Differential β-Arrestin–Dependent Conformational Signaling and Cellular Responses Revealed by Angiotensin Analogs

Brandon Zimmerman, Alexandre Beautrait, Benjamin Aguila, Ricardo Charles, Emanuel Escher, Audrey Claing, Michel Bouvier,* Stéphane A. Laporte*

*To whom correspondence should be addressed. E-mail: michel.bouvier{at}umontreal.ca (M.B.); stephane.laporte{at}mcgill.ca (S.A.L.)

This PDF file includes:

• Fig. S1. Analog-induced production of IP₁ and recruitment of β-arrestin as analyzed by confocal microscopy and immunoprecipitation.
• Fig. S2. Recruitment of β-arrestin to AT1R and conformational changes induced by AngII analogs.
• Fig. S3. siRNA-mediated knockdown of GRK2 and GRK6.
• Fig. S4. Role of GRK2 and GRK6 in the efficacy and potency on ligand-induced β- arrestin recruitment and conformational change.
• Fig. S5. Dose-response relationship of ERK1/2 activation by AngII and analogs.
• Fig. S6. Correlation plots between ligand affinity, BRET values, and ERK1/2 activation.
• Table S1. IP₁ dose-response curve data used to calculate σ values and β factors.
• Table S2. BRET dose-response data used to calculate σ values and β factors.
  

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© 2012 American Association for the Advancement of Science