Evidence map›Paper›PMID 24270425›Full record

ArticleThe Journal of clinical investigation2013

AKT activation promotes PTEN hamartoma tumor syndrome-associated cataract development.

Caterina Sellitto, Leping Li, Junyuan Gao, Michael L Robinson, Richard Z Lin, Richard T Mathias, Thomas W White

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

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  17. The Connexin50D47A Mutant Causes Cataracts by Calcium Precipitation.Investigative ophthalmology & visual science · 2019
    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 2 institutions in 1 country.

Caterina Sellitto
Leping Li
Junyuan Gao
Michael L Robinson
Richard Z Lin
Richard T Mathias
Thomas W White
Stony Brook University · USMiami University · US

Funding

Lens Intercellular Communication Connexins and CataractsR01EY013163 · NEI · STATE UNIVERSITY NEW YORK STONY BROOK · PI WHITE, THOMAS W · 2000 to 2019
$6.2M
VOLUME REGULATION IN NORMAL AND CATARACTOUS LENSESR01EY006391 · NEI · STATE UNIVERSITY NEW YORK STONY BROOK · PI MATHIAS, RICHARD T · 1985 to 2014
$5.4M
THE ROLE OF FGF RECPETORS IN LENS DEVELOPMENTR01EY012995 · NEI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI ROBINSON, MICHAEL L · 2000 to 2018
$4.9M
Gq-Coupled Receptors Inhibit PI 3-Kinase/Akt Signaling PathwayR01DK062722 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI LIN, RICHARD Z · 2002 to 2012
$3.1M
NEI NIH HHS EY006391NEI NIH HHS EY012995NEI NIH HHS EY013163NEI NIH HHS R01 EY006391NEI NIH HHS R01 EY012995NEI NIH HHS R01 EY013163NIDDK NIH HHS DK062722NIDDK NIH HHS R01 DK062722
6 · The paper itself

Abstract

Mutations in the human phosphatase and tensin homolog (PTEN) gene cause PTEN hamartoma tumor syndrome (PHTS), which includes cataract development among its diverse clinical pathologies. Currently, it is not known whether cataract formation in PHTS patients is secondary to other systemic problems, or the result of the loss of a critical function of PTEN within the lens. We generated a mouse line with a lens-specific deletion of Pten (PTEN KO) and identified a regulatory function for PTEN in lens ion transport. Specific loss of PTEN in the lens resulted in cataract. PTEN KO lenses exhibited a progressive age-related increase in intracellular hydrostatic pressure, along with, increased intracellular sodium concentrations, and reduced Na+/K+-ATPase activity. Collectively, these defects lead to lens swelling, opacities and ultimately organ rupture. Activation of AKT was highly elevated in PTEN KO lenses compared to WT mice. Additionally, pharmacological inhibition of AKT restored normal Na+/K+-ATPase activity in primary cultured lens cells and reduced lens pressure in intact lenses from PTEN KO animals. These findings identify a direct role for PTEN in the regulation of lens ion transport through an AKT-dependent modulation of Na+/K+-ATPase activity, and provide a new animal model to investigate cataract development in PHTS patients.

Indexed as

AgingAnimalsCataractDisease Models, AnimalDisease ProgressionEnzyme ActivationEye ProteinsHamartoma Syndrome, MultipleHydrostatic PressureIon TransportLens, CrystallineMiceMice, KnockoutOrgan SpecificityProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseAkt1 protein, mouseEye ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseSodiumSodium-Potassium-Exchanging ATPase

Identifiers

PMID24270425
PMCPMC3859396
OpenAlexW1990076368

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.