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Related Concept Videos

Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Related Experiment Video

Updated: Apr 5, 2026

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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Alternative Wnt Signaling Activates YAP/TAZ.

Hyun Woo Park1, Young Chul Kim2, Bo Yu3

  • 1Department of Pharmacology and Moores Cancer Center, University of California San Diego, La Jolla, CA 92093, USA.

Cell
|August 16, 2015
PubMed
Summary

The transcriptional co-activators YAP and TAZ are key regulators of organ size and tissue homeostasis, and their dysregulation contributes to human cancer. Here, we discover YAP/TAZ as bona fide downstream effectors of the alternative Wnt signaling pathway. Wnt5a/b and Wnt3a induce YAP/TAZ activation independent of canonical Wnt/β-catenin signaling. Mechanistically, we delineate the "alternative Wnt-YAP/TAZ signaling axis" that consists of Wnt-FZD/ROR-Gα12/13-Rho GTPases-Lats1/2 to promote YAP/TAZ activation and TEAD-mediated transcription. YAP/TAZ mediate the biological functions of alternative Wnt signaling, including gene expression, osteogenic differentiation, cell migration, and antagonism of Wnt/β-catenin signaling. Together, our work establishes YAP/TAZ as critical mediators of alternative Wnt signaling.

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Area of Science:

  • Cell biology
  • Molecular biology
  • Cancer research

Background:

  • The transcriptional co-activators YAP and TAZ regulate organ size and tissue homeostasis.
  • Dysregulation of YAP/TAZ is implicated in human cancer.
  • Alternative Wnt signaling pathways play crucial roles in cellular processes.

Purpose of the Study:

  • To identify downstream effectors of the alternative Wnt signaling pathway.
  • To elucidate the mechanism by which alternative Wnt signaling activates YAP/TAZ.
  • To establish YAP/TAZ as mediators of alternative Wnt signaling functions.

Main Methods:

  • Investigated the role of YAP/TAZ in response to Wnt5a/b and Wnt3a.
  • Delineated the signaling cascade from Wnt ligands to YAP/TAZ activation.
  • Assessed YAP/TAZ-mediated functions including gene expression and cell differentiation.

Main Results:

  • YAP/TAZ are bona fide downstream effectors of alternative Wnt signaling.
  • Wnt5a/b and Wnt3a activate YAP/TAZ independently of canonical Wnt/β-catenin signaling.
  • The identified signaling axis involves Wnt-FZD/ROR-Gα12/13-Rho GTPases-Lats1/2.

Conclusions:

  • YAP/TAZ mediate key biological functions of alternative Wnt signaling.
  • Alternative Wnt signaling promotes YAP/TAZ activation and TEAD-mediated transcription.
  • YAP/TAZ are critical mediators of alternative Wnt signaling, impacting gene expression, differentiation, and cell migration.