Evidence map›Paper›PMID 25875176›Full record

ArticlePloS one2015

Functional synergy between cholecystokinin receptors CCKAR and CCKBR in mammalian brain development.

Sayoko Nishimura, Kaya Bilgüvar, Keiko Ishigame, Nenad Sestan, Murat Günel, Angeliki Louvi

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

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  14. Article
  15. Cholecystokinin attenuates β-cell apoptosis in both mouse and human islets.Translational research : the journal of laboratory and clinical medicine · 2022
    Article
  16. Review
  17. Article
  18. Article
  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

6 authors at 1 institution in 1 country.

Sayoko NishimuraDepartment of Neurosurgery, Yale School of Medicine, New Haven, Connecticut, United States of America.
Kaya BilgüvarYale Program on Neurogenetics, Yale School of Medicine, New Haven, Connecticut, United States of America; Department of Genetics, Yale School of Medicine, New Haven, Connecticut, United States of America; Yale Center for Genome Analysis, Yale School of Medicine, New Haven, Connecticut, United States of America.
Keiko IshigameDepartment of Neurosurgery, Yale School of Medicine, New Haven, Connecticut, United States of America.
Nenad SestanDepartment of Neurobiology, Yale School of Medicine, New Haven, Connecticut, United States of America.
Murat GünelDepartment of Neurosurgery, Yale School of Medicine, New Haven, Connecticut, United States of America; Yale Program on Neurogenetics, Yale School of Medicine, New Haven, Connecticut, United States of America; Department of Genetics, Yale School of Medicine, New Haven, Connecticut, United States of America; Department of Neurobiology, Yale School of Medicine, New Haven, Connecticut, United States of America.
Angeliki LouviDepartment of Neurosurgery, Yale School of Medicine, New Haven, Connecticut, United States of America; Yale Program on Neurogenetics, Yale School of Medicine, New Haven, Connecticut, United States of America; Department of Neurobiology, Yale School of Medicine, New Haven, Connecticut, United States of America.
Yale University · US

Funding

Yale University Clinical and Translational Science Award ProgramUL1TR000142 · NCATS · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2012 to 2015
$31.8M
NCATS NIH HHS UL1 TR000142
6 · The paper itself

Abstract

Cholecystokinin (CCK), a peptide hormone and one of the most abundant neuropeptides in vertebrate brain, mediates its actions via two G-protein coupled receptors, CCKAR and CCKBR, respectively active in peripheral organs and the central nervous system. Here, we demonstrate that the CCK receptors have a dynamic and largely reciprocal expression in embryonic and postnatal brain. Using compound homozygous mutant mice lacking the activity of both CCK receptors, we uncover their additive, functionally synergistic effects in brain development and demonstrate that CCK receptor loss leads to abnormalities of cortical development, including defects in the formation of the midline and corpus callosum, and cortical interneuron migration. Using comparative transcriptome analysis of embryonic neocortex, we define the molecular mechanisms underlying these defects. Thus we demonstrate a developmental, hitherto unappreciated, role of the two CCK receptors in mammalian neocortical development.

Indexed as

Gene Expression Regulation, DevelopmentalTranscriptomeAnimalsAnimals, NewbornBone Morphogenetic Protein 7Cell MovementChemokine CXCL12CholecystokininCorpus CallosumEmbryo, MammalianGene Expression ProfilingHomozygoteHumansInterneuronsMiceMice, Knockoutbmp7 protein, mouseBone Morphogenetic Protein 7Chemokine CXCL12CholecystokininCxcl12 protein, mouseNeuropilin-2Receptor, Cholecystokinin AReceptor, Cholecystokinin BReceptors, N-Methyl-D-Aspartate

Identifiers

PMID25875176
PMCPMC4398320
OpenAlexW2056540233

What OpenQuestion holds

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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.