18/09/2026
Sala Marie Curie, 16:00h
Us convidem al pròxim seminari organitzat pel Programa d’Informàtica Biomèdica (GRIB) de l'Hospital del Mar Research Institut i de la UPF que tindrà lloc el pròxim divendres 18 de setembre a les 16:00 h a la Sala Marie Curie. El títol serà "Decoding Arrestin Activation: Phosphopeptide Barcodes Meet Membrane Lipids" i anirà a càrrec de la Dra. Qiuyan Chen, professora ajudant a la Indiana University School of Medicine.
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We invite you to the upcoming seminar organized by the Biomedical Informatics Program (GRIB) of the Hospital del Mar Research Institute and the UPF, which will take place on Friday September 18, at 4:00 pm in the Marie Curie room. The title of the seminar will be:"Decoding Arrestin Activation: Phosphopeptide Barcodes Meet Membrane Lipids", presented by Dr. Qiuyan Chen, Assistant Professor at Indiana University School of Medicine.

Biosketch:
Dr. Qiuyan Chen is an Assistant Professor at Indiana University School of Medicine studying the molecular mechanisms of GPCR signaling. She trained in pharmacology at Vanderbilt University and later at the University of Michigan and Purdue University, where she helped determine the first cryo-EM structure of a GPCR-kinase complex. Her lab combines structural and biophysical approaches, including cryo-EM, crystallography, EPR, and fluorescence methods, to understand GPCR regulation and develop more selective therapeutic strategies.
Abstract:
GPCRs are major drug targets, but we still do not fully understand how they engage arrestins, key proteins that switch off and redirect receptor signaling. Our work shows that arrestin activation is governed by two cooperating signals: the pattern of receptor phosphorylation and the surrounding membrane lipids. Using cryo-EM together with a simplified nanodisc system, we found that different phosphorylation "barcodes" produce distinct arrestin states, while the position of these motifs relative to the membrane strongly affects activation. Extending this analysis across the GPCR family suggests that these principles may help explain why different receptors engage arrestins in different ways. Together, our results reveal how chemical modifications on the receptor and the membrane environment combine to shape GPCR signaling.
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