Hippo signaling at a glance

Zhao, Bin; Li, Li; Guan, Kun‐Liang

doi:10.1242/jcs.069070

Cited by 115 publications

(115 citation statements)

References 98 publications

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“…High levels of YAP and TAZ can cause organ hypertrophy and eventually tumorigenesis (27). On the contrary, depletion of YAP and TAZ results in proliferation inhibition and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

The N-terminal Phosphodegron Targets TAZ/WWTR1 Protein for SCFβ-TrCP-dependent Degradation in Response to Phosphatidylinositol 3-Kinase Inhibition

Huang

Liu

et al. 2012

Journal of Biological Chemistry

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146

143

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Background: TAZ overexpression is implicated in cancer development. Results:The N-terminal phosphodegron is phosphorylated by GSK3, which creates a binding site for ␤-TrCP, resulting in TAZ ubiquitylation and degradation. Conclusion:The N-terminal phosphodegron regulates TAZ stability in response to the dysregulated PI3K pathway. Significance: Our study reveals the underlying mechanism of TAZ N-terminal phosphodegron regulation in elevated TAZ cancers with a dysregulated PTEN/PI3K pathway.

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“…High levels of YAP and TAZ can cause organ hypertrophy and eventually tumorigenesis (27). On the contrary, depletion of YAP and TAZ results in proliferation inhibition and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

The N-terminal Phosphodegron Targets TAZ/WWTR1 Protein for SCFβ-TrCP-dependent Degradation in Response to Phosphatidylinositol 3-Kinase Inhibition

Huang

Liu

et al. 2012

Journal of Biological Chemistry

Self Cite

146

143

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“…Mutation leads to neurofibromatosis type II; lesions in the CNS and eyes and skin [114,115] TSG in some cancers due to mutation and underexpression [10] Barely studied; point mutations were not critical [49] WWC1, KIBRA Polymorphisms associated with Alzheimer's disease [116] Not studied…”

Section: Nf2 Merlinmentioning

confidence: 99%

“…Moreover, cross talks of the Hippo pathway with other signalling pathways like Notch, EGF or Sonic hedgehog have also been described [49]. Due to the space constraints they will not be discussed.…”

Section: Hippo Pathway Cross Talk With Wnt/b-catenin and Egfr/kras Simentioning

confidence: 99%

The Hippo pathway in colorectal cancer

Wierzbicki

Rybarczyk

2015

Folia Histochem Cytobiol.

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Colorectal cancer (CRC) is one the most frequently diagnosed neoplastic diseases worldwide. Currently, aside from traditional chemotherapy, advanced CRCs are treated with modern drugs targeting cellular components such as epithelial growth factor receptor (EGFR). Since up to 70% of metastasized CRCs are drug resistant, the description of recent progress in cellular homeostasis regulation may shed new light on the development of new molecular targets in cancer treatment. The Hippo pathway has recently become subject of intense investigations since it plays a crucial role in cell proliferation, differentiation, apoptosis and tumourigenesis. Components of the Hippo pathway are deregulated in various human malignancies, and expression levels of its major signal transducers were proposed as prognostic factors in colorectal cancer. In this review we focused on recent data regarding Hippo pathway, its up-stream signals and down-stream effectors. Hippo negatively regulates its major effectors, YAP1 and TAZ kinases, which act as transcriptional co-activators inducing expression of genes involved not only in tissue repair and proliferation but are also oncoproteins involved in tumour development and progression. The deregulation of Hippo pathway components was found in many malignancies. The interactions between Hippo and Wnt/b-catenin signalling, crucial in the maintenance of cell homeostasis, have been described in relation to the control of intestinal stem cell proliferation and CRC development. The recently discovered positive feedback loop between activated YAP1 and increased EGFR/KRAS signalling found in oesophageal, ovarian and hepatocellular cancer has been related to the CRC progression and resistance to EGFR inhibitors during CRC therapy.

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“…This demonstrates the strength of morphogens as growth-promoting agents (Leevers and McNeill 2005;Crickmore and Mann 2008), which is the consequence of interlinks between growth and pattern generation signaling pathways. For instance, Wnt, TGF-b, Sonic Hedgehog (Shh), and Notch all impact on Hippo pathway activity (Alarcon et al 2009;Varelas et al 2010;Zhao et al 2010;Heallen et al 2011). Additionally, morphogens influence cell number through cellular differentiation that frequently results in cell cycle exit.…”

Section: Morphogens: Controlling Growth By Regulation Of Cell Prolifementioning

confidence: 99%

Mechanisms and pathways of growth failure in primordial dwarfism

Klingseisen¹,

Jackson²

2011

Genes Dev.

188

198

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The greatest difference between species is size; however, the developmental mechanisms determining organism growth remain poorly understood. Primordial dwarfism is a group of human single-gene disorders with extreme global growth failure (which includes Seckel syndrome, microcephalic osteodysplastic primordial dwarfism I [MOPD] types I and II, and Meier-Gorlin syndrome). Ten genes have now been identified for microcephalic primordial dwarfism, encoding proteins involved in fundamental cellular processes including genome replication (ORC1 [origin recognition complex 1], ORC4, ORC6, CDT1, and CDC6), DNA damage response (ATR [ataxia-telangiectasia and Rad3-related]), mRNA splicing (U4atac), and centrosome function (CEP152, PCNT, and CPAP). Here, we review the cellular and developmental mechanisms underlying the pathogenesis of these conditions and address whether further study of these genes could provide novel insight into the physiological regulation of organism growth.

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Hippo signaling at a glance

Cited by 115 publications

References 98 publications

The N-terminal Phosphodegron Targets TAZ/WWTR1 Protein for SCFβ-TrCP-dependent Degradation in Response to Phosphatidylinositol 3-Kinase Inhibition

The N-terminal Phosphodegron Targets TAZ/WWTR1 Protein for SCFβ-TrCP-dependent Degradation in Response to Phosphatidylinositol 3-Kinase Inhibition

The Hippo pathway in colorectal cancer

Mechanisms and pathways of growth failure in primordial dwarfism

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