The cross-talk between nitric oxide and Ca2+: a story with a complex past and a promising future (Q40885499)

24 September 2017

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title

The cross-talk between nitric oxide and Ca2+: a story with a complex past and a promising future (English)

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24 September 2017

1

Clementi E

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24 September 2017

Meldolesi J

2

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24 September 2017

publication date

1 August 1997

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Trends in Pharmacological Sciences

24 September 2017

published in

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24 September 2017

volume

18

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24 September 2017

issue

8

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24 September 2017

page(s)

266-269

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Nitric oxide synthase isozymes. Characterization, purification, molecular cloning, and functions.

24 September 2017

cites work

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Nitric oxide action on growth factor-elicited signals. Phosphoinositide hydrolysis and [Ca2+]i responses are negatively modulated via a cGMP-dependent protein kinase I pathway.

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Phosphorylation of the inositol 1,4,5-trisphosphate receptor. Cyclic GMP-dependent protein kinase mediates cAMP and cGMP dependent phosphorylation in the intact rat aorta

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Prostacyclin and sodium nitroprusside inhibit the activity of the platelet inositol 1,4,5-trisphosphate receptor and promote its phosphorylation

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Cyclic GMP-dependent protein kinase blocks pertussis toxin-sensitive hormone receptor signaling pathways in Chinese hamster ovary cells

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3':5'-cyclic guanosine monophosphate (cGMP) potentiates the inositol 1,4,5-trisphosphate-evoked Ca2+ release in guinea-pig hepatocytes

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Cyclic GMP induces oscillatory calcium signals in rat hepatocytes

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cGMP mobilizes intracellular Ca2+ in sea urchin eggs by stimulating cyclic ADP-ribose synthesis

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Anti-Ig-induced calcium influx in rat B lymphocytes mediated by cGMP through a dihydropyridine-sensitive channel

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7 January 2021

Possible regulation of capacitative Ca2+ entry into colonic epithelial cells by NO and cGMP.

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cGMP is not required for capacitative Ca2+ entry in Jurkat T-lymphocytes

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Inhibition by nitroprusside of platelet calcium mobilization: evidence for reduced sensitivity to nitric oxide in essential hypertension.

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7 January 2021

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7 January 2021

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Identifiers

DOI

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24 September 2017

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