Evidence map›Paper›PMID 23226316›Full record

ArticlePloS one2012

Expression of Caytaxin protein in Cayman Ataxia mouse models correlates with phenotype severity.

Kristine M Sikora, LaGina M Nosavanh, Prameela Kantheti, Margit Burmeister, Michael Hortsch

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. 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 34% 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, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Vocal development in dystonic rats.Physiological reports · 2015
    Article
  5. Article
  6. Article
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.

Kristine M SikoraProgram in Cellular and Molecular Biology, University of Michigan, Ann Arbor, Michigan, United States of America.
LaGina M Nosavanh
Prameela Kantheti
Margit Burmeister
Michael Hortsch
Michigan United · USUniversity of Michigan–Ann Arbor · US

Funding

CELLULAR AND MOLECULAR BIOLOGY AT MICHIGANT32GM007315 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PUTHENVEEDU, MANOJKUMAR A · 1985 to 2021
$12.8M
Molecular Characterization of Cayman Ataxia, ATCAYR01NS032130 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURMEISTER, MARGIT · 1994 to 2007
$1.9M
GENES FOR NEUROLOGICAL MUTATIONS ON MURINE CHROMOSOME 10R55NS032130 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURMEISTER, MARGIT · 1993 to 1993
–
NIGMS NIH HHS T32 GM007315NIGMS NIH HHS T32-GM007315NINDS NIH HHS NS32130NINDS NIH HHS R01 NS032130
6 · The paper itself

Abstract

Caytaxin is a highly-conserved protein, which is encoded by the Atcay/ATCAY gene. Mutations in Atcay/ATCAY have been identified as causative of cerebellar disorders such as the rare hereditary disease Cayman ataxia in humans, generalized dystonia in the dystonic (dt) rat, and marked motor defects in three ataxic mouse lines. While several lines of evidence suggest that Caytaxin plays a critical role in maintaining nervous system processes, the physiological function of Caytaxin has not been fully characterized. In the study presented here, we generated novel specific monoclonal antibodies against full-length Caytaxin to examine endogenous Caytaxin expression in wild type and Atcay mutant mouse lines. Caytaxin protein is absent from brain tissues in the two severely ataxic Atcay(jit) (jittery) and Atcay(swd) (sidewinder) mutant lines, and markedly decreased in the mildly ataxic/dystonic Atcay(ji-hes) (hesitant) line, indicating a correlation between Caytaxin expression and disease severity. As the expression of wild type human Caytaxin in mutant sidewinder and jittery mice rescues the ataxic phenotype, Caytaxin's physiological function appears to be conserved between the human and mouse orthologs. Across multiple species and in several neuronal cell lines Caytaxin is expressed as several protein isoforms, the two largest of which are caused by the usage of conserved methionine translation start sites. The work described in this manuscript presents an initial characterization of the Caytaxin protein and its expression in wild type and several mutant mouse models. Utilizing these animal models of human Cayman Ataxia will now allow an in-depth analysis to elucidate Caytaxin's role in maintaining normal neuronal function.

Indexed as

Gene Expression RegulationPhenotypeAmino Acid SequenceAnimalsAntibodies, MonoclonalAntibody SpecificityBase SequenceBrainCell Line, TumorCerebellar AtaxiaDisease Models, AnimalHomozygoteHumansMiceMolecular Sequence DataMutationAntibodies, MonoclonalATCAY protein, humanAtcay protein, mouseNerve Tissue ProteinsProtein Isoforms

Identifiers

PMID23226316
PMCPMC3511541
OpenAlexW2065613207

What OpenQuestion 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 OpenQuestion graph.