Evidence map›Paper›PMID 31034808›Full record

ArticleExperimental neurology2019

Gnal haploinsufficiency causes genomic instability and increased sensitivity to haloperidol.

Mohammad Moshahid Khan, Jianfeng Xiao, T J Hollingsworth, Damini Patel, Dana E Selley, Trevor L Ring, Mark S LeDoux

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  6. 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

7 authors at 3 institutions in 1 country.

Mohammad Moshahid KhanDepartment of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, USA; Division of Rehabilitation Sciences, Department of Physical Therapy, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, USA; Neuroscience Institute, University of Tennessee Health Science Center, Memphis, TN 38163, USA. Electronic address: mkhan26@uthsc.edu.
Jianfeng XiaoDepartment of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, USA; Neuroscience Institute, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
T J HollingsworthNeuroscience Institute, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Damini PatelDepartment of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Dana E SelleyDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Trevor L RingDepartment of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Mark S LeDouxDepartment of Psychology, University of Memphis, Memphis, TN 38152, USA. Electronic address: msledoux@memphis.edu.
University of Tennessee Health Science Center · USUniversity of Memphis · USVirginia Commonwealth University · US

Funding

VCU Center for Drug Addiction ResearchP30DA033934 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI Matthew Sean Halquist · 2014 to 2026
$13.8M
Genetics and Biology of CIZ1 in Cervical DystoniaR01NS082296 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEDOUX, MARK S · 2013 to 2016
$1.3M
The Role of THAP1 in DystoniaR01NS069936 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEDOUX, MARK S · 2010 to 2013
$1.3M
The Role of UBTF in Undiagnosed Neurodevelopmental DisordersR21GM118962 · NIGMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI HORI, RODERICK T · 2016 to 2017
$456k
Pathophysiology of Paroxysmal DyskinesiasR56NS094965 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEDOUX, MARK S · 2017 to 2017
$438k
Mouse Models of Paroxysmal Non-kinesigenic DyskinesiaR03NS101485 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI XIAO, JIANFENG · 2018 to 2019
$152k
NIDA NIH HHS P30 DA033934NIGMS NIH HHS R21 GM118962NINDS NIH HHS R01 NS069936NINDS NIH HHS R01 NS082296NINDS NIH HHS R03 NS101485NINDS NIH HHS R56 NS094965
6 · The paper itself

Abstract

GNAL encodes guanine nucleotide-binding protein subunit Gα(olf) which plays a key role in striatal medium spiny neuron (MSN)-dopamine signaling. GNAL loss-of-function mutations are causally-associated with isolated dystonia, a movement disorder characterized by involuntary muscle contractions leading to abnormal postures. Dopamine D2 receptor (D2R) blockers such as haloperidol are mainstays in the treatment of psychosis but may contribute to the development of secondary acute and tardive dystonia. Administration of haloperidol promotes cAMP-dependent signaling in D2R-expressing indirect pathway MSNs. At present, little is known about the cellular relationships among isolated, acute, and tardive dystonia. Herein, we report the effects of acute D2R blockade on motor behavior, DNA repair, cAMP-mediated histone H3 phosphorylation (Ser10), and cell death in Gnal

Indexed as

AnimalsBrainDopamine AntagonistsFemaleGenomic InstabilityGTP-Binding Protein alpha SubunitsHaloperidolHaploinsufficiencyMaleMiceTardive DyskinesiaDopamine AntagonistsGTP-Binding Protein alpha SubunitsHaloperidololfactory G protein subunit alpha olfCatalepsyDNA methylationDopamine receptorDystoniaGα(olf)HaloperidolHistoneStriatum

Identifiers

PMID31034808
PMCPMC7962478
OpenAlexW2940474588

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.