0B68 Fortini, Mark - Thomas Jefferson University - Thomas Jefferson University

Mark Fortini, PhD

Contact Dr. Fortini

233 S. 10th Street
830 BLSB
Philadelphia, PA 19107

(215) 503-7322

Most Recent Peer-reviewed Publications

  1. Disruption of Drosophila melanogaster Lipid Metabolism Genes Causes Tissue Overgrowth Associated with Altered Developmental Signaling
  2. Protein trafficking abnormalities in Drosophila tissues with impaired activity of the ZIP7 zinc transporter Catsup
  3. Dmon1 controls recruitment of Rab7 to maturing endosomes in Drosophila
  4. Introduction-Notch in development and disease
  5. Therapeutic approaches to modulating Notch signaling: Current challenges and future prospects
  6. Deficient Notch signaling associated with neurogenic pecanex is compensated for by the unfolded protein response in Drosophila
  7. Pharmacological and genetic reversal of age-dependent cognitive deficits attributable to decreased presenilin function
  8. In Vivo reconstitution of γ-secretase in Drosophila results in substrate specificity
  9. Erratum to Retraction Notice to: The Big Brain Aquaporin Is Required for Endosome Maturation and Notch Receptor Trafficking [ 0B68 Cell, 133, (2008), 852-863]
  10. Pharmacological analysis of Drosophila melanogaster γ-secretase with respect to differential proteolysis of notch and APP
  11. Endocytic regulation of Notch signaling
  12. Generation and characterization of monoclonal antibodies specific to Drosophila presenilin
  13. Notch Signaling: The Core Pathway and Its Posttranslational Regulation
  14. The Big Brain Aquaporin Is Required for Endosome Maturation and Notch Receptor Trafficking
  15. Endosomal entry regulates Notch receptor activation in Drosophila melanogaster
  16. Drosophila as a model for human diseases IRB and ICREA, Barcelona, Spain, October 5-7, 2006
  17. A role for presenilin in post-stress regulation: Effects of presenilin mutations on Ca2+ currents in Drosophila
  18. Anticipating trouble from gene transcription
  19. Modeling Clinically Heterogeneous Presenilin Mutations with Transgenic Drosophila
  20. γ-Cleavage-Independent Functions of Presenilin, Nicastrin, and Aph-1 Regulate Cell-Junction Organization and Prevent Tau Toxicity In Vivo