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YAP/TAZ mechanotransduction integrates with cell-cell communication pathways for fine-grained orchestration of stem cell decisions.
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The TAZ WW domain exhibits a binding preference for the second of the two PPxY motifs of LATS1 in vitro. We modelled the structure of the domain in complex with LATS1 PPxY2 peptide and, through molecular dynamics simulations, show that WW domain-PPxY2 complex is stable with some flexibility in the peptide region.
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In the present review, we focus on the functions of YAP/TAZ in cancer, discuss their potential as new therapeutic target for tumor treatment, and provide valuable suggestions for further study in this field.
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functional evaluation of a HTM cell monolayer using a permeability assay demonstrated that the inhibition of YAP and TAZ attenuated the DEX-induced impairment of permeability. These findings suggest that YAP and TAZ play pivotal roles in the DEX-induced cytoskeletal changes of HTM cells, and reveal novel potential mechanisms for the development and progression of glaucoma
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WWTR1 promotes cell proliferation and inhibits apoptosis of GC cells by regulating cell cycle/apoptosisassociated factors, and effectors in the TGFbeta pathway.
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EphA2-mediates glutaminolysis through YAP/TAZ activation in HER2-positive breast cancer and may serve as potential therapeutic targets in patients.
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Depletion of either YES-associated protein (YAP) or transcriptional coactivator with PDZ-motif (TAZ) sensitised cancer cell lines to MLN8237, resulting in apoptosis and reduction in aurora-A.
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High TAZ expression is associated with breast cancer.
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Nuclear localization of YAP and TAZ was reduced in DMOG-treated primary tubular epithelial cells.
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SnoN interacts with multiple components of the Hippo pathway to inhibit the binding of Lats2 to TAZ and the subsequent phosphorylation of TAZ, leading to TAZ stabilization.
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Results show that YAP and TAZ transcription are regulated by Cbx7 inhibiting glioblasoma cell migration.
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Besides its role in normal tissue development, TAZ plays critical roles in cell proliferation, differentiation, apoptosis, migration, invasion, epithelial-mesenchymal transition (EMT), and stemness in multiple human cancers.
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Together, these data illustrate that YAP/TAZ signaling is responsive to hydrogel stiffness and degradability, but the outcome is dependent on the dimensionality of cell-biomaterial interactions.
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Wnt signaling upregulated WBP2 by disrupting ITCH-WBP2 interactions via EGFR-mediated tyrosine phosphorylation of WBP2 and TAZ/YAP competitive binding.
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results highlight both CYR61 and TAZ genes as potential predictive biomarkers for stratification of the risk for development of adenocarcinoma and suggest a potential mechanistic route for Barrett's esophagus neoplastic progression
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Collectively, our study identified an unexpected transcriptional repression function of the BET bromodomain and a novel mechanism for TAZ upregulation.
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High TAZ expression is associated with non-small cell lung cancer.
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These findings demonstrate sufficiency of TAZ activation for driving fibroblast proliferation, contraction, and soluble profibrotic factor expression, and mechanical context-dependent crosstalk of TAZ with other pathways in regulating Col1a1 expression.
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A group of miRNAs have been demonstrated to directly target components of the Hippo signaling pathway, such as YAP, TAZ and LATS1/2 in oncogenesis. (Review)
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AXL/TAZ/YAP expression is associated with poor prognosis in male breast cancer patients.
