Computationally designed GPCR quaternary structures bias signaling pathway activation

Autor: Justine S. Paradis, Xiang Feng, Brigitte Murat, Robert E. Jefferson, Badr Sokrat, Martyna Szpakowska, Mireille Hogue, Nick D. Bergkamp, Franziska M. Heydenreich, Martine J. Smit, Andy Chevigné, Michel Bouvier, Patrick Barth

Publikováno v: Nature Communications, Vol 13, Iss 1, Pp 1-14 (2022)

Computational modeling and design of G Protein-Coupled Receptor quaternary structures reveals a signaling bias switch at the receptor dimer interface that selectively controls G protein vs β-arrestin activation.

Externí odkaz: https://doaj.org/article/c0d899ae8609439f8ce39b8bdc95e8a4

A new inhibitor of the β-arrestin/AP2 endocytic complex reveals interplay between GPCR internalization and signalling

Autor: Alexandre Beautrait, Justine S. Paradis, Brandon Zimmerman, Jenna Giubilaro, Ljiljana Nikolajev, Sylvain Armando, Hiroyuki Kobayashi, Lama Yamani, Yoon Namkung, Franziska M. Heydenreich, Etienne Khoury, Martin Audet, Philippe P. Roux, Dmitry B. Veprintsev, Stéphane A. Laporte, Michel Bouvier

Publikováno v: Nature Communications, Vol 8, Iss 1, Pp 1-16 (2017)

Beta-arrestins play central roles in the mechanisms regulating GPCR signalling and trafficking. Here the authors identify a selective inhibitor of the interaction between β-arrestin and the β2-adaptin subunit of the clathrin adaptor protein AP-2, w

Externí odkaz: https://doaj.org/article/6eba6ba8e03a459fb317fb0b5ab08460

Data from Synthetic Lethal Screens Reveal Cotargeting FAK and MEK as a Multimodal Precision Therapy for GNAQ-Driven Uveal Melanoma

Autor: J. Silvio Gutkind, Andrew E. Aplin, Takami Sato, Jonathan A. Pachter, Prashant Mali, Glenn Merlino, Chi-Ping Day, Kyle Ford, Xingyu Wu, Silvia Coma, Manoela Tiago, Nadia Arang, Frederico Gomes, Simone Lubrano, Ayush Kishore, Robert Saddawi-Konefka, Monica Acosta, Justine S. Paradis

Purpose:Uveal melanoma is the most common eye cancer in adults. Approximately 50% of patients with uveal melanoma develop metastatic uveal melanoma (mUM) in the liver, even after successful treatment of the primary lesions. mUM is refractory to curre

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6586666443c72d8c7650610b8c2c2ce1
https://doi.org/10.1158/1078-0432.c.6529851

Supplementary Fig 1 from Synthetic Lethal Screens Reveal Cotargeting FAK and MEK as a Multimodal Precision Therapy for GNAQ-Driven Uveal Melanoma

Autor: J. Silvio Gutkind, Andrew E. Aplin, Takami Sato, Jonathan A. Pachter, Prashant Mali, Glenn Merlino, Chi-Ping Day, Kyle Ford, Xingyu Wu, Silvia Coma, Manoela Tiago, Nadia Arang, Frederico Gomes, Simone Lubrano, Ayush Kishore, Robert Saddawi-Konefka, Monica Acosta, Justine S. Paradis

Supplementary figure S1. Synthetic lethality of FAK and ERK/MAPK pathway inhibition.

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a403519c803d895983e8ab05e66b7d8
https://doi.org/10.1158/1078-0432.22478118.v1

The RanBP2/RanGAP1-SUMO complex gates β-arrestin2 nuclear entry to regulate the Mdm2-p53 signaling axis

Autor: Stephane Angers, Kusumika Saha, Jane E. Findlay, Evelyne Lima-Fernandes, Michel Bouvier, Justine S. Paradis, Stefano Marullo, Cédric Auffray, George S. Baillie, Hervé Enslen, Mark G.H. Scott, Alessia Zamborlini, Anne Poupon, Elodie Blondel-Tepaz, Badr Sokrat, Milena Kosic, Louis Gaboury, Marie Leverve

Publikováno v: Oncogene
Oncogene, Nature Publishing Group, 2021, 40 (12), pp.2243-2257. ⟨10.1038/s41388-021-01704-w⟩
Oncogene, 2021, 40 (12), pp.2243-2257. ⟨10.1038/s41388-021-01704-w⟩

International audience; Mdm2 antagonizes the tumor suppressor p53. Targeting the Mdm2-p53 interaction represents an attractive approach for the treatment of cancers with functional p53. Investigating mechanisms underlying Mdm2-p53 regulation is there

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5adce6552ce02dc0e61877eaf3db50f5
https://doi.org/10.1038/s41388-021-01704-w