Hans Michael Maric on Muck Rack

Hans Michael Maric

As seen in: Nature
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Articles

Correction: USP10 drives cancer stemness and enables super-competitor signalling in colorectal cancer - Oncogene

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By Michaela Reissland, Saskia Tauch, Jeroen M. Bugter, Clemens Schulte, Daniel Solvie, Ashwin Narain, Anne-Claire Jacomin, Carsten P. Ade, Viktoria Buck, Vivian Li, Armin Wiegering, Martin Eilers, Hans Michael Maric, Mathias Rosenfeldt, Madelon M. Maurice, Ivan Dikic, Amir Orian
| Nature Verified
The affiliation of the author Gerti Beliu has been corrected from “Institute of Lung Health and Immunity, Helmholtz Center, Munich, Germany” to “Rudolf-Virchow-Center for Integrative and Translational Imaging, University of Wuerzburg, Wuerzburg, Germany.” The original article has been corrected.
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Inhibition of the YAP-MMB interaction and targeting NEK2 as potential therapeutic strategies for YAP-driven cancers - Oncogene

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By Marco Jessen, Clemens Schulte, Hans Michael Maric, Carsten P. Ade, Björn von Eyss
| Nature Verified
Abstract YAP activation in cancer is linked to poor outcomes, making it an attractive therapeutic target. Previous research focused on blocking the interaction of YAP with TEAD transcription factors. Here, we took a different approach by disrupting YAP’s binding to the transcription factor B-MYB using MY-COMP, a fragment of B-MYB containing the YAP binding domain fused to a nuclear localization signal. MY-COMP induced cell cycle defects, nuclear abnormalities, and polyploidization.
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Molecular characterization of AIFM2/FSP1 inhibition by iFSP1-like molecules - Cell Death & Disease

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By Clemens Schulte, Hans Michael Maric
| Nature Verified
Cell Lines. 4-hydroxytamoxifen (TAM)-inducible Gpx4−/− murine immortalized fibroblasts (Pfa1) were reported previously [24]. These cells harbor two loxP-flanked Gpx4 alleles and stably express TAM inducible Cre recombinase allowing the genetic deletion of Gpx4 at will. For all experiments using Gpx4−/− the well were treated with 4-hydroxitamoxifen (TAM) 1 µM.
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