PMID: 8594869Dec 1, 1995Paper

Ca2+/calmodulin-dependent protein kinase II activation and regulation of adrenal glomerulosa Ca2+ signaling

The American Journal of Physiology
R J FernP Q Barrett

Abstract

We recently reported that elevations in the intracellular Ca2+ concentration ([Ca2+]i) enhance low-voltage-activated, T-type, Ca2+ channel activity via Ca2+/calmodulin-dependent protein kinase II (CaMKII). Here, we document CaMKII activity in bovine adrenal glomerulosa (AG) cells and assess the importance of CaMKII in depolarization-induced Ca2+ signaling. AG cell extracts exhibited kinase activity toward a CaMKII-selective peptide substrate that was dependent on both Ca2+ [half-maximal concentration for Ca2+ activation (K0.5) = 1.5 microM] and calmodulin (K0.5 = 46 nM) and was sensitive to a calmodulin antagonist and a CaMKII peptide inhibitor. On cell treatment with elevated extracellular potassium (10-60 mM) or angiotensin II, Ca(2+)-independent CaMKII activity increased to 133-205% of basal activity. Ca(2+)-independent kinase activity in agonist-stimulated extracts was inhibited by the CaMKII inhibitor peptide, 1(-)[N,O-bis(1,5- isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN-62), a cell-permeable inhibitor of CaMKII, reduced the agonist-induced stimulation of Ca(2+)-independent CaMKII activity. KN-62 also diminished depolarization-induced increases in [Ca2+]i without affecting the membrane potential. These...Continue Reading

Citations

Nov 18, 2000·American Journal of Physiology. Cell Physiology·P Q BarrettJ J Pancrazio
Oct 13, 2005·American Journal of Physiology. Endocrinology and Metabolism·Stepan GambaryanUlrich Walter
Dec 21, 2000·American Journal of Physiology. Cell Physiology·D R YingstR Schiebinger
Feb 24, 2001·American Journal of Physiology. Cell Physiology·A D SchrierP Q Barrett
May 21, 2021·The Tohoku Journal of Experimental Medicine·Xin GaoHironobu Sasano

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