ArticleThe Journal of cell biology1998
Effects of forced expression of an NH2-terminal truncated beta-Catenin on mouse intestinal epithelial homeostasis.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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.
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Who cites it
77 citing papers in PubMed, 181 citations in OpenAlex.
- Mechano-gradients drive morphogen-noise correction to ensure robust patterning.Science advances · 2024Article
- Role of Wnt Signaling in Mouse Fetal Skin Wound Healing.Biomedicines · 2022Article
- Activation of PDGFRA signaling contributes to filamin C-related arrhythmogenic cardiomyopathy.Science advances · 2022Article
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- Cell competition corrects noisy Wnt morphogen gradients to achieve robust patterning in the zebrafish embryo.Nature communications · 2019Article
- Anoctamin 1/TMEM16A controls intestinal ClExperimental & molecular medicine · 2019Article
- Wnt/β-catenin-mediated signaling re-activates proliferation of matured cardiomyocytes.Stem cell research & therapy · 2018Article
- Comprehensive analysis of CTNNB1 in adrenocortical carcinomas: Identification of novel mutations and correlation to survival.Scientific reports · 2018Article
- Cell Adhesion Molecule CD166/ALCAM Functions Within the Crypt to Orchestrate Murine Intestinal Stem Cell Homeostasis.Cellular and molecular gastroenterology and hepatology · 2017Article
- Elevated levels of Wnt signaling disrupt thymus morphogenesis and function.Scientific reports · 2017Article
- Tuning Collective Cell Migration by Cell-Cell Junction Regulation.Cold Spring Harbor perspectives in biology · 2017Review
- Prostaglandin E2 promotes intestinal repair through an adaptive cellular response of the epithelium.The EMBO journal · 2017Article
- WDR26 is a new partner of Axin1 in the canonical Wnt signaling pathway.FEBS letters · 2016Article
- Type I Interferons Control Proliferation and Function of the Intestinal Epithelium.Molecular and cellular biology · 2016Article
- A hypermorphic epithelial β-catenin mutation facilitates intestinal tumorigenesis in mice in response to compounding WNT-pathway mutations.Disease models & mechanisms · 2015Article
- Nuclear signaling from cadherin adhesion complexes.Current topics in developmental biology · 2015Review
- A caspase-dependent pathway is involved in Wnt/β-catenin signaling promoted apoptosis in Bacillus Calmette-Guerin infected RAW264.7 macrophages.International journal of molecular sciences · 2014Article
- Apc regulates the function of hematopoietic stem cells largely through β-catenin-dependent mechanisms.Blood · 2013Article
- Loss of β-catenin induces multifocal periosteal chondroma-like masses in mice.The American journal of pathology · 2013Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
beta-Catenin functions as a downstream component of the Wnt/Wingless signal transduction pathway and as an effector of cell-cell adhesion through its association with cadherins. To explore the in vivo effects of beta-catenin on proliferation, cell fate specification, adhesion, and migration in a mammalian epithelium, a human NH2-terminal truncation mutant (DeltaN89 beta-catenin) was expressed in the 129/Sv embryonic stem cell-derived component of the small intestine of adult C57Bl/6-ROSA26 left and right arrow 129/Sv chimeric mice. DeltaN89 beta-Catenin was chosen because mutants of this type are more stable than the wild-type protein, and phenocopy activation of the Wnt/Wingless signaling pathway in Xenopus and Drosophila. DeltaN89 beta-Catenin had several effects. Cell division was stimulated fourfold in undifferentiated cells located in the proliferative compartment of the intestine (crypts of Lieberkühn). The proliferative response was not associated with any discernible changes in cell fate specification but was accompanied by a three- to fourfold increase in crypt apoptosis. There was a marked augmentation of E-cadherin at the adherens junctions and basolateral surfaces of 129/Sv (DeltaN89 beta-catenin) intestinal epithelial cells and an accompanying slowing of cellular migration along crypt-villus units. 1-2% of 129/Sv (DeltaN89 beta-catenin) villi exhibited an abnormal branched architecture. Forced expression of DeltaN89 beta-catenin expression did not perturb the level or intracellular distribution of the tumor suppressor adenomatous polyposis coli (APC). The ability of DeltaN89 beta-catenin to interact with normal cellular pools of APC and/or augmented pools of E-cadherin may have helped prevent the 129/Sv gut epithelium from undergoing neoplastic transformation during the 10-mo period that animals were studied. Together, these in vivo studies emphasize the importance of beta-catenin in regulating normal adhesive and signaling functions within this epithelium.
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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.