Evidence map›Paper›PMID 26322982›Full record

ArticlePloS one2015

Novel Alternative Splice Variants of Mouse Cdk5rap2.

Nadine Kraemer, Lina Issa-Jahns, Gerda Neubert, Ethiraj Ravindran, Shyamala Mani, Olaf Ninnemann, Angela M Kaindl

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Roles of Cep215/Cdk5rap2 in establishing testicular architecture for mouse male germ cell development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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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

7 authors at 2 institutions in 2 countries.

Nadine KraemerInstitute of Cell Biology and Neurobiology, Charité -Universitätsmedizin Berlin, Berlin, Germany; Department of Pediatric Neurology, Charité -Universitätsmedizin Berlin, Berlin, Germany.
Lina Issa-JahnsInstitute of Cell Biology and Neurobiology, Charité -Universitätsmedizin Berlin, Berlin, Germany; Department of Pediatric Neurology, Charité -Universitätsmedizin Berlin, Berlin, Germany.
Gerda NeubertInstitute of Cell Biology and Neurobiology, Charité -Universitätsmedizin Berlin, Berlin, Germany; Department of Pediatric Neurology, Charité -Universitätsmedizin Berlin, Berlin, Germany.
Ethiraj RavindranInstitute of Cell Biology and Neurobiology, Charité -Universitätsmedizin Berlin, Berlin, Germany; Department of Pediatric Neurology, Charité -Universitätsmedizin Berlin, Berlin, Germany.
Shyamala ManiCentre for Neuroscience, Indian Institute of Science, Bangalore, India.
Olaf NinnemannInstitute of Cell Biology and Neurobiology, Charité -Universitätsmedizin Berlin, Berlin, Germany.
Angela M KaindlInstitute of Cell Biology and Neurobiology, Charité -Universitätsmedizin Berlin, Berlin, Germany; Department of Pediatric Neurology, Charité -Universitätsmedizin Berlin, Berlin, Germany; Sozialpädiatrisches Zentrum (SPZ), Charité -Universitätsmedizin Berlin, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEIndian Institute of Science Bangalore · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autosomal recessive primary microcephaly (MCPH) is a rare neurodevelopmental disorder characterized by a pronounced reduction of brain volume and intellectual disability. A current model for the microcephaly phenotype invokes a stem cell proliferation and differentiation defect, which has moved the disease into the spotlight of stem cell biology and neurodevelopmental science. Homozygous mutations of the Cyclin-dependent kinase-5 regulatory subunit-associated protein 2 gene CDK5RAP2 are one genetic cause of MCPH. To further characterize the pathomechanism underlying MCPH, we generated a conditional Cdk5rap2 LoxP/hCMV Cre mutant mouse. Further analysis, initiated on account of a lack of a microcephaly phenotype in these mutant mice, revealed the presence of previously unknown splice variants of the Cdk5rap2 gene that are at least in part accountable for the lack of microcephaly in the mice.

Indexed as

Alternative SplicingAnimalsBase SequenceBrainCell Cycle ProteinsCell ProliferationGenetic Predisposition to DiseaseHumansMagnetic Resonance ImagingMiceMice, Inbred C57BLMice, KnockoutMicrocephalyNerve Tissue ProteinsNeural Stem CellsProtein IsoformsCdk5rap2 protein, mouseCell Cycle ProteinsNerve Tissue ProteinsProtein Isoforms

Identifiers

PMID26322982
PMCPMC4556188
OpenAlexW2142782148

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.