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      YAP and TAZ Negatively Regulate Prox1 During Developmental and Pathologic Lymphangiogenesis

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          Most cited references 40

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          Mechanisms and regulation of endothelial VEGF receptor signalling.

          Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are uniquely required to balance the formation of new blood vessels with the maintenance and remodelling of existing ones, during development and in adult tissues. Recent advances have greatly expanded our understanding of the tight and multi-level regulation of VEGFR2 signalling, which is the primary focus of this Review. Important insights have been gained into the regulatory roles of VEGFR-interacting proteins (such as neuropilins, proteoglycans, integrins and protein tyrosine phosphatases); the dynamics of VEGFR2 endocytosis, trafficking and signalling; and the crosstalk between VEGF-induced signalling and other endothelial signalling cascades. A clear understanding of this multifaceted signalling web is key to successful therapeutic suppression or stimulation of vascular growth.
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            Cancer biology and NuRD: a multifaceted chromatin remodelling complex.

            The nucleosome remodelling and histone deacetylase (NuRD; also known as Mi-2) complex regulates gene expression at the level of chromatin. The NuRD complex has been identified - using both genetic and molecular analyses - as a key determinant of differentiation in mouse embryonic stem cells and during development in various model systems. Similar to other chromatin remodellers, such as SWI/SNF and Polycomb complexes, NuRD has also been implicated in the regulation of transcriptional events that are integral to oncogenesis and cancer progression. Emerging molecular details regarding the recruitment of NuRD to specific loci during development, and the modulation of these events in cancer, are used to illustrate how the inappropriate localization of the complex could contribute to tumour biology.
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              Regulation of insulin-like growth factor signaling by Yap governs cardiomyocyte proliferation and embryonic heart size.

              The Hippo signaling pathway regulates growth of the heart and other tissues. Hippo pathway kinases influence the activity of various targets, including the transcriptional coactivator Yap, but the specific role of Yap in heart growth has not been investigated. We show that Yap is necessary and sufficient for embryonic cardiac growth in mice. Deletion of Yap in the embryonic mouse heart impeded cardiomyocyte proliferation, causing myocardial hypoplasia and lethality at embryonic stage 10.5. Conversely, forced expression of a constitutively active form of Yap in the embryonic heart increased cardiomyocyte number and heart size. Yap activated the insulin-like growth factor (IGF) signaling pathway in cardiomyocytes, resulting in inactivation of glycogen synthase kinase 3β, which led to increased abundance of β-catenin, a positive regulator of cardiac growth. Our results point to Yap as a critical downstream effector of the Hippo pathway in the control of cardiomyocyte proliferation and a nexus for coupling the IGF, Wnt, and Hippo signaling pathways with the developmental program for heart growth.
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                Author and article information

                Journal
                Circulation Research
                Circ Res
                Ovid Technologies (Wolters Kluwer Health)
                0009-7330
                1524-4571
                January 18 2019
                January 18 2019
                : 124
                : 2
                : 225-242
                Affiliations
                [1 ]From the Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon (H.C., J.H.A., D.-S.L., G.Y.K.)
                [2 ]Center for Vascular Research, Institute for Basic Science, Daejeon, Republic of Korea (J.K., G.Y.K.)
                [3 ]Department of Surgery (Y.-K.H.), Keck School of Medicine, University of Southern California, Los Angeles
                [4 ]Department of Biochemistry and Molecular Biology (Y.-K.H.), Keck School of Medicine, University of Southern California, Los Angeles
                [5 ]Department of Immunology, Genetics, and Pathology, Uppsala University, Sweden (T.M.).
                Article
                10.1161/CIRCRESAHA.118.313707
                © 2019

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