Activation of the Cardiac Calcium Release Channel (Ryanodine Receptor) by Poly-S-Nitrosylation

Xu, Le; Eu, Jerry P.; Meissner, Gerhard; Stamler, Jonathan S.

doi:10.1126/science.279.5348.234

Cited by 928 publications

(720 citation statements)

References 44 publications

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“…Furthermore, DNA microarray analysis showed that CHOP is induced by IL-1b plus IFN-g in primary rat b-cells. 85 In type II diabetes, impaired insulin action, which is often associated with obesity and physical inactivity, is a major factor in progression of the disease, but hyperglycemia occurs only when b-cells fail to compensate for the increased demand for insulin secretion. Overload of b-cells in conditions such as hyperglycemia, obesity and long-term treatment with sulfonylureas leads to b-cell dysfunction and to apoptosis through a process referred as 'b-cell exhaustion'.…”

Section: Diabetesmentioning

confidence: 99%

Roles of CHOP/GADD153 in endoplasmic reticulum stress

2003

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Endoplasmic reticulum (ER) is the site of synthesis and folding of secretory proteins. Perturbations of ER homeostasis affect protein folding and cause ER stress. ER can sense the stress and respond to it through translational attenuation, upregulation of the genes for ER chaperones and related proteins, and degradation of unfolded proteins by a quality-control system. However, when the ER function is severely impaired, the organelle elicits apoptotic signals. ER stress has been implicated in a variety of common diseases such as diabetes, ischemia and neurodegenerative disorders. One of the components of the ER stress-mediated apoptosis pathway is C/EBP homologous protein (CHOP), also known as growth arrestand DNA damage-inducible gene 153 (GADD153). Here, we summarize the current understanding of the roles of CHOP/ GADD153 in ER stress-mediated apoptosis and in diseases including diabetes, brain ischemia and neurodegenerative disease.

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Section: Diabetesmentioning

confidence: 99%

Roles of CHOP/GADD153 in endoplasmic reticulum stress

2003

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“…Concomitantly, NO derived from NOS 1 in the SR nitrosylates RyR channel proteins in a manner that promotes Ca efflux from the SR, causing contraction [19]. NO signaling by nitrosylation is fast, reversible, and affected by the overall nitroso-redox balance of the system [20]. The oxidase enzymes NADPH oxidase and xanthine oxidase, as well as mitochondrial oxidative phosphorylation, generate the biologically relevant reactive oxygen species superoxide, hydrogen peroxide and the hydroxyl radical [21].…”

Section: Nitric Oxidementioning

confidence: 99%

Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms

2010

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“…For example, NO oxidizes vicinal thiol groups to form disulfide (51). This oxidation reaction appears to occur via formation of an intermediate nitrosothiol to increase or decrease the activity of proteins such as p21 RAS (52), the olfactory cyclic nucleotide-gated channel (53), glyceraldehyde-3-phosphate dehydrogenase (54), caspase-3 (55), and ryanodine receptor (56).…”

Section: No and Signal-transduction Pathwaymentioning

confidence: 99%

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

Kadekaro

2004

Braz J Med Biol Res

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Nitric oxide (NO), a free radical gas produced endogenously from the amino acid L-arginine by NO synthase (NOS), has important functions in modulating vasopressin and oxytocin secretion from the hypothalamo-neurohypophyseal system. NO production is stimulated during increased functional activity of magnocellular neurons, in parallel with plastic changes of the supraoptic nucleus (SON) and paraventricular nucleus. Electrophysiological data recorded from the SON of hypothalamic slices indicate that NO inhibits firing of phasic and non-phasic neurons, while L-NAME, an NOS inhibitor, increases their activity. Results from measurement of neurohypophyseal hormones are more variable. Overall, however, it appears that NO, tonically produced in the forebrain, inhibits vasopressin and oxytocin secretion during normovolemic, isosmotic conditions. During osmotic stimulation, dehydration, hypovolemia and hemorrhage, as well as high plasma levels of angiotensin II, NO inhibition of vasopressin neurons is removed, while that of oxytocin neurons is enhanced. This produces a preferential release of vasopressin over oxytocin important for correction of fluid imbalance. During late pregnancy and throughout lactation, fluid homeostasis is altered and expression of NOS in the SON is down-and up-regulated, respectively, in parallel with plastic changes of the magnocellular system. NO inhibition of magnocellular neurons involves GABA and prostaglandin synthesis and the signal-transduction mechanism is independent of the cGMP-pathway. Plasma hormone levels are unaffected by icv 1H-[1, 2, 4]oxadiazolo-[4,3-a]quinoxalin-1-one (a soluble guanylyl cyclase inhibitor) or 8-Br-cGMP administered to conscious rats. Moreover, cGMP does not increase in homogenates of the neural lobe and in microdialysates of the SON when NO synthesis is enhanced during osmotic stimulation. Among alternative signal-transduction pathways, nitrosylation of target proteins affecting activity of ion channels is considered.

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Activation of the Cardiac Calcium Release Channel (Ryanodine Receptor) by Poly-S-Nitrosylation

Cited by 928 publications

References 44 publications

Roles of CHOP/GADD153 in endoplasmic reticulum stress

Roles of CHOP/GADD153 in endoplasmic reticulum stress

Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

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