About: Heme oxygenase/carbon monoxide signaling pathways: Regulation and functional significance

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Heme oxygenase/carbon monoxide signaling pathways: Regulation and functional significance
Creator	Otterbein, Leo Choi, Augustine Morse, Danielle Ryter, Stefan
Source	PMC
abstract	Carbon monoxide (CO), a gaseous second messenger, arises in biological systems during the oxidative catabolism of heme by the heme oxygenase (HO) enzymes. HO exists as constitutive (HO-2, HO-3) and inducible isoforms (HO-1), the latter which responds to regulation by multiple stress-stimuli. HO-1 confers protection in vitro and in vivo against oxidative cellular stress. Although the redox active compounds that are generated from HO activity (i.e. iron, biliverdin-IXα, and bilirubin-IXα) potentially modulate oxidative stress resistance, increasing evidence points to cytoprotective roles for CO. Though not reactive, CO regulates vascular processes such as vessel tone, smooth muscle proliferation, and platelet aggregation, and possibly functions as a neurotransmitter. The latter effects of CO depend on the activation of guanylate cyclase activity by direct binding to the heme moiety of the enzyme, stimulating the production of cyclic 3′:5′-guanosine monophosphate. CO potentially interacts with other intracellular hemoprotein targets, though little is known about the functional significance of such interactions. Recent progress indicates that CO exerts novel anti-inflammatory and anti-apoptotic effects dependent on the modulation of the p38 mitogen activated protein kinase (MAPK)-signaling pathway. By virtue of these effects, CO confers protection in oxidative lung injury models, and likely plays a role in HO-1 mediated tissue protection.
has issue date	2002-01-01(xsd:dateTime)
bibo:doi	10.1023/a:1015957026924
bibo:pmid	12162441
has license	no-cc
sha1sum (hex)	c0c7b00ab24cc387be12eab10e6eb3e304d24f7d
schema:url	https://doi.org/10.1023/a:1015957026924
resource representing a document's title	Heme oxygenase/carbon monoxide signaling pathways: Regulation and functional significance
has PubMed Central identifier	PMC7101540
has PubMed identifier	12162441
schema:publication	Mol Cell Biochem
resource representing a document's body	covid:c0c7b00ab24cc387be12eab10e6eb3e304d24f7d#body_text
is schema:about of	named entity 'exists' named entity 'regulates' named entity 'activity' named entity 'smooth muscle' named entity 'inducible' named entity 'catabolism' named entity 'targets' named entity 'enzyme' named entity 'functional' named entity 'Heme oxygenase' named entity 'stress' named entity 'paracrine' named entity 'transcriptional regulation' named entity 'sepsis' named entity 'LPS' named entity 'hypoxia' named entity 'MKK3' named entity 'intracellular' named entity 'HeLA cells' named entity 'isoform' named entity 'rat' named entity 'mRNA' named entity 'hyperoxia' named entity 'oxygenases' named entity 'HO-1' named entity 'HO-1' named entity 'anti-inflammatory' named entity 'smooth muscle cells' named entity 'glutamate toxicity' named entity 'Hypoxia' named entity 'metabolite' named entity 'anti-inflammatory' named entity 'macrophage' named entity 'endogenous' named entity 'LPS' named entity 'coal' named entity 'hyperoxia' named entity 'pulmonary artery' named entity 'mRNA expression' named entity 'TNFα' named entity 'regulatory protein' named entity 'hypoxic' named entity 'rat' named entity 'heme' named entity 'hypoxia' named entity 'ferritin' named entity 'p38 MAPK' named entity 'hypoxia' named entity 'interleukin-11' named entity 'peroxidases' named entity 'HIF-1' named entity 'HO-1' named entity 'heme' named entity 'lung' named entity 'effector' named entity 'lesion' named entity 'rat' named entity 'nitric oxide' named entity 'AP-1' named entity 'platelet derived growth factor' named entity 'Although' named entity 'oxidative stress' named entity 'cyclic' named entity 'models' named entity 'intracellular' named entity 'interacts' named entity 'guanylate cyclase' named entity 'ppm' named entity 'diatomic' named entity 'yeast two-hybrid analysis' named entity 'systemic vasculature' named entity 'stimulants' named entity 'TNFα' named entity 'L929' named entity 'HO-1' named entity 'hyperoxia' named entity 'interleukin-1' named entity 'Exogenous'

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