Pharmacologically controlling protein-protein interactions through epichaperomes for therapeutic vulnerability in cancer

Joshi, Gomes et al. employ a chemical modulation approach of the cellular interactome to a hyperconnectivity state and show association with the increased response of pancreatic cancer cell lines to specific drugs, including those that target the MAPK-pathways and PI3K-mTOR pathway. To achieve this,...

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Auteurs principaux: Suhasini Joshi, Erica DaGama Gomes, Tai Wang, Adriana Corben, Tony Taldone, Srinivasa Gandu, Chao Xu, Sahil Sharma, Salma Buddaseth, Pengrong Yan, Lon Yin L. Chan, Askan Gokce, Vinagolu K. Rajasekhar, Lisa Shrestha, Palak Panchal, Justina Almodovar, Chander S. Digwal, Anna Rodina, Swathi Merugu, NagaVaraKishore Pillarsetty, Vlad Miclea, Radu I. Peter, Wanyan Wang, Stephen D. Ginsberg, Laura Tang, Marissa Mattar, Elisa de Stanchina, Kenneth H. Yu, Maeve Lowery, Olivera Grbovic-Huezo, Eileen M. O’Reilly, Yelena Janjigian, John H. Healey, William R. Jarnagin, Peter J. Allen, Chris Sander, Hediye Erdjument-Bromage, Thomas A. Neubert, Steven D. Leach, Gabriela Chiosis
Format: article
Langue:EN
Publié: Nature Portfolio 2021
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Accès en ligne:https://doaj.org/article/c73d69998238486ba39d6f85c901b64d
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Résumé:Joshi, Gomes et al. employ a chemical modulation approach of the cellular interactome to a hyperconnectivity state and show association with the increased response of pancreatic cancer cell lines to specific drugs, including those that target the MAPK-pathways and PI3K-mTOR pathway. To achieve this, the authors employ chemical modulation of the interactome via epichaperome inhibition with the small molecule PU-H71.