Author

A. G. Stephen

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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Biophysics· 2 Cancer Biology· 2 Biochemistry· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 5 Research Focus:cell signaling & trafficking· 3 Organism:mouse· 2 Research Focus:protein folding & dynamics· 2 Assay:structural biology· 2 Approach:biophysical modeling· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:chromatin & epigenetic regulation· 1

Frequent Co-Authors

D. K. Simanshu· 4 shared F. McCormick· 3 shared S. Messing· 3 shared D. Esposito· 2 shared D. V. Nissley· 2 shared T. H. Tran· 2 shared A. Cheng· 1 shared A. Cuevas-Navarro· 1 shared

Activity by Year

2019-2022 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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4 shared papersBiophysics

D. K. Simanshu

Mutual co-authors in cluster

Author profile →

6 papers

Recent·Most cited

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

Allosteric regulation of switch-II controls K-Ras oncogenicity

M. H. Yang, T. H. Tran, B. Hunt, R. Agnor, C. W. Johnson, T. J. Waybright, J. A. Nowak, A. G. Stephen, D. K. Simanshu, K. M. Haigis

This study shows that the K104Q mutation reduces oncogenic K-Ras activity in vivo by disrupting GEF-mediated nucleotide exchange and stabilizing switch-II helix through an allosteric network.

bioRxiv · Sep 20, 2022 · PreprintCancer Biology

Structure of the SHOC2-MRAS-PP1C complex provides insights into RAF activation and Noonan syndrome

D. A. Bonsor, P. Alexander, K. Snead, N. Hartig, M. Drew, S. Messing, L. I. Finci, D. V. Nissley, F. McCormick, D. Esposito, P. Rodriguez-Viciana, A. G. Stephen, D. K. Simanshu

The paper presents the structure of the SHOC2-MRAS-PP1C complex and shows how it regulates RAF activation and is linked to Noonan syndrome mutations.

bioRxiv · May 10, 2022Biophysics

RASopathy Mutations Provide Functional Insight into the BRAF Cysteine-rich Domain and Demonstrate the Importance of Autoinhibition in BRAF Regulation

R. Spencer-Smith, E. M. Terrell, C. Insinna, C. Agamasu, M. E. Wagner, D. A. Ritt, J. Stauffer, A. G. Stephen, D. K. Morrison

This study examines RASopathy mutations in the BRAF cysteine-rich domain, showing they increase BRAF activity by relieving autoinhibition and enhancing PS binding, with autoinhibition being the main factor affecting mutation severity.

bioRxiv · Oct 1, 2021Cell Biology

KRAS interaction with RAF1 RAS-binding domain and cysteine-rich domain provides insights into RAS-mediated RAF activation

T. H. Tran, A. H. Chan, L. C. Young, L. Bindu, C. Neale, S. Messing, S. Dharmaiah, T. Taylor, J.-P. Denson, D. Esposito, D. V. Nissley, A. G. Stephen, F. McCormick, D. K. Simanshu

The paper determines crystal structures of KRAS mutants bound to RAF1 domains, revealing molecular interactions critical for RAS-mediated RAF activation.

bioRxiv · Jul 31, 2020Biophysics

PIP2 Influences the Conformational Dynamics of Membrane bound KRAS4b

M. A. McLean, A. G. Stephen, S. G. Sligar

This study shows that PIP2 in the membrane bilayer promotes KRAS4b G-domain interactions, altering its conformational dynamics and potentially regulating its activity.

bioRxiv · May 2, 2019Cancer Biology