Evidence map›Paper›PMID 30135513›Full record

ArticleScientific reports2018

Ndr kinases regulate retinal interneuron proliferation and homeostasis.

Hélène Léger, Evelyn Santana, N Adrian Leu, Eliot T Smith, William A Beltran, Gustavo D Aguirre, Francis C Luca

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  7. The NDR family of kinases: essential regulators of aging.Frontiers in molecular neuroscience · 2024
    Review
  8. Illumination of understudied ciliary kinases.Frontiers in molecular biosciences · 2024
    Review
  9. 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

7 authors at 1 institution in 1 country.

Hélène LégerDepartment of Biomedical Sciences, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, United States.ORCID 0000-0003-1116-8637
Evelyn SantanaDivision of Experimental Retinal Therapies, Department of Clinical Sciences and Advanced Medicine, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, United States.
N Adrian LeuCenter for Animal Transgenesis and Germ Cell Research, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, United States.
Eliot T SmithDepartment of Biomedical Sciences, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, United States.
William A BeltranDivision of Experimental Retinal Therapies, Department of Clinical Sciences and Advanced Medicine, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, United States.
Gustavo D AguirreDivision of Experimental Retinal Therapies, Department of Clinical Sciences and Advanced Medicine, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, United States.
Francis C LucaDepartment of Biomedical Sciences, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, United States. fluca@vet.upenn.edu.
University of Pennsylvania · US

Funding

KOMP2-Phase3 Production and Phenotyping by the DTCC Consortium TCP Transfer to UC DavisUM1OD023221 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KC KENT LLOYD · 2016 to 2026
$45.7M
MODELS OF HEREDITY RETINAL DEGENERATIONR01EY006855 · NEI · UNIVERSITY OF PENNSYLVANIA · PI GUSTAVO David AGUIRRE, William A. Beltran · 1992 to 2026
$20.7M
Scientific TransparencyP30EY001583 · NEI · UNIVERSITY OF PENNSYLVANIA · PI CLAIRE H MITCHELL · 1985 to 2026
$19.5M
Translational Research for Retinal Degeneration TherapiesR01EY017549 · NEI · UNIVERSITY OF PENNSYLVANIA · PI BELTRAN, WILLIAM A. · 2007 to 2024
$14.1M
Examining the role of Cbk1/NDR kinase in regulating mRNA localizationR01GM097327 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI LUCA, FRANCIS C · 2013 to 2016
$1.2M
NEI NIH HHS P30 EY001583NEI NIH HHS R01 EY006855NEI NIH HHS R01 EY017549NIGMS NIH HHS R01 GM097327NIH HHS UM1 OD023221
6 · The paper itself

Abstract

Ndr2/Stk38l encodes a protein kinase associated with the Hippo tumor suppressor pathway and is mutated in a naturally-occurring canine early retinal degeneration (erd). To elucidate the retinal functions of Ndr2 and its paralog Ndr1/Stk38, we generated Ndr1 and Ndr2 single knockout mice. Although retinal lamination appeared normal in these mice, Ndr deletion caused a subset of Pax6-positive amacrine cells to proliferate in differentiated retinas, while concurrently decreasing the number of GABAergic, HuD and Pax6-positive amacrine cells. Retinal transcriptome analyses revealed that Ndr2 deletion increased expression of neuronal stress genes and decreased expression of synaptic organization genes. Consistent with the latter, Ndr deletion dramatically reduced levels of Aak1, an Ndr substrate that regulates vesicle trafficking. Our findings indicate that Ndr kinases are important regulators of amacrine and photoreceptor cells and suggest that Ndr kinases inhibit the proliferation of a subset of terminally differentiated cells and modulate interneuron synapse function via Aak1.

Indexed as

Amacrine CellsAnimalsCell ProliferationELAV-Like Protein 4Gene Expression RegulationHomeostasisInterneuronsMice, Inbred C57BLMice, KnockoutPAX6 Transcription FactorPhotoreceptor CellsProtein Serine-Threonine KinasesRetinaRetinal Bipolar CellsAak1 protein, mouseElavl4 protein, mouseELAV-Like Protein 4NDR1 protein kinase, mouseNDR2 protein kinase, mousePax6 protein, mousePAX6 Transcription FactorProtein Serine-Threonine Kinases

Identifiers

PMID30135513
PMCPMC6105603
OpenAlexW2885972463

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.