Evidence map›Paper›PMID 32580238›Full record

ArticleBrain pathology (Zurich, Switzerland)2020

Abnormal scaffold attachment factor 1 expression and localization in spinocerebellar ataxias and Huntington's chorea.

Nicola Buckner, Kevin C Kemp, Helen L Scott, Gongyu Shi, Caroline Rivers, Andriana Gialeli, Liang-Fong Wong, Oscar Cordero-LLana, Nicholas Allen, Alastair Wilkins and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 49% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. 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

11 authors at 2 institutions in 1 country.

Nicola BucknerBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
Kevin C KempBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
Helen L ScottBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
Gongyu ShiBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
Caroline RiversBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
Andriana GialeliBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
Liang-Fong WongBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
Oscar Cordero-LLanaBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
Nicholas AllenSchool of Biosciences, Cardiff University, Cardiff, UK.
Alastair WilkinsInstitute of Clinical Neurosciences, Bristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.
James B UneyBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK.ORCID 0000-0002-1415-4639
University of Bristol · GBCardiff University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/M017532/1Biotechnology and Biological Sciences Research Council BB/R017883/1Medical Research Council MR/N0137941/1
6 · The paper itself

Abstract

SAFB1 is a DNA and RNA binding protein that is highly expressed in the cerebellum and hippocampus and is involved in the processing of coding and non-coding RNAs, splicing and dendritic function. We analyzed SAFB1 expression in the post-mortem brain tissue of spinocerebellar ataxia (SCA), Huntington's disease (HD), Multiple sclerosis (MS), Parkinson's disease patients and controls. In SCA cases, the expression of SAFB1 in the nucleus was increased and there was abnormal and extensive expression in the cytoplasm where it co-localized with the markers of Purkinje cell injury. Significantly, no SAFB1 expression was found in the cerebellar neurons of the dentate nucleus in control or MS patients; however, in SCA patients, SAFB1 expression was increased significantly in both the nucleus and cytoplasm of dentate neurons. In HD, we found that SAFB1 expression was increased in the nucleus and cytoplasm of striatal neurons; however, there was no SAFB1 staining in the striatal neurons of controls. In PD substantia nigra, we did not see any changes in neuronal SAFB1 expression. iCLIP analysis found that SAFB1 crosslink sites within ATXN1 RNA were adjacent to the start and within the glutamine repeat sequence. Further investigation found increased binding of SAFB1 to pathogenic ATXN1-85Q mRNA. These novel data strongly suggest SAFB1 contributes to the etiology of SCA and Huntington's chorea and that it may be a pathological marker of polyglutamine repeat expansion diseases.

Indexed as

AgedAged, 80 and overBrainCerebellumCorpus StriatumFemaleHumansHuntington DiseaseMaleMatrix Attachment Region Binding ProteinsMiddle AgedMultiple SclerosisNeuronsNuclear Matrix-Associated ProteinsParkinson DiseasePurkinje CellsMatrix Attachment Region Binding ProteinsNuclear Matrix-Associated ProteinsReceptors, EstrogenSAFB protein, humanHuntington’s choreaParkinson’s diseasepolyglutamineRNA binding protein (RBP)SAFB1spinocerebellar ataxia

Identifiers

PMID32580238
PMCPMC8018166
OpenAlexW3037674704

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.