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cyclic amp/hypoxia
Odkaz sa uloží do schránky
Strana 1 od 236 výsledky
A Key role for cyclic AMP-responsive element binding protein in hypoxia-mediated activation of the angiogenesis factor CCN1 (CYR61) in Tumor cells.
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Hypoxia is a prominent feature of solid tumors known to contribute to malignant progression and therapeutic resistance. Cancer cells adapt to hypoxia using various pathways, allowing tumors to thrive in a low oxygen state. Induction of new blood vessel formation via the secretion of proangiogenic
Adenosine and cyclic AMP in cerebral cortex of rats in hypoxia, status epilepticus and hypercapnia.
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The influence of hypercapnia, hypoxia and status epilepticus on cerebral cortex concentrations of adenosine, adenine nucleotides and cyclic AMP was studied on lightly anaesthetized (70% N2O) and artificially ventilated rats. Neither hypercapnia (arterial PCO2 about 80 and about 300 mmHg) nor hypoxia
Effects of cyclic AMP on the function of the cardiac gap junction during hypoxia.
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BACKGROUND
In the ischemic or hypoxic heart, an impairment of electrical cell-to-cell coupling and a dephosphorylation of the connexins that comprise the gap junction channel were observed. However, it remains to be elucidated whether the dephosphorylation of the connexin during hypoxia is due to
[Early cellular alterations induced by myocardial hypoxia: possible role of cyclic AMP (author's transl)].
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The ability of endogenous myocardial catecholamines to participate in the development of myocardial cellular alterations during a short period of severe hypoxia (30 min) was studied in isolated, Langendorff-perfused rat heart preparation, arrested by a high potassium concentration (16 mM) and
Hypoxia modulates cyclic AMP activation of BkCa channels in rat pulmonary arterial smooth muscle.
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The signal transduction mechanisms defining the role of cyclic nucleotides in the regulation of potassium channel activity in pulmonary vascular smooth muscle are currently an area of great interest. Normally, signaling mechanisms that elevate cyclic AMP (cAMP) open potassium channels. Modulation of
Hypoxia-activated cytochrome bd expression in Mycobacterium smegmatis is cyclic AMP receptor protein dependent.
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Mycobacteria are obligate aerobes and respire using two terminal respiratory oxidases, an aa3-type cytochrome c oxidase and a cytochrome bd-type menaquinol oxidase. Cytochrome bd is encoded by cydAB from the cydABDC gene cluster that is conserved throughout the mycobacterial genus. Here we report
Cyclic AMP represses the hypoxic induction of hypoxia-inducible factors in PC12 cells.
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Hypoxia-inducible factor 1 (HIF-1) is a master regulator for hypoxic activation of genes for angiogenesis, hormone synthesis, glycolysis and cell survival. In addition to hypoxic stimulus, various effectors and reagents were reported to affect HIF-1 activity. Here, we show that cyclic AMP (cAMP)
Hypoxia increases the cyclic AMP content of the cat carotid body in vitro.
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The cyclic AMP content of cat carotid bodies in vitro measured with a radioimmunoassay under control conditions (PO2: 230 torr) was 0.79 +/- 0.10 pmol/carotid body (n = 10). Lowering medium PO2 to 20 torr for 2 min significantly increased cyclic AMP content to 1.13 +/- 0.14 pmol/carotid body (n =
Adrenocortical activity and urinary cyclic AMP levels: effects of hypobaric hypoxia.
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Six highly motivated and trained military test subjects were exposed to a simulated altitude of 4267 m (477 torr) for 48 hours, prededed and followed by sea level runs lasting 32 hours. During each scenario tests subjects were required to perform their respective military tasks on a continual basis
The cyclic AMP response element in the Bcl-2 promoter confers inducibility by hypoxia in neuronal cells.
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In neuronal cells, expression of the anti-apoptotic Bcl-2 gene is induced by hypoxia and produces a protective effect. We show here that this effect is dependent upon the cyclic AMP response element (CRE) in the Bcl-2 promoter since mutation of this element abolishes the response and the isolated
Prolonged repolarization during hypoxemia in epicardial electrogram: difference from ischemia and a competitive action of cyclic AMP.
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The effects of regional hypoxemia and ischemia on epicardial electrogram were studied in anesthetized, open-chest dogs. The left circumflex artery (LCx) was cannulated and perfused with either arterial blood or hypoxic solution. A contact electrode for recording monophasic action potential (MAP) was
Myosin heavy chain isoforms expression and cyclic AMP concentrations in hypoxia-induced hypertrophied right ventricle in rats.
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We have previously demonstrated that the relative expression of myosin heavy chain-beta (MHC-beta) in both ventricles of rats exposed to long-term hypobaric hypoxia correlated significantly with the relative ventricular mass. In the present study, we investigated whether an increased expression of
Cyclic AMP modulates differentially the release of dopamine induced by hypoxia and other stimuli and increases dopamine synthesis in the rabbit carotid body.
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We have investigated the effects of different treatments that increase cyclic AMP levels on the in vitro synthesis and release of catecholamines in the rabbit carotid body. We also measured the rate of 45Ca2+ efflux from previously loaded carotid bodies under different conditions. Forskolin produced
Long-term modulation of inward currents in O2 chemoreceptors by chronic hypoxia and cyclic AMP in vitro.
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In mammals, ventilatory acclimatization to hypoxia is associated with an enhanced chemosensitivity of the O2-sensing carotid body, resulting in an increased respiratory drive. To test whether this sensitization involves long-term modulation of ion channel function in endogenous O2 chemoreceptors,
Cleavage of cyclic AMP-responsive element-binding protein H aggravates myocardial hypoxia reperfusion injury in a hepatocyte-myocardial cell co-culture system.
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