TY - DATA T1 - Supplementary Material for: The Type I Inositol 1,4,5-Trisphosphate Receptor Interacts with Protein 4.1N to Mediate Neurite Formation through Intracellular Ca2+ Waves PY - 2011/03/10 AU - Fiedler M.J. AU - Nathanson M.H. UR - https://karger.figshare.com/articles/dataset/Supplementary_Material_for_The_Type_I_Inositol_1_4_5-Trisphosphate_Receptor_Interacts_with_Protein_4_1N_to_Mediate_Neurite_Formation_through_Intracellular_Ca_sup_2_sup_Waves/5121733 DO - 10.6084/m9.figshare.5121733.v1 L4 - https://ndownloader.figshare.com/files/8706397 L4 - https://ndownloader.figshare.com/files/8706400 L4 - https://ndownloader.figshare.com/files/8706403 L4 - https://ndownloader.figshare.com/files/8706406 L4 - https://ndownloader.figshare.com/files/8706409 KW - Type I inositol 1,4,5-trisphosphate receptor KW - Protein 4.1N KW - Ca2+ waves KW - Neuron N2 - Ca2+ waves are an important mechanism for encoding Ca2+ signaling information, but the molecular basis for wave formation and how this regulates neuronal function is not entirely understood. Using nerve growth factor-differentiated PC12 cells as a model system, we investigated the interaction between the type I inositol 1,4,5-trisphosphate receptor (IP3R1) and the cytoskeletal linker, protein 4.1N, to examine the relationship between Ca2+ wave formation and neurite development. This was examined using RNAi and overexpressed dominant negative binding regions of each protein. Confocal microscopy was used to monitor neurite formation and Ca2+ waves. Knockdown of IP3R1 or 4.1N attenuated neurite formation, as did binding regions of IP3R1 and 4.1N, which colocalized with endogenous 4.1N and IP3R1, respectively. Upon stimulation with the IP3-producing agonist carbachol, both RNAi and dominant negative molecules shifted signaling events from waves to homogeneous patterns of Ca2+ release. These findings provide evidence that IP3R1 localization, via protein 4.1N, is necessary for Ca2+ wave formation, which in turn mediates neurite formation. ER -