Brian J. Knoll

TL;DR: It is suggested that beta-AR agonists and beta-blockers with inverse agonist properties may exert reciprocating effects on cellular signaling dependent on duration of administration.

TL;DR: Chronic administration of beta-blockers reduces inflammation and mucous metaplasia, cardinal features of asthma that may contribute to airflow obstruction and AHR, and provides a second disease model in which beta-blocks producing an acutely detrimental effect may provide a therapeutically beneficial effect with chronic administration.

TL;DR: It is demonstrated that, in a murine model of asthma, β2-AR signaling is required for the full development of three cardinal features of asthma: mucous metaplasia, AHR, and the presence of inflammatory cells in the lungs.

TL;DR: It is reported that chronic treatment with certain ‘β-blockers’ reduces airway hyperresponsiveness to methacholine in a murine model of asthma.

TL;DR: A pivotal role for rab11 is highlighted in regulating the traffic of a G protein-coupled receptor at the level of the RE, where modulation of rab11 activity dictates the balance between receptor recycling and downregulation during prolonged exposure to agonist.