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Scot A Marsters on Muck Rack

Scot A Marsters

As seen in: AIChE Journal, Nature, BioRxiv
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Articles

Epithelial cancer cells co-opt the death ligand TRAIL to avert extrinsic apoptosis while acquiring killing capacity

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By John M. Canty, Scot A Marsters, David Lawrence, Serena Lee, Hartmut Koeppen, Avi Ashkenazi
| Nature Verified
Abstract Cancer cells avert apoptosis to sustain growth, evade immunity, and resist therapy. However, how they escape specific extrinsic death signals remains unclear. We show that certain epithelial carcinomas co-opt the death-receptor ligand Apo2L/TRAIL to suppress apoptosis while acquiring killing capacity. Analysis of CRISPR knockout screens from the Cancer Dependency Map uniquely identified TRAIL as an essential tumor necrosis factor superfamily member in epithelial malignancies.
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TRAIL induces caspase-dependent cleavage of specific components of the clathrin-mediated endocytosis machinery

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By David Lawrence, Scot A Marsters, Cary Austin, Avi Ashkenazi
| BioRxiv
Abstract It has been reported that caspase activation by the proapoptotic ligand Apo2L/TRAIL disrupts the clathrin-mediated endocytosis machinery (CMEM).
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A nonenzymatic dependency on inositol-requiring enzyme 1 controls cancer cell cycle progression and tumor growth

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By Iratxe Zuazo-Gaztelu, David Lawrence, Ioanna Oikonomidi, Scot A Marsters
| BioRxiv
Abstract Endoplasmic-reticulum resident inositol-requiring enzyme alpha; (IRE1) supports protein homeostasis via a cytoplasmic kinase-RNase module. Known cancer dependency on IRE1 entails its enzymatic activation of the transcription factor XBP1s and of RNA decay. We discovered that some cancer cells require IRE1 but not its enzymatic activity.
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