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KCNMA1 activates calcium(2+). 49 / 49
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reach
"Our results (XREF_FIG and XREF_FIG) reveal that slo mediates the vast majority of all the Ca 2+ -activated K + currents in postembryonic neurons, and that absence of slo induced profound functional compensations from transient voltage gated K + currents, particularly in pupal neurons."
reach
"The identification of Slo1 gene KCNMA1 and the availability of cDNA of Slo1 for functional expression of BK channels in exogenous cells (Atkinson et al., 1991; Adelman et al., 1992; Butler et al., 1993) allowed the studies to distinguish the distinct Ca and voltage dependent activation mechanisms (Cui et al., 1997)."
reach
"To investigate the involvement of these Ca dependent kinases in the increase in CREB phosphorylation seen after BK channel inhibition, STO-609, which selectively inhibits Ca and calmodulin-dependent kinase kinase 2 (CaMKK2) which is upstream of CaMKIV [32] and the CaMKII peptide inhibitor, tatCN21 [29], were added to our system.As previously demonstrated in whole cells, BK channel inhibition with paxilline increased CREB phosphorylation sevenfold (**p = 0.0023)."
reach
"For the copper metalloporphyrin, the predicted results can be highly correlated with the experimental data, suggesting that at lower concentrations, the metal complex may inhibit SERCA2b, leading to an elevation of cytosolic calcium and activation of calcium-dependent Slo1 potassium channels."
sparser
"This extremely high positive correlation, together with previous data establishing that LCA-induced dilation of MCA is due to LCA activation of smooth muscle BK channels [ xref ], strongly suggest that the larger LCA-induced BK channel activation in myocytes of BA or CA vs . that of ACA, MCA, PCA or MA, is an important contributor to the larger LCA-induced dilation of the former group of arteries vs . the latter."
reach
"We provide evidence that PGE 2 causes : 1) increase in DSM spontaneous phasic contractions in a BK channel dependent manner, 2) elevation of the intracellular Ca 2+ concentration in freshly isolated DSM cells, and 3) inhibition of the amplitude and frequency of TBKCs in freshly isolated DSM cells."
reach
"We observed that the average intensity of G-CaMP increased over time during GAS infection in an SLO-dependent manner, with the average G-CaMP intensity at 4 h comparable with that in A23187-treated cells (Supplementary Fig. 5a, b) and indicating GAS internalization into the cytosol and/or endosomal membrane damage via SLO-induced cytosolic Ca mobilization."