TAZ Promotes Cell Proliferation and Epithelial-Mesenchymal Transition and Is Inhibited by the Hippo Pathway
By Q. Lei, Heng Zhang, Bin Zhao, Zhengyu Zha, F. Bai, X. Pei, Shimin Zhao, Y. Xiong, K. Guan. Molecular and Cellular Biology, 2008
956 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/8dbf2a047e02772855662dd24c8b33f3c46d8ef2
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Citations in the corpus
- A mechanical checkpoint controls multicellular growth through YAP/TAZ regulation by actin-processing factors. (2013, positive): “As TAZ overexpression has been shown to induce epithelial-tomesenchymal transition in cells cultured on plastic in 2D (Lei et al., 2008), this 3D phenotype likely reflects fully unleashed TAZ activity.”
- Hippo Pathway in Organ Size Control, Tissue Homeostasis, and Cancer. (2015, positive): “YAP induces expression of ZEB1/2 to stimulate the epithelial-to-mesenchymal transition (EMT), which is a key step for tumor metastasis (Gao et al., 2014; Lei et al., 2008; Liu et al., 2010b; Overholtzer et al., 2006).”
- The Hippo Signaling Pathway in Development and Disease (2019, background): “The existence of an evolutionarily conserved kinase cascade culminating on the phosphorylation of YAP and TAZ, the mammalian counterpart of Yki, was soon demonstrated in mammalian cells (Dong et al., 2007; Lei et al., 2008; Zhao et al., 2007).”
- The biology of YAP/TAZ: hippo signaling and beyond. (2014, background): “This function is conserved in mammalian cells: overexpression of nonphosphorylatable forms of YAP or TAZ increases the proliferation of several human or mouse cell lines in vitro (114, 165, 167, 267).”
- The Hippo transducer TAZ confers cancer stem cell-related traits on breast cancer cells. (2011, positive): “Others have shown that TAZ itself can sustain EMT (Chan et al., 2008; Lei et al., 2008); however, we found that acquisition of mesenchymal traits can be uncoupled from TAZ-induced CSC-like properties.”
- The Hippo signaling pathway components Lats and Yap pattern Tead4 activity to distinguish mouse trophectoderm from inner cell mass. (2009, background): “A Role for Hippo Signaling in Preimplantation Embryos The Hippo signaling pathway mediates cell contact-mediated growth inhibition in cultured cells (Lei et al., 2008; Ota and Sasaki, 2008; Zhao et al., 2007, 2008), but our evidence suggests a slightly different role during preimplantation developme”
- The 14-3-3 proteins: integrators of diverse signaling cues that impact cell fate and cancer development (2008, background): “With regard to YAP and TAZ, mutants unable to bind to 14-3-3 localize constitutively in the nucleus and exhibit constitutive activity that can result in the loss of cell contact inhibition, epithelial-to-mesenchymal transition and/or anchorageindependent growth [52,54,55], all of which are propertie”
- Mst1 and Mst2 maintain hepatocyte quiescence and suppress the development of hepatocellular carcinoma through inactivation of the Yap1 oncogene (2009, positive): “In this regard, it is notable that the transcriptional coactivator Taz—a potential oncogene (Chan et al., 2008; Lei et al., 2008) — shares 45% homology to Yap1 throughout its sequence, and in vitro studies suggest that these proteins can be regulated through comparable mechanisms (i.e. by…”
- The Hippo pathway: regulators and regulations. (2013, background): “Lats1/2 directly interact with and phosphorylate YAP/ TAZ (Huang et al. 2005; Dong et al. 2007; Zhao et al. 2007; Lei et al. 2008; Oh and Irvine 2008), in which the interaction may be mediated by PPxY motifs on Lats1/2 andWWdomains on YAP/TAZ (Hao et al.”
- The Hippo-YAP pathway in organ size control and tumorigenesis: an updated version. (2010, background): “YAP/TAZ are the major downstream effectors of the Hippo pathway.”
- The two faces of Hippo: targeting the Hippo pathway for regenerative medicine and cancer treatment (2013, positive): “Overexpression of YAP and/or TAZ can lead to acquisition of a mesenchymal phenotype in mammary epithelial cells suggesting Hippo signaling may play important roles in suppression of EMT 15, 61, 132 .”
- The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges (2019, background): “Similarly, ectopic expression of TAZ promotes cell proliferation, reduces cell contact inhibition and enhances EMT, where phosphorylation of TAZ by LATS reverses these effects [168].”