WNT/CTNNB1 signaling plays a critical role in the development of all multicellular animals. Here, we include both the embryonic stages, during which tissue morphogenesis takes place, and the postnatal stages of development, during which tissue homeostasis occurs. Thus, embryonic development concerns lineage development and cell fate specification, while postnatal development involves tissue maintenance and regeneration. Multiple tools are available to researchers who want to investigate, and ideally visualize, the dynamic and pleiotropic involvement of WNT/CTNNB1 signaling in these processes. Here, we discuss and evaluate the decisions that researchers need to make in identifying the experimental system and appropriate tools for the specific question they want to address, covering different types of WNT/CTNNB1 reporters in cells and mice. At a molecular level, advanced quantitative imaging techniques can provide spatio-temporal information that cannot be provided by traditional biochemical assays. We therefore also highlight some recent studies to show their potential in deciphering the complex and dynamic mechanisms that drive WNT/CTNNB1 signaling.
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http://dx.doi.org/10.1016/bs.ctdb.2023.02.001 | DOI Listing |
bioRxiv
November 2024
Section of Nephrology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Common intronic enhancer SNPs in Shroom3 associate with CKD in GWAS, although there is paucity of detailed mechanism. Previously, we reported a role for Shroom3 in mediating crosstalk between TGFβ1- & Wnt/Ctnnb1 pathways promoting renal fibrosis (TIF). However, beneficial roles for Shroom3 in proteinuria have also been reported suggesting pleiotropic effects.
View Article and Find Full Text PDFBiofactors
October 2024
Department of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.
The objective was to determine whether USP13 stabilizes WISP1 protein and contributes to tumorigenicity and metastasis in ESCC through the Wnt/CTNNB1 signaling pathway. ESCC cell lines (KYSE150 and TE10) were treated with the proteasome inhibitor MG-132, followed by siRNA screening of deubiquitinases (DUBs) to identify regulators of WISP1. Mass spectrometry, immunoprecipitation, and in vitro functional assays were conducted to explore the interaction between USP13 and WISP1 and to assess the effects of USP13 downregulation on cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and apoptosis.
View Article and Find Full Text PDFbioRxiv
March 2024
Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
WNT/β-catenin signaling is mediated by the transcriptional coactivator β-catenin (CTNNB1). CTNNB1 abundance is regulated by phosphorylation and proteasomal degradation promoted by a destruction complex composed of the scaffold proteins APC and AXIN1 or AXIN2, and the kinases CSNK1A1 and GSK3A or GSK3B. Loss of CSNK1A1 increases CTNNB1 abundance, resulting in hyperactive WNT signaling.
View Article and Find Full Text PDFmBio
December 2023
State Key Laboratory of Virology, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan, Hubei, China.
One of the conserved mechanisms at the stage of genome transcription of segmented negative-strand RNA viruses (sNSVs) is the cap-snatching process, which is vital for sNSVs transcription and provides drugable targets for the development of antivirals. However, the specificity of RNAs snatched by sNSV is still unclear. By transcriptomics analysis of whole blood samples from SFTS patients, we found WNT-CTNNB1 signaling pathway was regulated according to the course of the disease.
View Article and Find Full Text PDFPharmacol Res
November 2023
Department of Urology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. Electronic address:
Small nucleolar RNA host gene 15 (SNHG15) plays an oncogenic role in many cancers. However, the role of SNHG15 in bladder cancer (BLCA) remains unclear. In this study, the regulation of SNHG15 on the activities of BLCA cells (T24 and RT112) was investigated.
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