Evidence map›Paper›PMID 34802187›Full record

ArticleAnnals of clinical and translational neurology2021

Pharmacological perturbation reveals deficits in D2 receptor responses in Thap1 null mice.

Natalie M Frederick, Morgan M Pooler, Parth Shah, Alessandro Didonna, Puneet Opal

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 54% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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 2 institutions in 1 country.

Natalie M FrederickKen and Ruth Davee Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, 60611, USA.
Morgan M PoolerKen and Ruth Davee Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, 60611, USA.
Parth ShahKen and Ruth Davee Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, 60611, USA.
Alessandro DidonnaDepartment of Neurology, Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, 94158, USA.ORCID 0000-0001-7510-9658
Puneet OpalKen and Ruth Davee Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, 60611, USA.ORCID 0000-0001-9110-2202
Northwestern University · USUniversity of California, San Francisco · US

Funding

Understanding the Cellular Basis of Movement DisordersR01NS082351 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Puneet Opal · 2013 to 2026
$6.2M
Supplementary funding for U01NS104326 Clinical Trial Readiness for SCA1 and SCA3 (“READISCA”)U01NS104326 · NINDS · METHODIST HOSPITAL RESEARCH INSTITUTE · PI ASHIZAWA, TETSUO, DURR, ALEXANDRA · 2018 to 2022
$6.1M
Cellular pathways underlying polyglutamine degenerationR01NS062051 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI OPAL, PUNEET · 2010 to 2014
$1.7M
HLA genetics and Parkinson's diseaseR56NS121112 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DIDONNA, ALESSANDRO, OKSENBERG, JORGE R. · 2021 to 2021
$565k
Understanding pathophysiological mechanisms underlying neurodegenerationR56NS108639 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI OPAL, PUNEET · 2019 to 2019
$510k
Biohaven PharmaceuticalsConrad N. Hilton Foundation 17323FISM-Fondazione Italiana Sclerosi Multipla 2014/B/1FISM-Fondazione Italiana Sclerosi Multipla 2017/B/3International Progressive MS Alliance PA-2001-36176National Ataxia FoundationNational Multiple Sclerosis Society RG-1901-33219NIH HHS 1R01NS062051NIH HHS 1R01NS082351NIH HHS R56NS108639NIH HHS R56NS121112NIH HHS U01NS104326NINDS NIH HHS R01 NS062051NINDS NIH HHS R01 NS082351NINDS NIH HHS R56 NS108639NINDS NIH HHS R56 NS121112NINDS NIH HHS U01 NS104326
6 · The paper itself

Abstract

The primary dystonia DYT6 is caused by mutations in the transcription factor Thanatos-associated protein 1 (THAP1). To understand THAP1's functions, we generated mice lacking THAP1 in the nervous system. THAP1 loss causes locomotor deficits associated with transcriptional changes. Since many of the genes misregulated involve dopaminergic signaling, we pharmacologically challenged the two striatal canonical dopamine pathways: the direct, regulated by the D1 receptor, and the indirect, regulated by the D2 receptor. We discovered that depleting THAP1 specifically interferes with the D2 receptor responses, pointing to a selective misregulation of the indirect pathway in DYT6 with implications for pathogenesis and treatment.

Indexed as

DNA-Binding ProteinsAnimalsDisease Models, AnimalDopamine AgonistsDopamine AntagonistsDystonia Musculorum DeformansMiceMice, Inbred C57BLMice, KnockoutReceptors, Dopamine D1Receptors, Dopamine D2DNA-Binding ProteinsDopamine AgonistsDopamine AntagonistsDrd1 protein, mouseDRD2 protein, mouseReceptors, Dopamine D1Receptors, Dopamine D2THAP1 protein, mouse

Identifiers

PMID34802187
PMCPMC8670318
OpenAlexW3215640522

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.