calmodulin/نقص الأكسجة

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Mechanism of Ca2+-influx and Ca2+/calmodulin-dependent protein kinase IV activity during in utero hypoxia in cerebral cortical neuronal nuclei of the guinea pig fetus at term.

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Previously we showed that following hypoxia there is an increase in nuclear Ca(2+)-influx and Ca(2+)/calmodulin-dependent protein kinase IV activity (CaMK IV) in the cerebral cortex of term guinea pig fetus. The present study tests the hypothesis that clonidine administration will prevent

[Involvement of JNK signal pathway in hypoxia related upregulation of calcium/calmodulin-dependent serine protein kinase in endothelial cells].

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OBJECTIVE To investigate the expression of calcium/calmodulin-dependent serine protein kinase (CASK) induced by short-term hypoxia, and to explore the role of JNK pathway in this signal event. METHODS EA. hy926 cells were cultured in normoxic condition for 0, 12, 24, 48, 72 h after being exposed to

[Effects of chronic hypoxia on the expression of calmodulin and calcicum/calmodulin-dependent protein kinase II and the calcium activity in myocardial cells in young rats].

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OBJECTIVE Calcium plays an important role in the impairment of heart function and arrhythmia under the condition of acute hypoxia, but the mechanism is different from that of chronic hypoxia. This study aimed to evaluate the effect of chronic hypoxia on the expression of calmodulin (CaM) and

Mechanism of increased tyrosine (Tyr(99)) phosphorylation of calmodulin during hypoxia in the cerebral cortex of newborn piglets: the role of nNOS-derived nitric oxide.

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The present study aims to investigate the mechanism of calmodulin modification during hypoxia and tests the hypothesis that hypoxia-induced increase in Tyr(99) phosphorylation of calmodulin in the cerebral cortex of newborn piglets is mediated by NO derived from nNOS. Fifteen piglets were divided

[Effects of chronic hypoxia on calmodulin activity in rats].

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To investigate the effects of chronic hypoxia of calmodulin activity in rats, we divided 40 wistar rats into four major groups. One group acted as control. The other three groups were made hypoxic by placing them in an isobaric hypoxic chamber (O2 = 10%) for 1, 2 and 3 weeks respectively. Calmodulin

Effect of calmodulin antagonists on hypoxia and reoxygenation damage in isolated rabbit hearts.

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The effect of calmodulin antagonists trifluoperazine (2.5 X 10(-7) M and 2.5 X 10(-6) M) and R 24571 (10(-8) M and 10(-7) M) on Langendorff-perfused rabbit hearts subjected to 180 min hypoxia and 30 min reoxygenation was studied. Coronary flow, force of contraction, oxygen consumption and release of

A novel Ca2+/calmodulin antagonist HBC inhibits angiogenesis and down-regulates hypoxia-inducible factor.

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Recent reports have shown that Ca(2+)/calmodulin (Ca(2+)/CaM) signaling plays a crucial role in angiogenesis. We previously developed a new Ca(2+)/CaM antagonist, HBC (4-{3,5-bis-[2-(4-hydroxy-3-methoxyphenyl)ethyl]-4,5-dihydropyrazol-1-yl}benzoic acid), from a curcumin-based synthetic chemical

Interleukin-10 prevents the hypoxia-induced decreases in expressions of AMPA receptor subunit GluA1 and alpha subunit of Ca(2+)/calmodulin-dependent protein kinase II in hippocampal neurons.

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The goal of this study is to evaluate the effects of anti-inflammatory cytokine interleukin-10 (IL-10) on the repeated brief hypoxia-induced changes in expressions of AMPA receptor subunit GluA1 and α- and β-subunit of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). The hypoxia-induced

Effects of calcium, calcium entry blockers and calmodulin inhibitors on atrioventricular conduction disturbances induced by hypoxia.

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Effects of hypoxia on atrioventricular conduction were investigated in the Langendorff-perfused isolated heart of the rabbit with various extracellular calcium concentrations ([Ca2+]) as well as in the presence of verapamil, nifedipine, N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide (W-7) and

Mechanism of Ca(2+)/calmodulin-dependent protein kinase IV activation and of cyclic AMP response element binding protein phosphorylation during hypoxia in the cerebral cortex of newborn piglets.

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Previously we showed that hypoxia results in increased neuronal nuclear Ca(2+) influx, Ca(2+)/calmodulin-dependent protein kinase IV activity (CaM KIV) and phosphorylation of c-AMP response element binding (CREB) protein. The aim of the present study was to understand the importance of neuronal

[Cyclic AMP level, dissociation of membrane-bound calmodulin and regulation of calcium transport in the heart sarcoplasmatic reticulum in circulatory hypoxia].

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Slight alterations in calmodulin-stimulated and distinct alterations in cAMP-dependent regulation of calcium transport were found in dog heart microsomes under conditions of circulatory hypoxia as compared with myocardium of healthy animals. After addition into the incubation mixture of exogenous

Effect of neuronal nitric oxide synthase inhibition on CA2+/calmodulin kinase kinase and CA2+/calmodulin kinase IV activity during hypoxia in cortical nuclei of newborn piglets.

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The present study tests the hypothesis that cerebral tissue hypoxia results in increased Ca(2+)/calmodulin (CaM) kinase kinase activity and that the administration of nitric oxide synthase inhibitors (N-nitro-l-arginine [NNLA], or 7-nitroindazole sodium [7-NINA]) prior to the onset of hypoxia will

Protection of dopaminergic antagonists against anoxia-induced inhibition of Ca(2+)-calmodulin dependent protein kinase II activity in rat brain.

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OBJECTIVE To study the effect of dopamine receptor antagonists on anoxia-induced inhibition of Ca(2+)-calmodulin dependent protein kinase II (CCDPK II) activity in rat hippocampus and striatum. METHODS Using the rat hippocampal and striatal slices under 95% N2 + 5% CO2, the activity of CCDPK II was

Nitric oxide-mediated Ca2+/calmodulin-dependent protein kinase IV activity during hypoxia in neuronal nuclei from newborn piglets.

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The present study tested the hypothesis that hypoxia results in increased Ca(2+)/calmodulin-dependent protein kinase IV (CaM kinase IV) activity and that inhibition of nitric oxide (NO) synthase by N-nitro-L-arginine (NNLA) prevents the hypoxia- induced increase in neuronal nuclear CaM kinase IV

Calcium/calmodulin-dependent protein kinase II mediates cardioprotection of intermittent hypoxia against ischemic-reperfusion-induced cardiac dysfunction.

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Intermittent high-altitude (IHA) hypoxia-induced cardioprotection against ischemia-reperfusion (I/R) injury is associated with the preservation of sarcoplasmic reticulum (SR) function. Although Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) and phosphatase are known to modulate the

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