Evidence map›Paper›PMID 20181838›Full record

ArticleInvestigative ophthalmology & visual science2010

The tumor suppressor merlin is required for cell cycle exit, terminal differentiation, and cell polarity in the developing murine lens.

Luke A Wiley, Lisa K Dattilo, Kai B Kang, Marco Giovannini, David C Beebe

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2010. 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
0.8field-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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Defect of LSS Disrupts Lens Development in Cataractogenesis.Frontiers in cell and developmental biology · 2021
    Article
  4. Article
  5. Review
  6. Hippo-yap signaling in ocular development and disease.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Review
  7. Case series: Pyramidal cataracts, intact irides and nystagmus from three novelAmerican journal of ophthalmology case reports · 2018
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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 1 institution in 1 country.

Luke A WileyDepartments of Ophthalmology and Visual Sciences, Washington University, St. Louis, MO, USA.
Lisa K Dattilo
Kai B Kang
Marco Giovannini
David C Beebe
House Clinic · US

Funding

WASHINGTON UNIVERSITY CENTER VISION RESEARCHP30EY002687 · NEI · WASHINGTON UNIVERSITY · PI Philip Andrew Ruzycki · 1985 to 2026
$18.4M
REGULATION OF LENS AND EYE FORMATIONR01EY004853 · NEI · WASHINGTON UNIVERSITY · PI BASSNETT, STEVEN · 1985 to 2015
$7.0M
DEVELOPMENTAL CARDIOLOGY AND PULMONARY TRAINING PROGRAMT32HL007873 · NHLBI · WASHINGTON UNIVERSITY · PI MECHAM, ROBERT P. · 1998 to 2012
$3.6M
NEI NIH HHS EY002687NEI NIH HHS EY04853NEI NIH HHS P30 EY002687NEI NIH HHS R01 EY004853NHLBI NIH HHS 2 T32 HL007873NHLBI NIH HHS T32 HL007873
6 · The paper itself

Abstract

PURPOSE. Neurofibromatosis type 2 (NF2) is an autosomal-dominant CNS tumor syndrome that affects 1:25,000 children and young adults. More than 50% of NF2 patients also develop posterior subcapsular cataracts (PSCs). The authors deleted Nf2 from the lens to determine its role in fiber cell differentiation. METHODS. Nf2 was conditionally deleted from murine lenses using the LeCre transgene. Standard histology and immunohistochemical and immunofluorescent methods were used to analyze lens morphology and markers of cell cycle progression, differentiation, and cell junctions in wild-type and knockout lenses from embryonic day 10.5 through postnatal day 3. RESULTS. Fiber cells lacking Nf2 did not fully exit the cell cycle and continued to express epithelial cell markers, such as FoxE3 and E-cadherin, despite expressing the fiber cell marker Prox1. Many fiber cells lost their elongated morphology. Markers of apical-basal polarity, such as ZO-1, were mislocalized along the lateral and basal membranes of fiber cells. The lens vesicle failed to separate from the surface ectoderm, and prospective lens and corneal epithelial cells formed a multilayered mass of cells at the surface of the eye. Herniation of this membrane caused the fiber mass to erupt through the cornea. CONCLUSIONS. Nf2 is required for complete fiber cell terminal differentiation, maintenance of cell polarity, and separation of lens vesicle from corneal epithelium. Defects identified in fiber cell differentiation may explain the formation of PSCs in patients with NF2. The lens provides an assay system to identify pathways critical for fiber cell differentiation and to test therapies for the tumors that occur in patients with NF2.

Indexed as

AnimalsBiomarkersCadherinsCell CycleCell DifferentiationCell PolarityFemaleFluorescent Antibody Technique, IndirectForkhead Transcription FactorsGene DeletionGenotypeIn Situ Nick-End LabelingLens, CrystallineMaleMembrane ProteinsMiceBiomarkersCadherinsForkhead Transcription FactorsFoxe3 protein, mouseMembrane ProteinsNeurofibromin 2PhosphoproteinsTjp1 protein, mouseZonula Occludens-1 Protein

Identifiers

PMID20181838
PMCPMC2904013
OpenAlexW2009367207

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.