Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.17 (CaMKII)
 4,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of regucalcin, a calcium-binding protein isolated from rat liver cytosol, on cytosolic Ca2+/calmodulin-dependent protein kinase activity was investigated. The increase in cytosolic Ca2+/calmodulin-dependent protein kinase activity with passage of incubation time was clearly prevented by the presence of regucalcin (1.0 microM). An appreciable effect of regucalcin was seen at 0.5 microM. The cytosolic Ca2+/calmodulin-dependent protein kinase activity was fairly increased by increasing concentrations of added Ca2+ (0.25-1.0 mM). This increase was clearly blocked by the presence of regucalcin (1.0 microM). The inhibitory effect of regucalcin on the protein kinase activity was also seen with varying concentrations of calmodulin (2.5-15 micrograms). In the presence of regucalcin (1.0 microM), trifluoperazine (50 microM), an antagonist of calmodulin, significantly decreased the cytosolic Ca2+/calmodulin-dependent protein kinase activity. These results suggest that regucalcin can regulate the Ca2(+)-calmodulin effect in liver cytosol.
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PMID:Hepatic calcium-binding protein regucalcin decreases Ca2+/calmodulin-dependent protein kinase activity in rat liver cytosol. 217 80

The effect of regucalcin on Ca2+/calmodulin-dependent protein kinase activity in the cytosol of rat renal cortex was investigated. Regucalcin is a calcium-binding protein which exists in rat liver and renal cortex. Protein kinase activity in renal cortex cytosol was markedly increased by the addition of CaCl2 (0.5 mM) plus calmodulin (10 microg/ml) in the enzyme reaction mixture . This increase was completely prevented by the addition of trifluoperazine (25 microM), an antagonist of calmodulin. The cytosolic Ca2+/calmodulin-dependent protein kinase activity was clearly inhibited by the addition of regucalcin; an appreciable effect of regucalcin was seen at 0.01 microM. The cytosolic Ca2+/calmodulin-dependent protein kinase activity was fairly increased by increasing concentrations of added Ca2+ (100-1000 microM). This increase was markedly blocked by the presence of regucalcin (0.1 microM). The inhibitory effect of regucalcin on the protein kinase activity was also seen with varying concentrations of calmodulin (2-20 microg/ml). These results demonstrate that regucalcin can regulate Ca2+/calmodulin-dependent protein kinase activity in renal cortex cells.
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PMID:Inhibitory effect of regucalcin on Ca2+/calmodulin-dependent protein kinase activity in rat renal cortex cytosol. 945 Jun 68

The expression of calcium-binding protein regucalcin mRNA in the kidney cortex of rats ingested with saline was investigated. The alteration in regucalcin mRNA levels was analyzed by Northern blotting using liver regucalcin complementary DNA (0.9 kb of open reading frame). Rats were freely given saline as drinking water for 7 days. Regucalcin mRNA levels in the kidney cortex were suppressed by saline ingestion. When calcium chloride (10 mg Ca/100 g body weight) was intraperitoneally administered to rats ingested with saline for 7 days, the effect of calcium administration to increase regucalcin mRNA levels was weakened by saline ingestion. Such effect was also seen by the administration of 2.5 and 5 mg Ca/100 g. Regucalcin mRNA levels in the kidney cortex of spontaneous hypertensive rats (SHR) were not appreciably increased by the administration of calcium (10 mg/100 g). Meanwhile, calcium content in the kidney cortex was significantly elevated by the administration of calcium (10 mg/100 g) to normal rats. This increase was weakened in saline-ingested rats. Moreover, Ca2+/calmodulin-dependent protein kinase activity in the cytosol of kidney cortex was significantly decreased by saline ingestion. These results suggest the possibility that saline ingestion-induced suppression of regucalcin mRNA expression in the kidney cortex is partly involved in the attenuation of Ca2+ signalling.
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PMID:Stimulatory effect of calcium administration on regucalcin mRNA expression is attenuated in the kidney cortex of rats ingested with saline. 954 10

The role of regucalcin in the regulation of protein kinase activity in rat brain neuronal cells obtained from primary culture was investigated. Protein kinase activity was assayed using the 5500 g supernatant fraction of the cell homogenate. Protein kinase activity was significantly raised by the addition of calmodulin (5 microg/ml) or dioctanoylglycerol (5 microg/ml) in the presence of CaCl2 (10(-4) M), indicating that Ca2+/calmodulin-dependent protein kinase and protein kinase C is present in the neuronal cells. The addition of regucalcin (10(-9)-10(-7) M) in the enzyme reaction mixture caused a significant decrease in protein kinase activity in the absence of calmodulin or dioctanoylglycerol without Ca(2+) addition. Moreover, regucalcin completely prevented the activation of protein kinase by the addition of calmodulin or dioctonoylglyceral in the presence of CaCl(2) (10(-4) M). The presence of anti-regucalcin monoclonal antibody (25 or 50 ng/ml) caused a significant elevation of protein kinase activity without CaCl2 addition. Such an effect was significantly inhibited by the addition of trifluoperazine (2x10(-5) M), an antagonist of calmodulin, or staurosporine (10(-6) M), an inhibitor of protein kinase C. The present study demonstrates that endogenous regucalcin in rat brain neuronal cells has an inhibitory effect on Ca2+ dependent protein kinase activity.
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PMID:Inhibitory role of regucalcin in the regulation of Ca2+ dependent protein kinases activity in rat brain neurons. 1116 91

Doxorubicin (DOXO) is widely used to treat solid tumors. However, its clinical use is limited by side effects including serious cardiotoxicity due to cardiomyocyte damage. Resident cardiac progenitor cells (hCPCs) act as key regulators of homeostasis in myocardial cells. However, little is known about the function of hCPCs in DOXO-induced cardiotoxicity. In this study, we found that DOXO-mediated hCPC toxicity is closely related to calcium-related autophagy signaling and was significantly attenuated by blocking mTOR signaling in human hCPCs. DOXO induced hCPC apoptosis with reduction of SMP30 (regucalcin) and autophagosome marker LC3, as well as remarkable induction of the autophagy-related markers, Beclin-1, APG7, and P62/SQSTM1 and induction of calcium-related molecules, CaM (Calmodulin) and CaMKII (Calmodulin kinase II). The results of an LC3 puncta assay further indicated that DOXO reduced autophagosome formation via accumulation of cytosolic Ca2+. Additionally, DOXO significantly induced mTOR expression in hCPCs, and inhibition of mTOR signaling by rapamycin, a specific inhibitor, rescued DOXO-mediated autophagosome depletion in hCPCs with significant reduction of DOXO-mediated cytosolic Ca2+ accumulation in hCPCs, and restored SMP30 and mTOR expression. Thus, DOXO-mediated hCPC toxicity is linked to Ca2+-related autophagy signaling, and inhibition of mTOR signaling may provide a cardio-protective effect against DOXO-mediated hCPC toxicity.
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PMID:Doxorubicin Regulates Autophagy Signals via Accumulation of Cytosolic Ca2+ in Human Cardiac Progenitor Cells. 2773 42