Fig. 6: NPC1-dependent increases in CaV1.2 are abrogated by inhibiting CDK5-dependent phosphorylation of KV2.1. | Nature Communications

Fig. 6: NPC1-dependent increases in CaV1.2 are abrogated by inhibiting CDK5-dependent phosphorylation of KV2.1.

From: NPC1-dependent alterations in KV2.1–CaV1.2 nanodomains drive neuronal death in models of Niemann-Pick Type C disease

Fig. 6: NPC1-dependent increases in CaV1.2 are abrogated by inhibiting CDK5-dependent phosphorylation of KV2.1.The alternative text for this image may have been generated using AI.

A Schematic diagram detailing roscovitine (Rosc) mode of action. B Top, representative super-resolution Airyscan images taken at a focal plane near the PM of CTL (black) or U18-treated (red) neurons co-incubated with roscovitine (Rosc) (cyan) and co-immunolabeled for CaV1.2 and KV2.1. Bottom, quantification of PM KV2.1 and CaV1.2 clustering size, and % of the soma occupied by CaV1.2–KV2.1 (left, yellow) and CaV1.2–KV2.1 area in the dendrite region (right, orange) of CTL (black), U18 (red) and Rosc (cyan) neurons. N = 43 (CTL), n = 41 (U18), n = 43 (Rosc) and n = 38 (Rosc+U18) neurons and n = 89 (CTL), n = 94 (U18), n = 82 (Rosc) and n = 71 (Rosc+U18) dendrites were analyzed across 5 independent isolations. All error bars represent SEM. Statistical significance was calculated using a two-way ANOVA test. ns: not significant; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.#P < 0.05; ##P < 0.01; ####P < 0.0001. # indicates comparison with the CTL condition. CTL is control, U18 is U18666A, ROSC is Roscovitine.

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