Jeffrey L. Benovic, PhD

Contact Dr. Benovic

233 S. 10th Street
Philadelphia, PA 19107

(215) 503-4607
(215) 503-5393 fax

Most Recent Peer-reviewed Publications

  1. Emerging Paradigm of Intracellular Targeting of G Protein-Coupled Receptors
  2. Pepducins as a potential treatment strategy for asthma and COPD
  3. Biased signaling of the proton-sensing receptor OGR1 by benzodiazepines
  4. G protein-coupled receptor kinases: Past, present and future
  5. G protein-coupled receptor kinase 3 and protein kinase C phosphorylate the distal C-terminal tail of the chemokine receptor CXCR4 and mediate recruitment of β-arrestin
  6. Structural basis for ß-arrestins in gpcr trafficking
  7. Dysregulated GPCR signaling and therapeutic options in uveal melanoma
  8. Structural and Functional Analysis of a β2-Adrenergic Receptor Complex with GRK5
  9. G protein-coupled receptor kinase-2 (GRK-2) regulates serotonin metabolism through the monoamine oxidase AMX-2 in Caenorhabditis elegans
  10. c-Src, Insulin-Like Growth Factor I Receptor, G-Protein-Coupled Receptor Kinases and Focal Adhesion Kinase are Enriched Into Prostate Cancer Cell Exosomes
  11. β-arrestin-biased signaling through the β2-adrenergic receptor promotes cardiomyocyte contraction
  12. The αarrestin ARRDC3 regulates the endosomal residence time and intracellular signaling of the β2-adrenergic receptor
  13. From biased signalling to polypharmacology: Unlocking unique intracellular signalling using pepducins
  14. Interdicting Gq activation in airway disease by receptor-dependent and receptor-independent mechanisms
  15. Atomic structure of GRK5 reveals distinct structural features novel for G protein-coupled receptor kinases
  16. Structural biology: Arresting developments in receptor signalling
  17. New frontiers in kinases
  18. Herpes simplex virus enhances chemokine function through modulation of receptor trafficking and oligomerization
  19. Consequence of the tumor-associated conversion to cyclin D1b
  20. Development and characterization of pepducins as Gs-biased allosteric agonists