Evidence map›Paper›PMID 33335120›Full record

ArticleScientific reports2020

Analysis of mutant and total huntingtin expression in Huntington's disease murine models.

Valentina Fodale, Roberta Pintauro, Manuel Daldin, Roberta Altobelli, Maria Carolina Spiezia, Monica Bisbocci, Douglas Macdonald, Alberto Bresciani

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. 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
1.5field-weighted citation impact, top 20% 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, 22 citations in OpenAlex.

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  15. Deletion of SUMO1 attenuates behavioral and anatomical deficits by regulating autophagic activities in Huntington disease.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

8 authors at 2 institutions in 2 countries.

Valentina FodaleDepartment of Translational Biology, IRBM S.p.A., via Pontina Km 30, 600, Pomezia, Rome, Italy.
Roberta PintauroDepartment of Translational Biology, IRBM S.p.A., via Pontina Km 30, 600, Pomezia, Rome, Italy.
Manuel DaldinDepartment of Translational Biology, IRBM S.p.A., via Pontina Km 30, 600, Pomezia, Rome, Italy.
Roberta AltobelliDepartment of Translational Biology, IRBM S.p.A., via Pontina Km 30, 600, Pomezia, Rome, Italy.
Maria Carolina SpieziaDepartment of Translational Biology, IRBM S.p.A., via Pontina Km 30, 600, Pomezia, Rome, Italy.
Monica BisbocciDepartment of Translational Biology, IRBM S.p.A., via Pontina Km 30, 600, Pomezia, Rome, Italy.
Douglas MacdonaldCHDI Management/CHDI Foundation, Suite 700, 6080 Centre Drive, Los Angeles, CA, USA. douglas.macdonald@chdifoundation.org.
Alberto BrescianiDepartment of Translational Biology, IRBM S.p.A., via Pontina Km 30, 600, Pomezia, Rome, Italy.
IRBM Science Park · ITCHDI Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is a monogenetic neurodegenerative disorder that is caused by the expansion of a polyglutamine region within the huntingtin (HTT) protein, but there is still an incomplete understanding of the molecular mechanisms that drive pathology. Expression of the mutant form of HTT is a key aspect of diseased tissues, and the most promising therapeutic approaches aim to lower expanded HTT levels. Consequently, the investigation of HTT expression in time and in multiple tissues, with assays that accurately quantify expanded and non-expanded HTT, are required to delineate HTT homeostasis and to best design and interpret pharmacodynamic readouts for HTT lowering therapeutics. Here we evaluate mutant polyglutamine-expanded (mHTT) and polyglutamine-independent HTT specific immunoassays for validation in human HD and control fibroblasts and use to elucidate the CSF/brain and peripheral tissue expression of HTT in preclinical HD models.

Indexed as

Gene ExpressionMutationAnimalsBiomarkersBrainDisease Models, AnimalFibroblastsGene Knock-In TechniquesHumansHuntingtin ProteinHuntington DiseaseImmunoassayImmunohistochemistryMiceRatsReproducibility of ResultsBiomarkersHTT protein, humanHuntingtin Protein

Identifiers

PMID33335120
PMCPMC7746729
OpenAlexW3112803277

What OpenQuestion holds

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LicenceCC BY
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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.