Evidence map›Paper›PMID 30872746›Full record

ArticleScientific reports2019

Non-redundant functions of FAK and Pyk2 in intestinal epithelial repair.

Keena S Thomas, Katherine A Owen, Kathryn Conger, Ryan A Llewellyn, Amy H Bouton, James E Casanova

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Hippo pathway in intestinal diseases: focusing on ferroptosis.Frontiers in cell and developmental biology · 2023
    Review
  10. Article
  11. Epithelial wound healing in inflammatory bowel diseases: the next therapeutic frontier.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  12. Article
  13. 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

6 authors at 2 institutions in 1 country.

Keena S ThomasUniversity of Virginia School of Medicine, Department of Microbiology, Immunology and Cancer, Charlottesville, VA, 22908, USA.
Katherine A OwenUniversity of Virginia School of Medicine, Department of Cell Biology, Charlottesville, VA, 22908, USA.
Kathryn CongerUniversity of Virginia School of Medicine, Department of Cell Biology, Charlottesville, VA, 22908, USA.
Ryan A LlewellynUniversity of Virginia School of Medicine, Department of Microbiology, Immunology and Cancer, Charlottesville, VA, 22908, USA.
Amy H BoutonUniversity of Virginia School of Medicine, Department of Microbiology, Immunology and Cancer, Charlottesville, VA, 22908, USA. ahb8y@virginia.edu.
James E CasanovaUniversity of Virginia School of Medicine, Department of Cell Biology, Charlottesville, VA, 22908, USA. jec9e@virginia.edu.
University of Virginia · USLa Jolla Institute for Immunology · US

Funding

TRAINING IN CELL AND MOLECULAR BIOLOGYT32GM008136 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI STUKENBERG, P. TODD · 1985 to 2020
$8.5M
NIGMS NIH HHS T32 GM008136
6 · The paper itself

Abstract

Adhesion signaling between epithelial cells and the extracellular matrix plays a critical role in maintaining tissue homeostasis and the response to tissue damage. Focal adhesion kinase (FAK) and its close relative Pyk2 are non-receptor tyrosine kinases that mediate adhesion signaling to promote cell proliferation, motility and survival. FAK has also been shown to act as a mechanosensor by modulating cell proliferation in response to changes in tissue compliance. We previously showed that mice lacking FAK in the intestinal epithelium are phenotypically normal under homeostatic conditions but hypersensitive to experimental colitis induced by dextran sulfate sodium (DSS). Here we report that Pyk2-deficient mice are also phenotypically normal under homeostatic conditions and are similarly hypersensitive to DSS-induced colitis. These data indicate that normal intestinal development and homeostatic maintenance can occur in the presence of either FAK or Pyk2, but that both kinases are necessary for epithelial repair following injury. In contrast, mice lacking both FAK and Pyk2 develop spontaneous colitis with 100% penetrance by 4 weeks of age. Normal colonic phenotype and function are restored upon treatment of the double knockout mice with antibiotics, implicating commensal bacteria or bacterial products in the etiology of the spontaneous colitis exhibited by these mice.

Indexed as

AnimalsAnti-Bacterial AgentsCells, CulturedColitisDisease Models, AnimalFocal Adhesion Kinase 1Focal Adhesion Kinase 2Gastrointestinal MicrobiomeGene Knockout TechniquesHomeostasisIntestinal MucosaMiceAnti-Bacterial AgentsFocal Adhesion Kinase 1Focal Adhesion Kinase 2Ptk2b protein, mousePtk2 protein, mouse

Identifiers

PMID30872746
PMCPMC6418130
OpenAlexW2922093008

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.