Evidence map›Paper›PMID 36417513›Full record

ArticleScience advances2022

Functional specialization of different PI3K isoforms for the control of neuronal architecture, synaptic plasticity, and cognition.

Carla Sánchez-Castillo, María I Cuartero, Alba Fernández-Rodrigo, Víctor Briz, Sergio López-García, Raquel Jiménez-Sánchez, Juan A López, Mariona Graupera, José A Esteban

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  16. IL-6 Enhances the Activation of PI3K-AKT/mTOR-GSK-3β by Upregulating GRPR in Hippocampal Neurons of Autistic Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 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

9 authors at 2 institutions in 1 country.

Carla Sánchez-CastilloDepartment of Molecular Neuropathology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.ORCID 0000-0002-3697-5825
María I CuarteroDepartment of Molecular Neuropathology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.
Alba Fernández-RodrigoDepartment of Molecular Neuropathology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.ORCID 0000-0003-3834-0687
Víctor BrizDepartment of Molecular Neuropathology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.ORCID 0000-0001-6936-0918
Sergio López-GarcíaDepartment of Molecular Neuropathology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.ORCID 0000-0003-0314-6219
Raquel Jiménez-SánchezDepartment of Molecular Neuropathology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.
Juan A LópezProteomics Unit, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.ORCID 0000-0002-9097-6060
Mariona GrauperaEndothelial Pathobiology and Microenviroment Group, Josep Carreras Leukaemia Research Institute (IJC), 08916 Badalona, Barcelona, Spain.
José A EstebanDepartment of Molecular Neuropathology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.ORCID 0000-0002-3759-3300
Centro de Biología Molecular Severo Ochoa · ESInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal connectivity and activity-dependent synaptic plasticity are fundamental properties that support brain function and cognitive performance. Phosphatidylinositol 3-kinase (PI3K) intracellular signaling controls multiple mechanisms mediating neuronal growth, synaptic structure, and plasticity. However, it is still unclear how these pleiotropic functions are integrated at molecular and cellular levels. To address this issue, we used neuron-specific virally delivered Cre expression to delete either p110α or p110β (the two major catalytic isoforms of type I PI3K) from the hippocampus of adult mice. We found that dendritic and postsynaptic structures are almost exclusively supported by p110α activity, whereas p110β controls neurotransmitter release and metabotropic glutamate receptor-dependent long-term depression at the presynaptic terminal. In addition to these separate functions, p110α and p110β jointly contribute to

Identifiers

PMID36417513
PMCPMC9683729
OpenAlexW4310087928

What Socratic 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 Socratic graph.