Evidence map›Paper›PMID 27097329›Full record

ArticlePloS one2016

MeCP2 Related Studies Benefit from the Use of CD1 as Genetic Background.

Clementina Cobolli Gigli, Linda Scaramuzza, Anna Gandaglia, Elisa Bellini, Marina Gabaglio, Daniela Parolaro, Charlotte Kilstrup-Nielsen, Nicoletta Landsberger, Francesco Bedogni

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  6. Article
  7. Article
  8. iScience · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. A Novel Mecp2Molecular neurobiology · 2019
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

9 authors at 3 institutions in 2 countries.

Clementina Cobolli GigliSan Raffaele Rett Research Unit, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.
Linda ScaramuzzaSan Raffaele Rett Research Unit, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.
Anna GandagliaSan Raffaele Rett Research Unit, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.
Elisa BelliniSan Raffaele Rett Research Unit, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.
Marina GabaglioDepartment of Biotechnology and Life Sciences, University of Insubria, Busto Arsizio, Italy.
Daniela ParolaroDepartment of Biotechnology and Life Sciences, University of Insubria, Busto Arsizio, Italy.
Charlotte Kilstrup-NielsenDepartment of Biotechnology and Life Sciences, University of Insubria, Busto Arsizio, Italy.
Nicoletta LandsbergerSan Raffaele Rett Research Unit, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.ORCID http://orcid.org/0000-0003-0820-3155
Francesco BedogniSan Raffaele Rett Research Unit, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.
San Raffaele University of Rome · ITUniversity of Insubria · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MECP2 mutations cause a number of neurological disorders of which Rett syndrome (RTT) represents the most thoroughly analysed condition. Many Mecp2 mouse models have been generated through the years; their validity is demonstrated by the presence of a broad spectrum of phenotypes largely mimicking those manifested by RTT patients. These mouse models, between which the C57BL/6 Mecp2tm1.1Bird strain probably represents the most used, enabled to disclose much of the roles of Mecp2. However, small litters with little viability and poor maternal care hamper the maintenance of the colony, thus limiting research on such animals. For this reason, past studies often used Mecp2 mouse models on mixed genetic backgrounds, thus opening questions on whether modifier genes could be responsible for at least part of the described effects. To verify this possibility, and facilitate the maintenance of the Mecp2 colony, we transferred the Mecp2tm1.1Bird allele on the stronger CD1 background. The CD1 strain is easier to maintain and largely recapitulates the phenotypes already described in Mecp2-null mice. We believe that this mouse model will foster the research on RTT.

Indexed as

Genetic BackgroundModels, AnimalAllelesAnimalsBehavior, AnimalFemaleGene DeletionMaleMethyl-CpG-Binding Protein 2MiceNeuronsPhenotypeSpecies SpecificityMethyl-CpG-Binding Protein 2

Identifiers

PMID27097329
PMCPMC4838291
OpenAlexW2341349973

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.