Evidence map›Paper›PMID 15525772›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Developmental roles of p73 in Cajal-Retzius cells and cortical patterning.

Gundela Meyer, Alfredo Cabrera Socorro, Carlos Gustavo Perez Garcia, Luis Martinez Millan, Nancy Walker, Daniel Caput

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.8field-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

54 citing papers in PubMed, 128 citations in OpenAlex.

  1. Review
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  11. Mining the jewels of the cortex's crowning mystery.Current opinion in neurobiology · 2020
    Review
  12. The C terminus of p73 is essential for hippocampal development.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Review
  14. Article
  15. TheFrontiers in genetics · 2019
    Review
  16. Article
  17. Lateral Thalamic Eminence: A Novel Origin for mGluR1/Lot Cells.Cerebral cortex (New York, N.Y. : 1991) · 2017
    Article
  18. Article
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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

6 authors at 3 institutions in 2 countries.

Gundela MeyerDepartment of Anatomy, University La Laguna, 38071 La Laguna, Tenerife, Spain. gmeyer@ull.es
Alfredo Cabrera Socorro
Carlos Gustavo Perez Garcia
Luis Martinez Millan
Nancy Walker
Daniel Caput
Universidad de La Laguna · ESSanofi (France) · FRUniversity of the Basque Country · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To examine the role of the p53 homolog p73 in brain development, we studied p73-/-, p73+/-, E2F1-/-, and reeler mutant mice. p73 in developing brain is expressed in Cajal-Retzius (CR) cells, the cortical hem, and the choroid plexus. p73-expressing CR cells are lost in p73-/- embryos, although Reelin is faintly expressed in the marginal zone. Ectopic neurons in the p73-/- preplate and cortical hem at embryonic day 12 implicate p73 in the early developmental program of the cortex; however, preplate partition and early cortical plate formation are not disturbed. Postnatal p73-/- mice show a mild hypoplasia of the rostral cortex and a severely disrupted architecture of the posterior telencephalon. In the developing p73-/- hippocampus, the most striking abnormality is the absence of the hippocampal fissure, suggesting a role of p73 in cortical folding. p73+/- mice have a less severe cortical phenotype; they display a dorsal shift of the entorhinal cortex and a reduced size of occipital and posterior temporal areas, which acquire entorhinal-like features such as Reelin-positive cells in layer II. CR cells appear unaffected by heterozygosity. We relate the malformations of the posterior pole in p73 mutant mice to alterations of p73 expression in the cortical hem and suggest that p73 forms part of an early signaling network that controls neocortical and archicortical regionalization. In mice deficient for the transcription factor E2F1, a main activator of the TAp73 (transactivating p73) isoform, we find a defect of the caudal cortical architecture resembling the p73+/- phenotype along with reduced TAp73 protein levels and propose that an E2F1-TAp73 dependent pathway is involved in cortical patterning.

Indexed as

AnimalsBrainCell Adhesion Molecules, NeuronalCell Cycle ProteinsCerebral CortexDNA-Binding ProteinsE2F1 Transcription FactorE2F Transcription FactorsExtracellular Matrix ProteinsGenes, Tumor SuppressorLimbic SystemMiceMice, Inbred C57BLMice, KnockoutMice, Neurologic MutantsNerve Tissue ProteinsCell Adhesion Molecules, NeuronalCell Cycle Proteinsdelta Np73, mouseDNA-Binding ProteinsE2f1 protein, mouseE2F1 Transcription FactorE2F Transcription FactorsExtracellular Matrix ProteinsNerve Tissue ProteinsNuclear ProteinsProtein IsoformsReelin ProteinReln protein, mouseSerine EndopeptidasesTranscription FactorsTrp73 protein, mouseTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID15525772
PMCPMC6730229
OpenAlexW2040927571

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.