IndraLab

Statements



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"These results suggest that besides the common natures of the BK channel family such as regulation by cytoplasmic Ca (2+) and membrane potential, the BK channel in RPTECs is directly inhibited by intracellular ATP independent of phosphorylation processes and sulfonylurea receptor."

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"XREF_BIBR Interestingly, it has been demonstrated recently that the N-terminus of intermediate conductance Ca 2+ -activated K + channels reduces BK channel NP o by the same open channel block underlying beta2- and beta3 induced inactivation."

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"Notably, direct application of H 2 O 2 (30 muM) increased Ca 2+ spark frequency in VSMCs from wild-type mice, but did not increase BK channel currents in these same cells treated with ryanodine to block Ca 2+ sparks, further supporting the conclusion that oxidant activated PKG increases BK channel mediated vasodilation of arteries through an increase in Ca 2+ spark frequency rather than a direct effect on the BK channel."

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"Our newly developed model recapitulates this important property (see Figure 3C for an example of this slow depolarization) and places action potential firing under the control of PI(4,5)P if Ca levels are sufficiently low to deactivate KCNMA1 channels."

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"It is likely that reduced Ca 2+ current in cac mutants would result in weakened activation of Slo (BK) K + current, thus indirectly trigger slo like upregulation of Sh I A."

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"Cav3 calcium influx induced a 50 mV negative shift in KCa1.1 voltage for activation, an interaction that was blocked by Cav3 or KCa1.1 channel blockers, or high internal EGTA."

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"For example, at the frog NMJ, presynaptic BK channels and N-type Ca 2+ channels show an identical and overlapping banding pattern of distribution [XREF_BIBR]; blocking N-type Ca 2+ channels with omega-conotoxin GVIA inhibits neurotransmitter release as well as BK channel currents [XREF_BIBR]."

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"From XREF_FIG D and 7 B it can be seen that, although the Ca 2+ bowl mutations greatly reduce the Ca 2+ sensitivity of Slo1 channels, the channels still retain Ca 2+ sensitivity."

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"The data support the concept that mAChR activation triggers indirect functional KCa1.1 channel inhibition mediated by intracellular Ca (2+), thus increasing the excitability in human DSM cells."

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"Furthermore, the transient BK channel opening probability (Po) was significantly reduced in LNCaP-NE cells by a previous inactivation of T-type Ca 2+ channels at -40 mV (XREF_FIG, right panel)."

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"It is concluded that inhibition of voltage gated as well as calcium activated (Slo) potassium channels leads to activation of gene transcription in striatal neurons which may trigger long-term changes in transmitter plasticity."

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"High concentrations of Ca 2+ also block Slo1 currents."

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"Slowpoke (Slo) potassium channels display extraordinarily high conductance, are synergistically activated by a positive transmembrane potential and high intracellular Ca 2+ concentrations and are important targets for insecticides and antiparasitic drugs."

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"Blocking KCa1.1 disturbs calcium homeostasis, leading to the sustained phosphorylation of Akt and the recruitment of talin to beta 1 integrins."

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"High conductance calcium activated (maxi-K) channels are potently blocked by a family of indole diterpenes that includes paxilline."

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"Previous studies (Meera et al. 1996) have indicated that physiological Ca 2+ i acts as a switch to functionally couple the beta 1 subunits with the alpha subunits, thus allowing lower levels of Ca 2+ i to activate the BK channel by shifting the P o vs. Ca 2+ i curve to the left."

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"Binding of Ca (v) beta1 markedly slows Slo1 activation kinetics, and it causes a significant decrease in Ca (2+) sensitivity in inside-out and in dialyzed cells, even in the absence of pore forming subunits of voltage gated Ca (2+) channels."

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"We showed previously in a pituitary cell line that the Ca (++)/calmodulin-dependent protein kinase CaMK IV specifically repressed splicing of the BK channel STREX exon."

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"Finally, this study provides another important piece of evidence supporting the idea that an NO induced reduction of calcium influx via VOC enables the BK channel to limit the anticontractile effect of NO."

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"We describe the case of a 25-year-old Caucasian male with autism spectrum disorder and severe intellectual disability presenting large-conductance calcium-activated potassium channel haploinsufficiency due to a de novo balanced translocation (46, XY, t [9; 10] [q23;q22]) disrupting the KCNMA1 gene."