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Leonardo Morsut

Researcher at University of Southern California

Publications -  29
Citations -  10627

Leonardo Morsut is an academic researcher from University of Southern California. The author has contributed to research in topics: Synthetic biology & Biology. The author has an hindex of 14, co-authored 23 publications receiving 8503 citations. Previous affiliations of Leonardo Morsut include University of California & University of Padua.

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Role of YAP/TAZ in mechanotransduction

TL;DR: YAP/TAZ are identified as sensors and mediators of mechanical cues instructed by the cellular microenvironment and are functionally required for differentiation of mesenchymal stem cells induced by ECM stiffness and for survival of endothelial cells regulated by cell geometry.
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CRISPR-Mediated Modular RNA-Guided Regulation of Transcription in Eukaryotes

TL;DR: The results establish that the CRISPR system can be used as a modular and flexible DNA-binding platform for the recruitment of proteins to a target DNA sequence, revealing the potential of CRISpri as a general tool for the precise regulation of gene expression in eukaryotic cells.
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Precision Tumor Recognition by T Cells With Combinatorial Antigen-Sensing Circuits.

TL;DR: A combinatorially activated T cell circuit in which a synthetic Notch receptor for one antigen induces the expression of a CAR for a second antigen opens the door to immune recognition of a wider range of tumors.
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Engineering Customized Cell Sensing and Response Behaviors Using Synthetic Notch Receptors.

TL;DR: It is found that chimeric forms of Notch, in which both the extracellular sensor module and the intracellular transcriptional module are replaced with heterologous protein domains, can serve as a general platform for generating novel cell-cell contact signaling pathways.
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FAM/USP9x, a Deubiquitinating Enzyme Essential for TGFβ Signaling, Controls Smad4 Monoubiquitination

TL;DR: This study defines a regulative ubiquitination step controlling Smads that is parallel to those impinging on R-Smad phosphorylation, and points to Smad4 monoubiquitinated and deubiquitination as a way for cells to set their TGFbeta responsiveness.