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Thanos P. Mourikis on Muck Rack

Thanos P. Mourikis

As seen in: Nature, Cell Press
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Articles

Author Correction: Direct and selective pharmacological disruption of the YAP-TEAD interface by IAG933 inhibits Hippo-dependent and RAS-MAPK-altered cancers | Nature Cancer

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By Emilie A. Chapeau, Giorgio G. Galli, Markus Wartmann, Thanos P. Mourikis, Sabrina Baltschukat, Daniel Bauer, David P. Kodack, Clemens Scheufler, Holger Sellner, Luca Tordella, Nicolas Soldermann
| Nature Verified
Correction to: Nature Cancer https://doi.org/10.1038/s43018-024-00754-9, published online 2 April 2024 In the version of the article initially published, in Fig. 1f, the MSTO-211H graph was originally a duplicate of NCI-H226. This has now been amended, and the correct MSTO-211H graph can be found in the HTML and PDF versions of the article.
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Direct and selective pharmacological disruption of the YAP–TEAD interface by IAG933 inhibits Hippo-dependent and RAS–MAPK-altered cancers - Nature Cancer

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By Giorgio G. Galli, Markus Wartmann, Thanos P. Mourikis, Daniel Bauer, David P. Kodack, Luca Tordella, Emilie A. Chapeau, Sabrina Baltschukat, Clemens Scheufler, Holger Sellner, Nicolas Soldermann
| Nature Verified
Abstract The YAP–TEAD protein–protein interaction mediates YAP oncogenic functions downstream of the Hippo pathway. To date, available YAP–TEAD pharmacologic agents bind into the lipid pocket of TEAD, targeting the interaction indirectly via allosteric changes. However, the consequences of a direct pharmacological disruption of the interface between YAP and TEADs remain largely unexplored.
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Mapping the Human Kinome in Response to DNA Damage

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By Byrne C.J, Michel Owusu, Thanos P. Mourikis, Peter Bannauer
| Cell Press Verified
Highlights • Catalog of the human kinome in response to different types of genotoxic stress • Synthetic vulnerability or resistance for kinases and DNA-damaging chemotherapeutics • Identification of MARK3 as a kinase in the DNA damage response Summary We provide a catalog for the effects of the human kinome on cell survival in response to DNA-damaging agents, covering all major DNA repair pathways.
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