Regulatory role of dynamin-2 in VEGFR-2/KDR-mediated endothelial signaling Resham Bhattacharya * , Ningling Kang-Decker † , Deborah A. Hughes * , Priyabrata Mukherjee * , Vijay Shah † , Mark A. McNiven * and Debabrata Mukhopadhyay * ,1 * Department of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center, Rochester, Minnesota, USA; and † GI Research Unit, Department of Medicine, Mayo Clinic Foundation, Rochester, Minnesota, USA 1 Correspondence: Department Biochemistry and Molecular Biology, Gugg 1401A, Mayo Clinic Foundation, 200 First St. SW, Rochester, MN 55905, USA. E-mail: mukhopadhyay.debabrata@mayo.edu <h3>SPECIFIC AIMS</h3> KDR is the key receptor that initiates signaling events for VPF/VEGF causing endothelial cell migration, proliferation, and tube formation leading to angiogenesis. Currently, there are at least 80 different drugs in clinical trials targeting KDR. Nonetheless, there is a huge gap in the understanding of mechanisms that regulate compartmentalization and thus signaling of this receptor. Dynamin-2 is a signal-transducing GTPase that has been widely reported to be involved in clathrin- and caveolin-mediated receptor endocytosis. Therefore, the aim of this project was to elucidate the role of dynamin-2 in KDR endocytosis, compartmentalization, and signaling. <h3>PRINCIPAL FINDINGS</h3> <h3>1. KDR is present on the plasma membrane and endosomes as well as
/lp/fed-of-american-socs-for-experimental-biology/regulatory-role-of-dynamin-2-in-vegfr-2-kdr-mediated-endothelial-odPu0sVZ6o