Author

A. D. Hamilton

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 Research Focus:cancer & tumor microenvironment· 2 Organism:human· 2 Research Focus:protein folding & dynamics· 2 Assay:ChIP-seq· 1 Research Focus:chromatin & epigenetic regulation· 1 Assay:proteomics· 1 Approach:statistical model· 1

Frequent Co-Authors

S. Kumar· 2 shared A. J. Afzal· 1 shared C.-H. Lee· 1 shared D. Maity· 1 shared D. Reinberg· 1 shared G. Esposito· 1 shared I. Chehade· 1 shared J. Ahmed· 1 shared

Activity by Year

2017-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 19 mutual co-author links

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2 shared papersCancer Biology

S. Kumar

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Author profile →

3 papers

Recent·Most cited

Single-molecule nanopore dielectrophoretic trapping of α-Synuclein with lipid membranes

J. Wu, T. Yamashita, A. D. Hamilton, S. Thompson, J. Luo

This paper uses single-molecule nanopore dielectrophoresis to study α-Synuclein folding and unfolding in lipid membranes and how metal ions and peptidomimetics affect these processes.

bioRxiv · Jan 24, 2022Biochemistry

Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumor suppressor function

L. Palanikumar, L. Karpauskaite, S. Hassan, M. Alam, M. Al-Sayegh, I. Chehade, D. Maity, L. Ali, Z. Falls, R. Samudrala, M. Kalmouni, Y. Hunashal, J. Ahmed, S. Karapetyan, R. Pasricha, , M. Magzoub

This study identifies a small-molecule amyloid inhibitor that disrupts mutant p53 aggregation, restores its function, and reduces tumor growth in xenograft models.

bioRxiv · Aug 10, 2020Cancer Biology

Allosteric activation dictates PRC2 activity independent of its recruitment to chromatin

C.-H. Lee, J.-R. Yu, S. Kumar, Y. Jin, S. Kaneko, A. D. Hamilton, D. Reinberg

This study shows that PRC2 activity is controlled by allosteric activation, independent of its chromatin recruitment, and identifies vulnerabilities in PRC2-addicted cancers.

bioRxiv · Oct 28, 2017Biochemistry