The Wnt, TGF-β, and Notch signaling pathways are essential for the regulation of cellular polarity, differentiation, proliferation, and migration. Differential activation and mutual crosstalk of these pathways during animal development are crucial instructive forces in the initiation of the body axis and the development of organs and tissues. Due to the ability to initiate cell proliferation, these pathways are vulnerable to somatic mutations selectively producing cells, which ultimately slip through cellular and organismal checkpoints and develop into cancer. The architecture of the Wnt, TGF-β, and Notch signaling pathways is simple. The transmembrane receptor, activated by the extracellular stimulus, induces nuclear translocation of the transcription factor, which subsequently changes the expression of target genes. Nevertheless, these pathways are regulated by a myriad of factors involved in various feedback mechanisms or crosstalk. The most prominent group of regulators is the ubiquitin-proteasome system (UPS). To open the door to UPS-based therapeutic manipulations, a thorough understanding of these regulations at a molecular level and rigorous confirmation in vivo are required. In this quest, mouse models are exceptional and, thanks to the progress in genetic engineering, also an accessible tool. Here, we reviewed the current understanding of how the UPS regulates the Wnt, TGF-β, and Notch pathways and we summarized the knowledge gained from related mouse models.

• Klíčová slova
• cancer, gene inactivation, mouse model, ubiquitin–proteasome system,
• MeSH
• beta-katenin metabolismus   MeSH
• buněčná diferenciace fyziologie   MeSH
• homeostáza genetika   MeSH
• ligasy metabolismus   MeSH
• myši embryologie   genetika   MeSH
• proliferace buněk fyziologie   MeSH
• proteiny Wnt metabolismus   MeSH
• receptory Notch metabolismus   MeSH
• signální dráha Wnt fyziologie   MeSH
• transformující růstový faktor beta metabolismus   MeSH
• transkripční faktory metabolismus   MeSH
• ubikvitin metabolismus   MeSH
• ubikvitinligasy metabolismus   fyziologie   MeSH
• vývojová regulace genové exprese genetika   MeSH
• zvířata MeSH
• Check Tag
• myši embryologie   genetika   MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• beta-katenin MeSH
• ligasy MeSH
• proteiny Wnt MeSH
• receptory Notch MeSH
• transformující růstový faktor beta MeSH
• transkripční faktory MeSH
• ubikvitin MeSH
• ubikvitinligasy MeSH