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Fig. 4 | Molecular Brain

Fig. 4

From: A T-type channel-calmodulin complex triggers αCaMKII activation

Fig. 4

Cav3 channel-mediated calcium influx leads to αCaMKII aggregation. tsA-201 cells are cotransfected with GFP-αCaMKII, CaM, Cav3.1, and Kir2.1 and exposed to low [K]o (1.0 mM) or high [K]o (50 mM). Plots of the mean pixel variance of GFP-αCaMKII fluorescence in ROIs in the cytoplasm and nuclear regions shown at right. a, b In cells coexpressing Cav3.1 GFP-αCaMKII exhibits a diffuse cytoplasmic distribution in low [K]o that changes to aggregates in high [K]o, a pattern that is fully reversible upon returning to low [K]o. c, d Magnified images of the distribution of GFP-αCaMKII in low [K]o and after perfusing high [K]o, with plots indicating a restriction of clusters primarily to cytoplasm and peri-nuclear regions. e-i Formation of GFP-αCaMKII aggregates induced by high [K]o is prevented in cells lacking Cav3.1 (e, f), and blocked by substitution of CaM with CaM1234 (g, h), or by coexpression of CaMKIIN (0.3 μg) as an inhibitor of αCaMKII phosphorylation (i, j). Values are mean ± SD derived from n = 3 plates with 12–29 ROIs. Scale bars 10 μm.* p < 0.05

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