Author

P. Castel

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Biochemistry· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:proteomics· 3 Research Focus:cell signaling & trafficking· 2 Organism:human· 2 Approach:biophysical modeling· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1

Frequent Co-Authors

A. Cheng· 2 shared A. Cuevas-Navarro· 2 shared A. Urisman· 2 shared F. McCormick· 2 shared R. Van· 2 shared A. Berger· 1 shared A. G. Stephen· 1 shared A. K. Riley· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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2 shared papersBiochemistry

A. Cheng

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

The deubiquitinase USP9X regulates RIT1 protein abundance and oncogenic phenotypes

A. K. Riley, M. Grant, A. Snell, A. Vichas, S. Moorthi, A. Urisman, P. Castel, L. Wan, A. Berger

This study shows that USP9X stabilizes RIT1 protein and that its depletion reduces RIT1 abundance and sensitizes cells to EGFR inhibitors.

bioRxiv · Nov 30, 2023Cancer Biology

Ras-dependent RAF-MAPK hyperactivation by pathogenic RIT1 is a therapeutic target in Noonan syndrome-associated cardiac hypertrophy

A. Cuevas-Navarro, M. Wagner, R. Van, M. Swain, M. R. Allison, A. Cheng, S. Messing, D. K. Simanshu, M. J. Sale, F. McCormick, A. G. Stephen, P. Castel

This study identifies how pathogenic RIT1 mutations drive RAF-MAPK hyperactivation in Noonan syndrome, showing MEK inhibition can alleviate cardiac hypertrophy in a mouse model.

bioRxiv · Nov 2, 2022Biochemistry

The RAS GTPase RIT1 compromises mitotic fidelity through spindle assembly checkpoint suppression

A. Cuevas-Navarro, R. Van, A. Cheng, A. Urisman, P. Castel, F. McCormick

This study shows that RIT1, a Ras GTPase, suppresses the spindle assembly checkpoint, leading to mitotic errors and chromosome segregation defects.

bioRxiv · Nov 17, 2020Biochemistry