Probenecid Disrupts a Novel Pannexin 1-Collapsin Response Mediator Protein 2 Interaction and Increases Microtubule Stability.

摘要: Neurite formation relies on finely-tuned control of the cytoskeleton. Here we identified a novel protein-protein interaction between ion and metabolite channel protein Pannexin 1 (Panx1) collapsin response mediator 2 (Crmp2), positive regulator microtubule polymerization stabilization. Panx1 Crmp2 co-precipitated from both Neuro-2a (N2a) cells mouse ventricular zone (VZ) tissue. In vitro binding assays purified proteins revealed occurs directly C-terminus (Panx1 CT) Crmp2. Because is well-established microtubule-stabilizing protein, previously observed marked increase in neurite following treatment with blocker, probenecid, N2a VZ neural precursor (NPCs), investigated impact probenecid Panx1-Crmp2 interaction. Probenecid significantly disrupted by immunoprecipitation (IP) proximity ligation analysis, without altering overall expression levels. presence was concentrated at distal ends growing neurites. Moreover, increased tubulin stability cells. These results reveal that disrupts stabilizer, Crmp2, also increases stability.