Mark Fortini, PhD

Contact Dr. Fortini

233 South 10th Street
Suite 830
Philadelphia, PA 19107

(215) 503-7322
fax

Research and Clinical Interests
Developmental signaling pathways involved in normal cellular patterning and cancer; proteolytic mechanisms in neurogenesis and neurodegeneration; trafficking and post-translational regulation of cell-surface receptors and ligands.

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Publications

Most recent Peer-reviewed Publications

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

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