2011
DOI: 10.1074/jbc.m110.175257
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Functional Roles of a C-terminal Signaling Complex of CaV1 Channels and A-kinase Anchoring Protein 15 in Brain Neurons

Abstract: Regulation of Ca V 1.2 channels in cardiac myocytes by the ␤-adrenergic pathway requires a signaling complex in which the proteolytically processed distal C-terminal domain acts as an autoinhibitor of channel activity and mediates up-regulation by the ␤-adrenergic receptor and PKA bound to A-kinase anchoring protein 15 (AKAP15). We examined the significance of this distal C-terminal signaling complex for Ca V 1.2 and Ca V 1.3 channels in neurons. AKAP15 co-immunoprecipitates with Ca V 1.2 and Ca V 1.3 channels… Show more

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Cited by 37 publications
(50 citation statements)
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“…channels (42). AKAP7α has not been reported to interact with any proteins other than ion channels and PKA.…”
Section: Discussionmentioning
confidence: 99%
“…channels (42). AKAP7α has not been reported to interact with any proteins other than ion channels and PKA.…”
Section: Discussionmentioning
confidence: 99%
“…A kinase-anchoring proteins are also found in a complex with native Ca V 1.3 channels (Marshall et al, 2011) Pharmacology of Voltage-Gated Calcium Channels 837 and are stimulated by PKA. This has been shown in adrenal chromaffin cells (Mahapatra et al, 2012) and in the SAN (Mangoni et al, 2003).…”
Section: +mentioning
confidence: 99%
“…Direct intracellular perfusion (dialysis) of the myocytes through the patch pipette often yielded incomplete inhibition of the β-AR effect: 50% to 70% with 1 µmol/L PKI, 0.5 mmol/L Rp-cAMPS, or a cocktail of PKA and phosphorylation inhibitors. [87][88][89][90] Other works reported full inhibition of effects of β-AR agonists in frog and rat ventricular cardiomyocytes by dialyzing cells with 2 to 5 mmol/L Rp-cAMPS, 16 µmol/L PKI (which is >3 orders of magnitude higher than its K i ), 20 µmol/L PKI peptide (PKI [15][16][17][18][19][20][21][22] ; K i =36 nmol/L), [91][92][93] or with 1 µmol/L H-89 applied externally. 94 Although the latter studies used rather high doses of inhibitors, the accumulated data strongly support the view that a major part and possibly all of the β-AR enhancement of cardiac Ca V 1.2 is mediated by activation of PKA.…”
Section: Pka Inhibitors and β-Ar Regulationmentioning
confidence: 99%
“…One is the role of PKA in basal I Ca . In the best reconstitution setting (α 1C Δ1800 coexpressed with dCT and AKAP7), the reduction of basal I Ca was ≈30% with 1 µmol/L PKI [14][15][16][17][18][19][20][21][22] peptide and ≈50% with a mixture of higher concentrations of 2 PKI peptides. Such sensitivity to blockers resembles embryonic cardiomyocytes or other heterologous expression studies but is somewhat higher than in adult cardiomyocytes.…”
Section: Regulation By Pka Activators or Pka-csmentioning
confidence: 99%
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