Nature Communications (Jun 2021)
Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumor suppressor function
- L. Palanikumar,
- Laura Karpauskaite,
- Mohamed Al-Sayegh,
- Ibrahim Chehade,
- Maheen Alam,
- Sarah Hassan,
- Debabrata Maity,
- Liaqat Ali,
- Mona Kalmouni,
- Yamanappa Hunashal,
- Jemil Ahmed,
- Tatiana Houhou,
- Shake Karapetyan,
- Zackary Falls,
- Ram Samudrala,
- Renu Pasricha,
- Gennaro Esposito,
- Ahmed J. Afzal,
- Andrew D. Hamilton,
- Sunil Kumar,
- Mazin Magzoub
Affiliations
- L. Palanikumar
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Laura Karpauskaite
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Mohamed Al-Sayegh
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Ibrahim Chehade
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Maheen Alam
- Department of Biology, SBA School of Science and Engineering, Lahore University of Management Sciences
- Sarah Hassan
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Debabrata Maity
- Department of Chemistry, New York University
- Liaqat Ali
- Core Technology Platforms, New York University Abu Dhabi, Saadiyat Island Campus
- Mona Kalmouni
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Yamanappa Hunashal
- Chemistry Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Jemil Ahmed
- Department of Chemistry and Biochemistry and Knoebel Institute for Healthy Aging, The University of Denver
- Tatiana Houhou
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Shake Karapetyan
- Physics Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Zackary Falls
- Department of Biomedical Informatics, School of Medicine and Biomedical Sciences, State University of New York (SUNY)
- Ram Samudrala
- Department of Biomedical Informatics, School of Medicine and Biomedical Sciences, State University of New York (SUNY)
- Renu Pasricha
- Core Technology Platforms, New York University Abu Dhabi, Saadiyat Island Campus
- Gennaro Esposito
- Chemistry Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Ahmed J. Afzal
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- Andrew D. Hamilton
- Department of Chemistry, New York University
- Sunil Kumar
- Department of Chemistry and Biochemistry and Knoebel Institute for Healthy Aging, The University of Denver
- Mazin Magzoub
- Biology Program, Division of Science, New York University Abu Dhabi, Saadiyat Island Campus
- DOI
- https://doi.org/10.1038/s41467-021-23985-1
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 24
Abstract
Amyloid aggregation of mutant p53 contributes to its loss of tumor suppressor function and oncogenic gain-of-function. Here, the authors use a protein mimetic to abrogate mutant p53 aggregation and rescue p53 function, which inhibits cancer cell proliferation in vitro and halts tumor growth in vivo.
