Evidence map›Paper›PMID 29322087›Full record

ArticleCellular and molecular gastroenterology and hepatology2018

The Endosomal Protein Endotubin Is Required for Enterocyte Differentiation.

Christopher M Cox, Ruifeng Lu, Kaan Salcin, Jean M Wilson

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 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
0.6field-weighted citation impact, top 33% 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, 18 citations in OpenAlex.

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  14. Article
  15. Formation of Giant Lysosome in Neonatal Ileal Enterocytes Requires Endotubin.Cellular and molecular gastroenterology and hepatology · 2018
    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

4 authors at 2 institutions in 2 countries.

Christopher M CoxDepartment of Cell and Molecular Medicine, University of Arizona, Tucson, Arizona.
Ruifeng LuDepartment of Cell and Molecular Medicine, University of Arizona, Tucson, Arizona.
Kaan SalcinDepartment of Cell and Molecular Medicine, University of Arizona, Tucson, Arizona.
Jean M WilsonDepartment of Cell and Molecular Medicine, University of Arizona, Tucson, Arizona.
University of Arizona · USMcGill University · CA

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Teri L Bankhead · 1985 to 2026
$110.2M
Endocytic Regulation of Intestinal DevelopmentR01DK109701 · NIDDK · UNIVERSITY OF ARIZONA · PI WILSON, JEAN M · 2017 to 2021
$2.1M
Regulation of Intestinal Tight Junction Structure by Membrane TrafficR01DK084047 · NIDDK · UNIVERSITY OF ARIZONA · PI WILSON, JEAN M · 2011 to 2015
$1.7M
NCI NIH HHS P30 CA023074NIDDK NIH HHS R01 DK084047NIDDK NIH HHS R01 DK109701
6 · The paper itself

Abstract

BACKGROUND &

aimsDuring late embryonic development and through weaning, enterocytes of the ileum are highly endocytic. Defects in endocytosis and trafficking are implicated in neonatal disease, however, the mechanisms regulating trafficking during the developmental period are incompletely understood. The apical endosomal protein endotubin (EDTB) is highly expressed in the late embryonic and neonatal ileum. In epithelial cells in vitro, EDTB regulates both trafficking of tight junction proteins and proliferation through modulation of YAP activity. However, EDTB function during the endocytic stage of development of the intestine is unknown.

methodsBy using Villin-CreERT2, we induced knockout of EDTB during late gestation and analyzed the impact on endocytic compartments and enterocyte structure in neonates using immunofluorescence, immunocytochemistry, and transmission electron microscopy.

resultsDeletion of the apical endosomal protein EDTB in the small intestine during development impairs enterocyte morphogenesis, including loss of the apical endocytic complex, defective formation of the lysosomal compartment, and some cells had large microvillus-rich inclusions similar to those observed in microvillus inclusion disease. There also was a decrease in apical endocytosis and mislocalization of proteins involved in apical trafficking.

conclusionsOur results show that EDTB-mediated trafficking within the epithelial cells of the developing ileum is important for maintenance of endocytic compartments and enterocyte integrity during early stages of gut development.

Indexed as

AEC, apical endocytic complexAP, alkaline phosphataseCRISPR/Cas9, clustered regularly interspaced short palindromic repeats/cas9 endonucleaseEDTB, endotubinEEA1, early endosomal antigen 1EndosomesEndotubinGFP, green fluorescent proteinG, guideGTPase, guanosine triphosphataseKO, knockoutLAMP1, lysosome-associated membrane protein 1MAMDC4, MAM domain containing 4MVID, microvillus inclusion diseasePBS, phosphate-buffered salinePCR, polymerase chain reactionP, postnatal dayRabSDS, sodium dodecyl sulfateTBST, tris-buffered saline with 0.1% tween-20TEM, transmission electron microscopicTight JunctionTJ, tight junctionTrafficking

Identifiers

PMID29322087
PMCPMC5756061
OpenAlexW2768923125

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LicenceCC BY-NC-ND
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Registered trials

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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.