Evidence map›Paper›PMID 25049392›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Ataxia and Purkinje cell degeneration in mice lacking the CAMTA1 transcription factor.

Chengzu Long, Chad E Grueter, Kunhua Song, Song Qin, Xiaoxia Qi, Y Megan Kong, John M Shelton, James A Richardson, Chun-Li Zhang, Rhonda Bassel-Duby and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

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  9. Genetic Mapping of Behavioral Traits Using the Collaborative Cross Resource.International journal of molecular sciences · 2022
    Article
  10. Frontiers in cellular neuroscience · 2022
    Article
  11. Review
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  19. Impaired Mitochondrial Fatty Acid Synthesis Leads to Neurodegeneration in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  20. 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 2 countries.

Chengzu LongDepartments of Molecular Biology.
Chad E GrueterDepartments of Molecular Biology.
Kunhua SongDepartments of Molecular Biology.
Song QinDepartments of Molecular Biology.
Xiaoxia QiDepartments of Molecular Biology.
Y Megan KongDepartments of Molecular Biology.
John M SheltonInternal Medicine, and.
James A RichardsonPathology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Chun-Li ZhangDepartments of Molecular Biology.
Rhonda Bassel-DubyDepartments of Molecular Biology.
Eric N OlsonDepartments of Molecular Biology.
The University of Texas Southwestern Medical Center · USInstitute of Macromolecular Chemistry · UA

Funding

Metabolic Control by Myogenic MicroRNAs, Mediator and MyokinesR01DK099653 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA, OLSON, ERIC N · 2013 to 2016
$1.9M
NIDDK NIH HHS R01 DK099653
6 · The paper itself

Abstract

Members of the calmodulin-binding transcription activator (CAMTA) family of proteins function as calcium-sensitive regulators of gene expression in multicellular organisms ranging from plants to humans. Here, we show that global or nervous system deletion of CAMTA1 in mice causes severe ataxia with Purkinje cell degeneration and cerebellar atrophy, partially resembling the consequences of haploinsufficiency of the human CAMTA1 locus. Gene-expression analysis identified a large collection of neuronal genes that were dysregulated in the brains of CAMTA1-mutant mice, and elucidation of a consensus sequence for binding of CAMTA proteins to DNA revealed the association of CAMTA-binding sites with many of these genes. We conclude that CAMTA1 plays an essential role in the control of Purkinje cell function and survival. CAMTA1-mutant mice provide a model to study the molecular mechanisms of neurodegenerative diseases and for screening potential therapeutic interventions for such disorders.

Indexed as

AnimalsAtaxiaAT Rich SequenceBase SequenceBinding SitesCalcium-Binding ProteinsGene Expression RegulationIntegrasesInverted Repeat SequencesMaleMiceMice, KnockoutMolecular Sequence DataMotor ActivityNestinNucleotide MotifsCalcium-Binding ProteinsCAMTA1 protein, mouseCre recombinaseIntegrasesNestinTrans-ActivatorsTranscription FactorsCAMTA2dimerizationneural genespalindromic DNA

Identifiers

PMID25049392
PMCPMC4128133
OpenAlexW1990674349

What OpenQuestion holds

Textmetadata
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.