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Prkg1 cascade role in platelet activation and thrombosis.
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These data thus demonstrate the existence of two differently distributed cGKI isoforms in the dorsal root ganglion, and may provide insight into the cellular and molecular mechanisms of pain.
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This study demonstrates that H- ras deletion protects against AngII-induced cardiac remodeling, possibly via a mechanism in which PKG-Ibeta overexpression could play a partial role, and points to H-Ras and/or downstream proteins as potential therapeutic targets in cardiovascular disease.
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that PKG-I expressed in nociceptors is not only a key determinant of dorsal root ganglion hyperexcitability and spinal synaptic plasticity but also an important modulator of cortical neuronal activity in pathological pain states
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Despite robust evidence for PKG Ialpha oxidation during NOS uncoupling in cell models, it is unlikely that PKG Ialpha oxidation occurs to a significant extent in vivo during diet-induced obesity and so is unlikely to mediate the associated cardiovascular dysfunction.
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analysis of the role of binding interface with protein kinase G-Ialpha leucine zipper in vascular function
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Brown adipose tissue, via Nox4-derived hydrogen peroxide, induces cyclic GMP-dependent protein kinase G type-1alpha activation, resulting in reduced vascular contractility.
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disulfide formation at Cys(43) does not directly activate PKGIalpha, and the C43S-mutant PKGIalpha has a higher Ka for cGMP. Results highlight that mutant enzymes should be carefully biochemically characterized before making in vivo inferences.
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PKG Ialpha disulfide formation triggers cardiac injury, and this initiation of maladaptive signaling can be blocked by pharmacological therapies that elevate cGMP, which binds kinase to limit its oxidation.
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Cyclic GMP kinase deletion causes iron deficiency anemia, duodenal ulcers, and bleeding in the knockout mice.
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Protein kinase G has a role in regulating production of H2S, which governs oxygen sensing
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cGMP/protein kinase G signaling suppresses Itpr1 phosphorylation and promotes endoplasmic reticulum stress in photoreceptors of Cnga3-deficient mice.
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these results demonstrate that myocardial PKG1alpha oxidation prevents a beneficial response to pathological stress, may explain variable responses to PKG1alpha pathway stimulation in heart disease
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Data show that cGMP-dependent kinase (cGK-Ialpha) knockdown partially rescued TNF-alpha-induced decrease in 42-kDa cGMP-dependent protein kinase-anchoring protein (GKAP42) and impairment of insulin signals.
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miR-20a expression is up-regulated in response to hypoxia in both mouse and human pulmonary arterial smooth muscle cells
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These findings characterize PKG as a novel regulator of AR-mediated transcription by enhancing AR cofactor p44/WDR77's function.
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A functional leucine zipper domain in PKG-1alpha is essential for maintenance of a low pulmonary vascular tone in normoxia.
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For the initial phase of angiotenin II-induced cardiac hypertrophy, lack of cardiomyocyte cGKI activity does not worsen hypertrophic growth.
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the key role of PKG-I in transforming growth factor beta1 induction by like weak inducer of apoptosis in kidney cells
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Results indicate that cGMP, acting primarily through cGKIalpha, is an important suppressor of kidney fibrosis.
