Evidence map›Paper›PMID 26681494›Full record

ArticleDevelopment (Cambridge, England)2016

Crim1 regulates integrin signaling in murine lens development.

Ying Zhang, Jieqing Fan, Joshua W K Ho, Tommy Hu, Stephen C Kneeland, Xueping Fan, Qiongchao Xi, Michael A Sellarole, Wilhelmine N de Vries, Weining Lu and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. A zebrafish model ofFrontiers in cell and developmental biology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The role ofNeural regeneration research · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Essential Role of CRIM1 on Endometrial Receptivity in Goat.International journal of molecular sciences · 2021
    Article
  13. Heterozygous Loss of Yap1 in Mice Causes Progressive Cataracts.Investigative ophthalmology & visual science · 2020
    Article
  14. Article
  15. The extracellular matrix in development.Development (Cambridge, England) · 2020
    Review
  16. Crim1Mammalian genome : official journal of the International Mammalian Genome Society · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. 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

14 authors at 9 institutions in 2 countries.

Ying ZhangDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Jieqing FanDepartment of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Joshua W K HoDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA Center for Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA Victor Chang Cardiac Research Institute, and The University of New South Wales, Sydney, New South Wales 2010, Australia.
Tommy HuDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Stephen C KneelandHoward Hughes Medical Institute and The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.
Xueping FanRenal Section, Department of Medicine, Boston University Medical Center, Boston, MA 02118, USA.
Qiongchao XiDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Michael A SellaroleVictor Chang Cardiac Research Institute, and The University of New South Wales, Sydney, New South Wales 2010, Australia.
Wilhelmine N de VriesVictor Chang Cardiac Research Institute, and The University of New South Wales, Sydney, New South Wales 2010, Australia.
Weining LuRenal Section, Department of Medicine, Boston University Medical Center, Boston, MA 02118, USA.
Salil A LachkeDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA.
Richard A LangDepartment of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Simon W M JohnVictor Chang Cardiac Research Institute, and The University of New South Wales, Sydney, New South Wales 2010, Australia.
Richard L MaasDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA maas@genetics.med.harvard.edu.
Harvard University · USCincinnati Children's Hospital Medical Center · USUNSW Sydney · AUVictor Chang Cardiac Research Institute · AUBoston Medical Center · USBoston University · USBrigham and Women's Hospital · USJackson Laboratory · USUniversity of Delaware · US

Funding

Factors Determining Intraocular Pressure and Glaucoma SusceptibilityR01EY011721 · NEI · JACKSON LABORATORY · PI JOHN, SIMON W · 2002 to 2018
$12.4M
POST TRANSCRIPTIONAL CONTROL OF GENE EXPRESSION IN THE LENS (LENS GENE EXPRESSIONR01EY021505 · NEI · WASHINGTON UNIVERSITY · PI LACHKE, SALIL · 2011 to 2024
$5.3M
The Role of Tdrd7 in Mammalian Lens DevelopmentR01EY010123 · NEI · BRIGHAM AND WOMEN'S HOSPITAL · PI MAAS, RICHARD L · 1993 to 2016
$5.1M
Molecular Pathogenesis of Vesicoureteral RefluxR01DK078226 · NIDDK · BOSTON MEDICAL CENTER · PI LU, WEINING · 2008 to 2018
$2.5M
FACTORS DETERMINING INTRAOCULAR PRESSURER29EY011721 · NEI · JACKSON LABORATORY · PI JOHN, SIMON W · 1997 to 2001
$227k
Howard Hughes Medical InstituteNEI NIH HHS EY010123NEI NIH HHS EY021505NEI NIH HHS EY11721NEI NIH HHS R01 EY010123NEI NIH HHS R01 EY011721NEI NIH HHS R01 EY021505NEI NIH HHS R29 EY011721NEI NIH HHS T32 EY714517NIDDK NIH HHS R01 DK078226
6 · The paper itself

Abstract

The developing lens is a powerful system for investigating the molecular basis of inductive tissue interactions and for studying cataract, the leading cause of blindness. The formation of tightly controlled cell-cell adhesions and cell-matrix junctions between lens epithelial (LE) cells, between lens fiber (LF) cells, and between these two cell populations enables the vertebrate lens to adopt a highly ordered structure and acquire optical transparency. Adhesion molecules are thought to maintain this ordered structure, but little is known about their identity or interactions. Cysteine-rich motor neuron 1 (Crim1), a type I transmembrane protein, is strongly expressed in the developing lens and its mutation causes ocular disease in both mice and humans. How Crim1 regulates lens morphogenesis is not understood. We identified a novel ENU-induced hypomorphic allele of Crim1, Crim1(glcr11), which in the homozygous state causes cataract and microphthalmia. Using this and two other mutant alleles, Crim1(null) and Crim1(cko), we show that the lens defects in Crim1 mouse mutants originate from defective LE cell polarity, proliferation and cell adhesion. Crim1 adhesive function is likely to be required for interactions both between LE cells and between LE and LF cells. We show that Crim1 acts in LE cells, where it colocalizes with and regulates the levels of active β1 integrin and of phosphorylated FAK and ERK. The RGD and transmembrane motifs of Crim1 are required for regulating FAK phosphorylation. These results identify an important function for Crim1 in the regulation of integrin- and FAK-mediated LE cell adhesion during lens development.

Indexed as

AnimalsBone Morphogenetic Protein ReceptorsCell LineGene Expression Regulation, DevelopmentalImmunohistochemistryIn Situ Nick-End LabelingLens, CrystallineMiceMice, Inbred C57BLOrganogenesisPhosphorylationSignal TransductionBone Morphogenetic Protein ReceptorsCrim1 protein, mouseCataractCell adhesionCrim1Cysteine-rich transmembrane BMP regulator 1Eye developmentIntegrinLensMouse

Identifiers

PMID26681494
PMCPMC4725338
OpenAlexW2416328526

What OpenQuestion holds

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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.