ZNRF3 promotes Wnt receptor turnover in an R-spondin-sensitive manner
By Huai-Xiang Hao, Yang Xie, Yue Zhang, O. Charlat, Emma Oster, Monika Avello, Hong Lei, C. Mickanin, Dong Liu, H. Ruffner and 9 more. Nature, 2012
909 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/993d4b55dc00cd52621c7a12e7d21e138eed0268
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Citations in the corpus
- An integral program for tissue renewal and regeneration: Wnt signaling and stem cell control (2014, background): “R-spondins, acting through Lgr family receptors (11–13), inhibit the transmembrane E3 ubiquitin ligases Rnf43/Znrf3 that ordinarily ubiquitinate and thus degrade Frizzled receptors (14, 15).”
- The R-spondin/Lgr5/Rnf43 module: regulator of Wnt signal strength (2014, neutral): “Although the Frizzled receptor clearly is a substrate for Rnf43/Znrf3-associated enzyme activity and their physical interaction was detected (Hao et al. 2012), the exact mechanism of this interaction is unknown.”
- Wnt signaling in development and tissue homeostasis (2018, background): “Rnf43 and Znrf3 are recently characterized Wnt-β -catenin target genes that encode transmembrane E3-ubiquitin-ligases (Hao et al., 2012; Koo et al., 2012) involved in ubiquitin-dependent Frizzled endocytosis and proteasomal degradation, thereby reducing receptor levels at the plasma membrane.”
- The intestinal crypt, a prototype stem cell compartment. (2013, background): “Simultaneous conditional deletion in crypt stem cells of Rnf43 and Znrf3 resulted in rapidly expanding stem/Paneth compartments that ultimate grew into large adenomas.”
- Functional repair of CFTR by CRISPR/Cas9 in intestinal stem cell organoids of cystic fibrosis patients. (2013, background): “…the CRISPR/Cas9 system for genome engineering in various species (Chang et al., 2013; Cho et al., 2013; Cong et al., 2013; Friedland et al., 2013; Hou et al., 2013; Hwang et al., 2013; Jinek et al., 2013; Li et al., 2013; Mali et al., 2013; Nekrasov et al., 2013; Shen et al., 2013; Wang et al.,…”
- Wnt/β-catenin signaling in cancers and targeted therapies (2021, background): “Znrf3 and Rnf43 were not essential in the intestine but dysregulation of Znrf3/Rnf43 was important for the growth of CRC.(26,27,123) Mutations of Rnf43, resulting in E3 ubiquitin ligases function loss, promoted CRC development and poor prognosis.”