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