Keystone Symposia

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This meeting took place in 2020



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MEETING CANCELLED: Targeted Protein Degradation (X8)


Organizer(s) Rajesh Chopra, Nathanael Gray, Anita Gandhi and Georg Winter
March 29—April 1, 2020
Snowbird Resort • Snowbird, UT USA
Discounted Abstract Deadline: Nov 21, 2019
Abstract Deadline: Dec 19, 2019
Scholarship Deadline: Nov 21, 2019
Discounted Registration Deadline: Jan 29, 2020

Sponsored by Incyte Corporation, Merck & Co., Inc., Novartis Institutes for BioMedical Research and Vertex Pharmaceuticals Incorporated


Summary of Meeting:
This Keystone Symposia conference will highlight the recent exciting advances in targeting proteins for degradation as an alternative to conventional inhibitory small molecules and antibodies. Protein degradation can be undertaken by bifunctional molecules that bind the target for ubiquitin-mediated degradation by complexing them with Cereblon (CRBN), von Hippel-Lindau or other E3 ligases. Alternatively, ligase receptors such as CRBN or DCAF15 can also be used as a ‘template’ to bind IMiD or sulphonamide-like compounds to degrade multiple context specific proteins by the selected E3 ligases. The ‘template approach’ results in the degradation of neo-substrates, some of which would be difficult to drug using conventional approaches. The chemical properties necessary for drug discovery, the rules by which neo-substrates are selected by ligase receptors and defining the optimal components of the ubiquitin proteasome for protein degradation are still to be fully elucidated. This conference will bring together early pioneers in the field, emerging scientists and experts from industry and academics to describe how these challenges are being addressed. Furthermore, experts who have used IMiD agents and proteasome inhibition in the clinic in real world practical applications of protein degradation agents have been invited to speak at this conference. Another unique aspect of this conference is with it being paired with the Keystone Symposia conference on Ubiquitin Biology. Protein ubiquitination regulates nearly every critical cellular pathway and emerging evidence has demonstrated that defects within the ubiquitin proteasome system can directly lead to human disease. This has fueled a recent expansion of drug development efforts to harness the ubiquitin proteasome system to both aid in its functionality during disease progression and to specify individual targets for degradation. By pairing these meetings, participants will be able to network and foster new collaborations between these two related areas of science.

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