Title : Receptor-mediated regulation of the TRPM7 channel through its endogenous protein kinase domain.

Pub. Date : 2004 Apr 20

PMID : 15069188






10 Functional Relationships(s)
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1 TRPM7 is a ubiquitously expressed and constitutively active divalent cation-selective ion channel, whose basal activity is regulated by intracellular levels of Mg(2+) and Mg.ATP. Magnesium transient receptor potential cation channel subfamily M member 7 Homo sapiens
2 TRPM7 is a ubiquitously expressed and constitutively active divalent cation-selective ion channel, whose basal activity is regulated by intracellular levels of Mg(2+) and Mg.ATP. Magnesium transient receptor potential cation channel subfamily M member 7 Homo sapiens
3 TRPM7 is a ubiquitously expressed and constitutively active divalent cation-selective ion channel, whose basal activity is regulated by intracellular levels of Mg(2+) and Mg.ATP. Adenosine Triphosphate transient receptor potential cation channel subfamily M member 7 Homo sapiens
4 Consistent with the involvement of G(s)/G(i) in controlling adenylyl cyclase activity, elevations of intracellular cAMP levels enhance TRPM7 activity and prevent receptor-mediated modulation of TRPM7 activity by muscarinic and adrenergic agonists. Cyclic AMP transient receptor potential cation channel subfamily M member 7 Homo sapiens
5 Consistent with the involvement of G(s)/G(i) in controlling adenylyl cyclase activity, elevations of intracellular cAMP levels enhance TRPM7 activity and prevent receptor-mediated modulation of TRPM7 activity by muscarinic and adrenergic agonists. Cyclic AMP transient receptor potential cation channel subfamily M member 7 Homo sapiens
6 This cAMP-dependent effect requires the functional integrity of both protein kinase A (PKA) and the endogenous kinase domain of TRPM7 because cAMP-mediated effects are abolished when treating cells with the PKA inhibitors H89 or KT5720 as well as in cells expressing phosphotransferase-deficient TRPM7 constructs. Cyclic AMP transient receptor potential cation channel subfamily M member 7 Homo sapiens
7 This cAMP-dependent effect requires the functional integrity of both protein kinase A (PKA) and the endogenous kinase domain of TRPM7 because cAMP-mediated effects are abolished when treating cells with the PKA inhibitors H89 or KT5720 as well as in cells expressing phosphotransferase-deficient TRPM7 constructs. Cyclic AMP transient receptor potential cation channel subfamily M member 7 Homo sapiens
8 This cAMP-dependent effect requires the functional integrity of both protein kinase A (PKA) and the endogenous kinase domain of TRPM7 because cAMP-mediated effects are abolished when treating cells with the PKA inhibitors H89 or KT5720 as well as in cells expressing phosphotransferase-deficient TRPM7 constructs. Cyclic AMP transient receptor potential cation channel subfamily M member 7 Homo sapiens
9 This cAMP-dependent effect requires the functional integrity of both protein kinase A (PKA) and the endogenous kinase domain of TRPM7 because cAMP-mediated effects are abolished when treating cells with the PKA inhibitors H89 or KT5720 as well as in cells expressing phosphotransferase-deficient TRPM7 constructs. Cyclic AMP transient receptor potential cation channel subfamily M member 7 Homo sapiens
10 Taken together, our results demonstrate that TRPM7 activity is up- and down-regulated through its endogenous kinase in a cAMP- and PKA-dependent manner. Cyclic AMP transient receptor potential cation channel subfamily M member 7 Homo sapiens