ArticlePloS one2012
mTrop1/Epcam knockout mice develop congenital tufting enteropathy through dysregulation of intestinal E-cadherin/β-catenin.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers.
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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.
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.
Who cites it
56 citing papers in PubMed, 82 citations in OpenAlex.
- Trop-1/EpCAM Thr115 is a driver of hyperproliferative cell repair and of severe lung damage in COVID-19.iScience · 2026Article
- EpCAM deficiency causes the inflammation of lungs due to the reduction of pIgR in airway epithelium.Respiratory research · 2026Article
- Farnesoid X Receptor Agonist Tropifexor Improves Intestinal Defense Response and Epithelial Barrier Function in Neonatal Piglets Receiving Parenteral Nutrition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- Regulation of the Function and Expression of EpCAM.Biomedicines · 2024Review
- Tmprss2 maintains epithelial barrier integrity and transepithelial sodium transport.Life science alliance · 2024Article
- EpCAM proteolysis and release of complexed claudin-7 repair and maintain the tight junction barrier.The Journal of cell biology · 2023Article
- Cytosolic EpCAM cooperates with H-Ras to regulate epithelial to mesenchymal transition through ZEB1.PloS one · 2023Article
- EPCAM and TROP2 share a role in claudin stabilization and development of intestinal and extraintestinal epithelia in mice.Biology open · 2022Article
- EpCAM Is Essential to Maintaining the Immune Homeostasis of IntestinesFrontiers in immunology · 2022Article
- Article
- Monogenic mutations in four cases of neonatal-onset watery diarrhea and a mutation review in East Asia.Orphanet journal of rare diseases · 2021Article
- Functional Implications of the Dynamic Regulation of EpCAM during Epithelial-to-Mesenchymal Transition.Biomolecules · 2021Review
- EMT-Induced Gemcitabine Resistance in Pancreatic Cancer Involves the Functional Loss of Equilibrative Nucleoside Transporter 1.Molecular cancer therapeutics · 2021Article
- EpCAM is essential for maintenance of the small intestinal epithelium architecture via regulation of the expression and localization of proteins that compose adherens junctions.International journal of molecular medicine · 2021Article
- EpCAM (CD326) Regulates Intestinal Epithelial Integrity and Stem Cells via Rho-Associated Kinase.Cells · 2021Article
- Congenital Tufting Enteropathy: Biology, Pathogenesis and Mechanisms.Journal of clinical medicine · 2020Review
- Trop2: Jack of All Trades, Master of None.Cancers · 2020Review
- New mutation inWorld journal of clinical cases · 2020Article
- EpCAM as Modulator of Tissue Plasticity.Cells · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Congenital tufting enteropathy (CTE) is a life-threatening hereditary disease that is characterized by enteric mucosa tufting degeneration and early onset, severe diarrhea. Loss-of-function mutations of the human EPCAM gene (TROP1, TACSTD1) have been indicated as the cause of CTE. However, loss of mTrop1/Epcam in mice appeared to lead to death in utero, due to placental malformation. This and indications of residual Trop-1/EpCAM expression in cases of CTE cast doubt on the role of mTrop1/Epcam in this disease. The aim of this study was to determine the role of TROP1/EPCAM in CTE and to generate an animal model of this disease for molecular investigation and therapy development. Using a rigorous gene-trapping approach, we obtained mTrop1/Epcam -null (knockout) mice. These were born alive, but failed to thrive, and died soon after birth because of hemorrhagic diarrhea. The intestine from the mTrop1/Epcam knockout mice showed intestinal tufts, villous atrophy and colon crypt hyperplasia, as in human CTE. No structural defects were detected in other organs. These results are consistent with TROP1/EPCAM loss being the cause of CTE, thus providing a viable animal model for this disease, and a benchmark for its pathogenetic course. In the affected enteric mucosa, E-cadherin and β-catenin were shown to be dysregulated, leading to disorganized transition from crypts to villi, with progressive loss of membrane localization and increasing intracellular accumulation, thus unraveling an essential role for Trop-1/EpCAM in the maintenance of intestinal architecture and functionality.Supporting information is available for this article.
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Registered trials
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.