IndraLab

Statements


PRKG activates KCNMA1. 12 / 12
| 11 1

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"It has been suggested that, particularly at lower levels of vessel contractility, NO-induced PKG-mediated activation of the BK channel is weaker than NO-induced [Ca ] decrease–mediated deactivation of the BK channel and that the overall decrease in BK channel activity determines the role of BK channels as limiters of the effect of NO."

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"The resulting increase in PKG activity enhanced Ca 2+ spark activity and sufficiently increased BK channel activity to exert an opposing influence on myogenic vasoconstriction."

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"At a high contraction level, NO induces a PKG mediated increase in BK channel activity, well established by many studies,1, 5, 6 that is stronger than the small [Ca 2+] i decrease mediated decrease of BK channel activity."

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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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"XREF_BIBR, XREF_BIBR PKA, PKG, and PKC also modulate BK channel activity indirectly by modulating the frequency of Ca 2+ sparks generated by sarcoplasmic reticulum ryanodine sensitive Ca 2+ -release channels."

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"Mechanistically, PKG has been linked to the activation of the mitochondrial K ATP channel [ xref ] and a recent paper further suggests that PKG activates the cardiomyocyte-specific BK channel at the mitochondria, increasing K + influx into the matrix, opposing mitochondrial Ca 2+ overloading and ROS production [ xref ]."
| PMC

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"With the approach of the present study, especially at lower levels of contractility, NO induces a PKG mediated increase in BK channel activity that is weaker than the large [Ca 2+] i decrease mediated decrease in BK channel activity."

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"Quercetin relaxes rat tail main artery partlyviaa PKG mediated stimulation of KCa1.1 channels."

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"It was suggested that at higher levels of vessel contractility, NO-induced PKG-mediated activation of the BK channel is stronger than NO-induced [Ca ] decrease–mediated deactivation of the BK channel and that the overall increase in BK channel activity determines the role of BK channels as facilitators of the effect of NO."

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"Mechanistically, PKG has been linked to the activation of the mitochondrial K channel [102] and a recent paper further suggests that PKG activates the cardiomyocyte-specific BK channel at the mitochondria, increasing K influx into the matrix, opposing mitochondrial Ca overloading and ROS production [103]."
| PMC

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"The list of PKG targets in smooth muscle cells includes proteins involved in the regulation of the cytoplasmic Ca concentration and the Ca -dependence of smooth muscle contraction.One of the main targets of PKG is the BK channel, which is activated by PKG-dependent phosphorylation [68,69,70]."

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"Conversely, β-adrenergic agonists, adenosine, calcitonin gene-related peptide, and nitric oxide (NO) mainly produce vasorelaxation via PKA- or PKG-dependent activation of the BK channel in VSMCs [130,131,132,133,134,135,136]."