuclein aggregation and associated toxicity eliciting the disease processes that we term PD.

Indexed as

actinautophagycell deathcytoskeletondopamineGTPasekinasetrafficking

Identifiers

PMID25071441
PMCPMC4087324
OpenAlexW2017708065

What OpenQuestion holds

Textmetadata
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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.