Jialu Wang

TL;DR: This review focuses on GPCRs most relevant to the cardiovascular system and discusses traditional components of GPCR signaling and highlight evolving concepts in the field, such as ligand bias, &bgr;-arrestin–mediated signaling, and conformational heterogeneity.

TL;DR: The data suggest that β-arrestins function as a regulatory hub, determining the balance between mechanistically different pathways that result in activation of ERK1/2, and caution against extrapolating results obtained from βArr 1/2- or G protein–deleted cells to GPCR behavior in native systems.

TL;DR: A previously unrecognized role for Gαi in β1AR signaling is demonstrated and the concept of β-arrestin-bias may need to be refined to incorporate the selective bias of receptors towards distinct G protein subtypes.

TL;DR: In this article, the authors showed that stretch-triggered AT1R-Gαi coupling is required for the recruitment of β-arrestin2 and activation of downstream signaling pathways, such as EGFR transactivation and ERK phosphorylation.

TL;DR: A selection methodology to enrich for functionally modulatory antibodies using a yeast-displayed library of synthetic camelid antibody fragments called “nanobodies” is described, and multiple nanobodies are discovered that act as antagonists of the angiotensin II type 1 receptor (AT1R).