0B68 Penn, Raymond B - Thomas Jefferson University - Thomas Jefferson University
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Raymond B. Penn, PhD

Contact Dr. Penn

Center for Translational Medicine
1025 Walnut Street, Suite 317
Philadelphia, PA 19107

(215) 955-9982
(215) 503-5731 fax

Most Recent Peer-reviewed Publications

  1. Far from "disappointing"
  2. GPCRs and arrestins in Airways: Implications for asthma
  3. cAMP regulation of airway smooth muscle function
  4. A-kinase anchoring proteins regulate compartmentalized cAMP signaling in airway smooth muscle
  5. The GPCR OGR1 (GPR68) mediates diverse signalling and contraction of airway smooth muscle in response to small reductions in extracellular pH
  6. β 2-adrenergic receptor agonists modulate human airway smooth muscle cell migration via vasodilator-stimulated phosphoprotein
  7. pH-dependent regulation of the α-subunit of H +-K +-ATPase (HK α2)
  8. New perspectives regarding β 2-adrenoceptor ligands in the treatment of asthma
  9. Anti-mitogenic effects of β-agonists and PGE2on airway smooth muscle are PKA dependent
  10. Deletion of the pH sensor GPR4 decreases renal acid excretion
  11. Asthma and gender impact accumulation of T cell subtypes
  12. Regulation of T cells in airway disease by beta-agonist
  13. Glucocorticoid- and protein kinase A-dependent transcriptome regulation in airway smooth muscle
  14. Agonizing over agonism: Should asthmatics turn their β-receptors on or off?
  15. Endogenous Gs-coupled receptors in smooth muscle exhibit differential susceptibility to GRK2/3-mediated desensitization
  16. Embracing emerging paradigms of G protein-coupled receptor agonism and signaling to address airway smooth muscle pathobiology in asthma
  17. β-Arrestins specifically constrain β2-adrenergic receptor signaling and function in airway smo 05D1 oth muscle
  18. Adenosine induces airway hyperresponsiveness through activation of A3 receptors on mast cells
  19. Interactive effects of steroids and β-agonists on accumulation of type 2 T cells
  20. Mitogenic effects of cytokines on smooth muscle are critically dependent on protein kinase A and are unmasked by steroids and cyclooxygenase inhibitors
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