Elucidation of a universal size-control mechanism in Drosophila and mammals.
By Jixin Dong, G. Feldmann, Jianbin Huang, Shian Wu, Nailing Zhang, S. Comerford, M. Gayyed, R. Anders, A. Maitra, Duojia Pan. Cell, 2007
2,401 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9c37e891164fc4bc9e546fdde04e8c9a8523505c
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- The TEAD/TEF family protein Scalloped mediates transcriptional output of the Hippo growth-regulatory pathway. (2008, background): “Wts, facilitated by the Mob family protein Mats (Lai et al., 2005), phosphorylates the transcriptional coacti- 388 Developmental Cell 14, 388–398, March 2008 ª2008 Elsevier I vator Yorkie (Yki) (Huang et al., 2005) and inactivates Yki function by excluding it from the nucleus (Dong et al., 2007).”
- The biology of YAP/TAZ: hippo signaling and beyond. (2014, background): “Phosphorylation of YAP S127 creates a binding consensus for 14-3-3 proteins (14, 49, 266), which would then contribute to keep YAP/TAZ in the cytoplasm.”
- Mechanisms of Hippo pathway regulation (2016, positive): “The underlying biochemical mechanism is that Wts phosphorylates Yki and leads to Yki’s interaction with 14-3-3 and cytoplasmic retention (Dong et al. 2007).”
- The Hippo pathway target, YAP, promotes metastasis through its TEAD-interaction domain (2012, background): “Serine 127 is critical for LATS-mediated cytoplasmic sequestration of YAP by the Hippo pathway (1, 9, 28), and several groups have reported increased YAP activity after mutating serine 127 to alanine (1, 10, 24, 30).”
- Mst1 and Mst2 maintain hepatocyte quiescence and suppress the development of hepatocellular carcinoma through inactivation of the Yap1 oncogene (2009, positive): “Yap1 is amplified in a number of human tumor types and transgenic overexpression of Yap1 in mice leads to liver overgrowth and HCC as well as expansion of progenitor cells in multiple organs (Camargo et al., 2007; Dong et al., 2007; Overholtzer et al., 2006; Zender et al., 2006).”
- Hippo signaling is a potent in vivo growth and tumor suppressor pathway in the mammalian liver (2010, methodology): “These results are significant because although previous studies have indicated that overexpression of an activated form of yap is sufficient to induce liver growth and tumor formation (13, 23), whether hippo signaling is normally required to repress liver growth and tumor formation has not been prev”
- The Hippo signaling pathway components Lats and Yap pattern Tead4 activity to distinguish mouse trophectoderm from inner cell mass. (2009, background): “Since null mutations in either gene do not disrupt preimplantation development (McPherson et al., 2004; St. John et al., 1999; Yabuta et al., 2007), we overexpressed a catalytically inactive (kinase dead; KD) variant of Lats2, designed to dominantly inhibit both Lats1 and Lats2.”
- The Hippo signaling pathway in stem cell biology and cancer (2014, positive): “While it was already suggested based on the Drosophila data that the Hippo pathway is involved in mammalian tumorigenesis, Dong et al [12] provided functional evidence that the mammalian Hippo pathway is a potent regulator of organ size and that its dysregulation leads to tumorigenesis in the liver.”
- The TEAD/TEF family of transcription factor Scalloped mediates Hippo signaling in organ size control. (2008, background): “Furthermore, the nuclear levels of endogenous Yki increased in wts or hpo mutant clones (Dong et al., 2007).”
- TAZ Promotes Cell Proliferation and Epithelial-Mesenchymal Transition and Is Inhibited by the Hippo Pathway (2008, background): “Therefore, we propose that TAZ is phosphorylated and inhibited by Lats but not by AKT.”
- The Hippo-YAP pathway in organ size control and tumorigenesis: an updated version. (2010, background): “Functions of YAP in organ size regulation and tumorigenesis have been confirmed in mammals, using transgenic mouse models (Camargo et al. 2007; Dong et al. 2007).”
- 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”
- The role of YAP transcription coactivator in regulating stem cell self-renewal and differentiation. (2010, background): “Consistently, elevated YAP protein levels have been found in many human cancers, especially in the liver (Zender et al. 2006; Dong et al. 2007; Zhao et al. 2007; Steinhardt et al. 2008; Xu et al. 2009).”
- CDK8/9 drive Smad transcriptional action, turnover and YAP interactions in BMP and TGFβ pathways (2009, positive): “We show that ALP activation of Smad1 involves YAP (Yes-associated protein, also known as YAP1 or YAP65), the end target of the Hippo pathway (Huang et al., 2005), which mediates cell-contact growth inhibition, organ size control, and tumor suppression ( Dong et al., 2007; Overholtzer et al., 2006; ”