Evidence map›Paper›PMID 34648564›Full record

ArticlePloS one2021

Global Rhes knockout in the Q175 Huntington's disease mouse model.

Taneli Heikkinen, Timo Bragge, Juha Kuosmanen, Teija Parkkari, Sanna Gustafsson, Mei Kwan, Jose Beltran, Afshin Ghavami, Srinivasa Subramaniam, Neelam Shahani and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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

14 authors at 3 institutions in 1 country.

Taneli HeikkinenCharles River Discovery Services, Kuopio, Finland.
Timo BraggeCharles River Discovery Services, Kuopio, Finland.ORCID 0000-0002-8634-0297
Juha KuosmanenCharles River Discovery Services, Kuopio, Finland.
Teija ParkkariCharles River Discovery Services, Kuopio, Finland.
Sanna GustafssonCharles River Discovery Services, Kuopio, Finland.
Mei KwanPsychogenics, Paramus, New Jersey, United States of America.
Jose BeltranPsychogenics, Paramus, New Jersey, United States of America.
Afshin GhavamiPsychogenics, Paramus, New Jersey, United States of America.
Srinivasa SubramaniamThe Scripps Research Institute, Department of Neuroscience, Jupiter, Florida, United States of America.
Neelam ShahaniThe Scripps Research Institute, Department of Neuroscience, Jupiter, Florida, United States of America.ORCID 0000-0003-1907-4811
Uri Nimrod Ramírez-JarquínThe Scripps Research Institute, Department of Neuroscience, Jupiter, Florida, United States of America.
Larry ParkCHDI Management/CHDI Foundation, New York, New York, United States of America.
Ignacio Muñoz-SanjuánCHDI Management/CHDI Foundation, New York, New York, United States of America.
Deanna M MarchioniniCHDI Management/CHDI Foundation, New York, New York, United States of America.ORCID 0000-0003-2071-1064
CHDI Foundation · USPsychogenics (United States) · USScripps Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) results from an expansion mutation in the polyglutamine tract in huntingtin. Although huntingtin is ubiquitously expressed in the body, the striatum suffers the most severe pathology. Rhes is a Ras-related small GTP-binding protein highly expressed in the striatum that has been reported to modulate mTOR and sumoylation of mutant huntingtin to alter HD mouse model pathogenesis. Reports have varied on whether Rhes reduction is desirable for HD. Here we characterize multiple behavioral and molecular endpoints in the Q175 HD mouse model with genetic Rhes knockout (KO). Genetic RhesKO in the Q175 female mouse resulted in both subtle attenuation of Q175 phenotypic features, and detrimental effects on other kinematic features. The Q175 females exhibited measurable pathogenic deficits, as measured by MRI, MRS and DARPP32, however, RhesKO had no effect on these readouts. Additionally, RhesKO in Q175 mixed gender mice deficits did not affect mTOR signaling, autophagy or mutant huntingtin levels. We conclude that global RhesKO does not substantially ameliorate or exacerbate HD mouse phenotypes in Q175 mice.

Indexed as

AnimalsBiomechanical PhenomenaBody WeightBrainDisease Models, AnimalDopamine and cAMP-Regulated Phosphoprotein 32FemaleGTP-Binding ProteinsHuntingtin ProteinHuntington DiseaseMagnetic Resonance ImagingMaleMiceMice, Inbred C57BLMice, KnockoutPhenotypeDopamine and cAMP-Regulated Phosphoprotein 32GTP-Binding ProteinsHtt protein, mouseHuntingtin ProteinPpp1r1b protein, mouseRasd2 protein, mouseTOR Serine-Threonine Kinases

Identifiers

PMID34648564
PMCPMC8516231
OpenAlexW3207288490

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.