Evidence map›Paper›PMID 22155156›Full record

ArticleMolecular and cellular neurosciences2012

PTEN regulates retinal interneuron morphogenesis and synaptic layer formation.

Kiyo Sakagami, Bryan Chen, Steven Nusinowitz, Hong Wu, Xian-Jie Yang

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-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

24 citing papers in PubMed, 38 citations in OpenAlex.

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  16. Pten Regulates Retinal Amacrine Cell Number by Modulating Akt, Tgfβ, and Erk Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
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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

5 authors at 2 institutions in 1 country.

Kiyo SakagamiJules Stein Eye Institute, University of California, Los Angeles, CA 90095, USA.
Bryan Chen
Steven Nusinowitz
Hong Wu
Xian-Jie Yang
University of California, Los Angeles · USDoheny Eye Institute · US

Funding

Vision Research Core at UCLAP30EY000331 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Gregory Darin Field, DAVID S WILLIAMS · 1985 to 2026
$16.8M
CYTOKINE SIGNAL TRANSDUCTION IN RETINAL DEVELOPMENTR01EY012270 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIAN-JIE · 2000 to 2008
$2.7M
Hedgehog Signaling in Photoreceptor Differentiation and MaintenanceR01EY019052 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIAN-JIE · 2010 to 2013
$1.5M
NEI NIH HHS EY019052NEI NIH HHS EY12270NEI NIH HHS P30 EY000331NEI NIH HHS R01 EY012270NEI NIH HHS R01 EY019052
6 · The paper itself

Abstract

The lipid phosphatase PTEN is a critical negative regulator of extracellular signal-induced PI3K activities, yet the roles of PTEN in the neural retina remain poorly understood. Here, we investigate the function of PTEN during retinal development. Deletion of Pten at the onset of neurogenesis in retinal progenitors results in the reduction of retinal ganglion cells and rod photoreceptors, but increased Müller glial genesis. In addition, PTEN deficiency leads to elevated phosphorylation of Akt, especially in the developing inner plexiform layer, where high levels of PTEN are normally expressed. In Pten mutant retinas, various subtypes of amacrine cells show severe dendritic overgrowth, causing specific expansion of the inner plexiform layer. However, the outer plexiform layer remains relatively undisturbed in the Pten deficient retina. Physiological analysis detects reduced rod function and augmented oscillatory potentials originating from amacrine cells in Pten mutants. Furthermore, deleting Pten or elevating Akt activity in individual amacrine cells is sufficient to disrupt dendritic arborization, indicating that Pten activity is required cell autonomously to control neuronal morphology. Moreover, inhibiting endogenous Akt activity attenuates inner plexiform layer formation in vitro. Together, these findings demonstrate that suppression of PI3K/Akt signaling by PTEN is crucial for proper neuronal differentiation and normal retinal network formation.

Indexed as

Amacrine CellsAnimalsGene Knockout TechniquesInterneuronsMiceMice, Inbred C57BLMorphogenesisMutationNeurogenesisNeuronsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRetinaRetinal Ganglion CellsRetinal Rod Photoreceptor CellsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID22155156
PMCPMC3278565
OpenAlexW2067840547

What OpenQuestion holds

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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.