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a(CHEBI:"reactive oxygen species")

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Entity

Name
reactive oxygen species
Namespace
chebi
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/chebi-names.belns

Appears in Networks 11

Alpha-synuclein oligomers: a new hope v1.0.0

Activation and regulation of the inflammasomes v1.0.0

Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease v1.0.0

Alzheimer’s disease and the autophagic-lysosomal system v1.0.0

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

In-Edges 25

a(HBP:HBP00093) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Another report by Zhang and collaborators also highlighted glial activation and production of reactive oxygen species in response to oligomer-like preparations of aggregated a-syn [168]. PubMed:28803412

Appears in Networks:
Annotations
Confidence
High
MeSH
Microglia

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Neurons from these animals exhibited increased oxidative stress, increased generation of ROS, DNA fragmentation, neuronal apoptosis, and impairment in learning, compared to single-transgenic mAPP mice. PubMed:30444369

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Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

In another study, neurons from Tg mAPP/ABAD mice were shown to exhibit decreased activity of cyclooxygenase (COX) enzyme, spontaneous release of ROS, loss of mitochondrial membrane potential, a decrease in ATP production and release of cytochrome c from mitochondria with subsequent induction of caspase-3-like activity followed by apoptotic cell death. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

path(HBP:"mitochondrial dysfunction") increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Dysfunctional mitochondria are critically harmful to cells, as this leads to decreased synthesis of cellular ATP and accumulation of ROS, which further overburden and damage other functional mitochondria. PubMed:29758300

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act(a(MESH:Peroxisomes)) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Excessive amounts of free radicals and radical-derived reactive species may also arise from the activity of NAD(P)H oxidases (NOx) and/or xanthine oxidase, as well as from nitric oxide synthase (NOS), P450 metabolism and peroxisomes. PubMed:24563850

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bp(GO:"inflammatory response") increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Excessive amounts of ROS may also arise from inflammatory processes [75]. PubMed:24563850

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act(p(FPLX:"NADPH_oxidase")) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Excessive amounts of free radicals and radical-derived reactive species may also arise from the activity of NAD(P)H oxidases (NOx) and/or xanthine oxidase, as well as from nitric oxide synthase (NOS), P450 metabolism and peroxisomes. PubMed:24563850

Appears in Networks:

act(p(FPLX:NOS)) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Excessive amounts of free radicals and radical-derived reactive species may also arise from the activity of NAD(P)H oxidases (NOx) and/or xanthine oxidase, as well as from nitric oxide synthase (NOS), P450 metabolism and peroxisomes. PubMed:24563850

Appears in Networks:

act(p(HGNC:XDH)) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Excessive amounts of free radicals and radical-derived reactive species may also arise from the activity of NAD(P)H oxidases (NOx) and/or xanthine oxidase, as well as from nitric oxide synthase (NOS), P450 metabolism and peroxisomes. PubMed:24563850

Appears in Networks:

act(p(HGNCGENEFAMILY:"Cytochrome P450 family 1")) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Excessive amounts of free radicals and radical-derived reactive species may also arise from the activity of NAD(P)H oxidases (NOx) and/or xanthine oxidase, as well as from nitric oxide synthase (NOS), P450 metabolism and peroxisomes. PubMed:24563850

Appears in Networks:

act(complex(GO:"NADPH oxidase complex")) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

We indeed found that there is an overexpression (w15%) of Nox1 protein (a component of NADPH oxidase complex) by Western blot, suggesting the role of NADPH oxidase complex as a potential source of ROS PubMed:28528849

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act(complex(GO:"NADPH oxidase complex")) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

These findings suggest that the ROS production induced by extracellular TauRDΔK oligomers might cause the activation of NADPH oxidase complex PubMed:28528849

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p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) causesNoChange a(CHEBI:"reactive oxygen species") View Subject | View Object

By contrast, monomers of TauRDΔK even at 10 mM concentration did not cause any significant ROS increase (Fig. 5B). PubMed:28528849

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p(HBP:"Tau oligomers", var("p.Lys280del")) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

We observed an oligomer-dependent increase in the ROS production in the mature rat primary hippocampal neurons in all cellular compartments (Fig. 5A). PubMed:28528849

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Annotations
MeSH
Hippocampus
MeSH
Neurons

a(CHEBI:"alpha-tocopherol") decreases a(CHEBI:"reactive oxygen species") View Subject | View Object

It has antiox-idant effects via the interference of reactive components and ROS by redox cycling of quinine, and subsequently generating hydroquinone [209]. PubMed:29179999

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a(CHEBI:"1,8-cineole") decreases a(CHEBI:"reactive oxygen species") View Subject | View Object

The mitochondrial membrane potential, ROS and NO levels were down-regulated by 1,8-cineole in A 25-35-stimulated cells [250]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"vitamin D") decreases a(CHEBI:"reactive oxygen species") View Subject | View Object

The phosphorylation of the NF-B inflamma-tory pathway in A 25-35-stimulated microglial cells was inhibited by vitamin D2 via reducing ROS and inflammatory cytokines [207] PubMed:29179999

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Annotations
Cell Ontology (CL)
microglial cell

a(PUBCHEM:14193399) decreases a(CHEBI:"reactive oxygen species") View Subject | View Object

Glaucocalyxin B, found in Rabdosia japonica, considerably atten-uated the expression of NO, TNF-, IL-1, COX-2 and iNOS in LPS-induced microglia cells [169–172]. Moreover, the activation of NF-B, p38 MAPK and ROS generation was interrupted by glauco- calyxin B in LPS-induced microglia cells [172]. PubMed:29179999

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell

a(PUBCHEM:440312) decreases a(CHEBI:"reactive oxygen species") View Subject | View Object

Besides, it significantly decreased the generation of ROS and affected LPS-induced activation of MAPK, including p38 and NF-B signaling[243]. PubMed:29179999

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bp(GO:"ion transport") association a(CHEBI:"reactive oxygen species") View Subject | View Object

Higher levels of ROS biomarkers are characteristic of AD patients in clinical and preclinical studies, resulting in the alteration of membrane proper- ties, such as fluidity, ion transport, enzyme activities, protein cross- linking, tau protein hyperphosphorylation, autophagic dysfunction and eventually neuron cell death [20]. PubMed:27288790

Appears in Networks:

bp(MESH:"Membrane Fluidity") association a(CHEBI:"reactive oxygen species") View Subject | View Object

Higher levels of ROS biomarkers are characteristic of AD patients in clinical and preclinical studies, resulting in the alteration of membrane proper- ties, such as fluidity, ion transport, enzyme activities, protein cross- linking, tau protein hyperphosphorylation, autophagic dysfunction and eventually neuron cell death [20]. PubMed:27288790

Appears in Networks:

path(MESH:"Alzheimer Disease") positiveCorrelation a(CHEBI:"reactive oxygen species") View Subject | View Object

Higher levels of ROS biomarkers are characteristic of AD patients in clinical and preclinical studies, resulting in the alteration of membrane proper- ties, such as fluidity, ion transport, enzyme activities, protein cross- linking, tau protein hyperphosphorylation, autophagic dysfunction and eventually neuron cell death [20]. PubMed:27288790

Appears in Networks:

act(complex(GO:"NF-kappaB complex")) increases act(a(CHEBI:"reactive oxygen species")) View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(complex(GO:"NF-kappaB complex")) increases act(a(CHEBI:"reactive oxygen species")) View Subject | View Object

Furthermore NF-κB specific inhibitor prevents iNOS and ROS upregulation in Aβ stimulated cultures of astrocytes or mixed cortical cells PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:Schizophrenia) association a(CHEBI:"reactive oxygen species") View Subject | View Object

Beyond METH, redox-related changes that result from an imbalance between reactive oxygen species (ROS) production and ROS clearance are implicated in schizophrenia PubMed:30061532

Appears in Networks:

Out-Edges 23

a(CHEBI:"reactive oxygen species") increases act(p(HGNC:TRPM2)) View Subject | View Object

This channel senses intracellular ROS and responds by opening itself to facilitate Ca2+ influx into the cell; this is intriguing considering that both ion fluxes and the oxidative state (see below) have important roles in NLRP3 inflammasome activation. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Caspase subgraph

a(CHEBI:"reactive oxygen species") increases bp(GO:"apoptosome assembly") View Subject | View Object

In particular, ROS facilitate the assembly of the apoptosome in several ways. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Apoptosis signaling subgraph

a(CHEBI:"reactive oxygen species") increases bp(GO:"negative regulation of inflammatory response") View Subject | View Object

Specifically, ROS have been shown to regulate a wide variety of signalling pathways including anti- inflammatory responses and adaptation to hypoxia [77,78], autop- hagy [79], immune cell function [80], cellular differentiation [81], integrins [82], as well as oncogenes signalling [83]. PubMed:24563850

Appears in Networks:

a(CHEBI:"reactive oxygen species") regulates bp(GO:"response to hypoxia") View Subject | View Object

Specifically, ROS have been shown to regulate a wide variety of signalling pathways including anti- inflammatory responses and adaptation to hypoxia [77,78], autop- hagy [79], immune cell function [80], cellular differentiation [81], integrins [82], as well as oncogenes signalling [83]. PubMed:24563850

Appears in Networks:

a(CHEBI:"reactive oxygen species") regulates bp(GO:autophagy) View Subject | View Object

Specifically, ROS have been shown to regulate a wide variety of signalling pathways including anti- inflammatory responses and adaptation to hypoxia [77,78], autop- hagy [79], immune cell function [80], cellular differentiation [81], integrins [82], as well as oncogenes signalling [83]. PubMed:24563850

Appears in Networks:

a(CHEBI:"reactive oxygen species") regulates bp(GO:"leukocyte activation") View Subject | View Object

Specifically, ROS have been shown to regulate a wide variety of signalling pathways including anti- inflammatory responses and adaptation to hypoxia [77,78], autop- hagy [79], immune cell function [80], cellular differentiation [81], integrins [82], as well as oncogenes signalling [83]. PubMed:24563850

Appears in Networks:

a(CHEBI:"reactive oxygen species") regulates bp(GO:"cell differentiation") View Subject | View Object

Specifically, ROS have been shown to regulate a wide variety of signalling pathways including anti- inflammatory responses and adaptation to hypoxia [77,78], autop- hagy [79], immune cell function [80], cellular differentiation [81], integrins [82], as well as oncogenes signalling [83]. PubMed:24563850

Appears in Networks:

a(CHEBI:"reactive oxygen species") regulates bp(GO:"integrin activation") View Subject | View Object

Specifically, ROS have been shown to regulate a wide variety of signalling pathways including anti- inflammatory responses and adaptation to hypoxia [77,78], autop- hagy [79], immune cell function [80], cellular differentiation [81], integrins [82], as well as oncogenes signalling [83]. PubMed:24563850

Appears in Networks:

a(CHEBI:"reactive oxygen species") increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(CHEBI:"reactive oxygen species") increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(CHEBI:"reactive oxygen species") increases act(p(FPLX:PKC)) View Subject | View Object

ROS activate various downstream signaling molecules, such as PKC and mitogen-activated protein kinases (MAPKs) that induce nuclear translocation of NF-B and the expression of pro-inflammatory genes [41]. PubMed:29179999

Appears in Networks:

a(CHEBI:"reactive oxygen species") increases act(p(FPLX:ERK)) View Subject | View Object

ROS activate various downstream signaling molecules, such as PKC and mitogen-activated protein kinases (MAPKs) that induce nuclear translocation of NF-B and the expression of pro-inflammatory genes [41]. PubMed:29179999

Appears in Networks:

a(CHEBI:"reactive oxygen species") increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

ROS activate various downstream signaling molecules, such as PKC and mitogen-activated protein kinases (MAPKs) that induce nuclear translocation of NF-B and the expression of pro-inflammatory genes [41]. PubMed:29179999

Appears in Networks:

a(CHEBI:"reactive oxygen species") increases act(p(FPLX:"IKK_complex")) View Subject | View Object

Under different envi- ronmental conditions such as Aβ/ROS/cytokines accumulation, the IκB kinase (IKK) complex becomes activated and mediates the phosphoryla- tion of IκBs, then IκBs are degradated and the remaining NF-κB dimer is activated and thus translocates to the nucleus where it binds to the DNA consensus sequence of various target genes [9–11]. PubMed:27288790

Appears in Networks:

a(CHEBI:"reactive oxygen species") positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Higher levels of ROS biomarkers are characteristic of AD patients in clinical and preclinical studies, resulting in the alteration of membrane proper- ties, such as fluidity, ion transport, enzyme activities, protein cross- linking, tau protein hyperphosphorylation, autophagic dysfunction and eventually neuron cell death [20]. PubMed:27288790

Appears in Networks:

a(CHEBI:"reactive oxygen species") association bp(MESH:"Membrane Fluidity") View Subject | View Object

Higher levels of ROS biomarkers are characteristic of AD patients in clinical and preclinical studies, resulting in the alteration of membrane proper- ties, such as fluidity, ion transport, enzyme activities, protein cross- linking, tau protein hyperphosphorylation, autophagic dysfunction and eventually neuron cell death [20]. PubMed:27288790

Appears in Networks:

a(CHEBI:"reactive oxygen species") association bp(GO:"ion transport") View Subject | View Object

Higher levels of ROS biomarkers are characteristic of AD patients in clinical and preclinical studies, resulting in the alteration of membrane proper- ties, such as fluidity, ion transport, enzyme activities, protein cross- linking, tau protein hyperphosphorylation, autophagic dysfunction and eventually neuron cell death [20]. PubMed:27288790

Appears in Networks:

a(CHEBI:"reactive oxygen species") increases p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) View Subject | View Object

Higher levels of ROS biomarkers are characteristic of AD patients in clinical and preclinical studies, resulting in the alteration of membrane proper- ties, such as fluidity, ion transport, enzyme activities, protein cross- linking, tau protein hyperphosphorylation, autophagic dysfunction and eventually neuron cell death [20]. PubMed:27288790

Appears in Networks:

a(CHEBI:"reactive oxygen species") decreases bp(GO:autophagy) View Subject | View Object

Higher levels of ROS biomarkers are characteristic of AD patients in clinical and preclinical studies, resulting in the alteration of membrane proper- ties, such as fluidity, ion transport, enzyme activities, protein cross- linking, tau protein hyperphosphorylation, autophagic dysfunction and eventually neuron cell death [20]. PubMed:27288790

Appears in Networks:

a(CHEBI:"reactive oxygen species") increases act(p(FPLX:NFkappaB)) View Subject | View Object

Previous find- ings have identified ROS as a common denominator of NF-κB activating signals, as Chetsawang B found that NF-κB was increased in H 2 O 2 -treat- ed SH-SY5Y cells [22,23]. PubMed:27288790

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

a(CHEBI:"reactive oxygen species") regulates act(p(FPLX:NFkappaB)) View Subject | View Object

ROS has been found not only the regulators of NF-κB, interestingly, iNOS is also regulated by NF-κB. PubMed:27288790

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a(CHEBI:"reactive oxygen species") increases p(HGNC:NFKBIA, pmod(Ph)) View Subject | View Object

ROS generation leads to phosphorylation of NF-κB cytoplasmic inhibitor IκBα. NF-κB is thus liberated and transports to the nucleus. PubMed:27288790

Appears in Networks:

a(CHEBI:"reactive oxygen species") association path(MESH:Schizophrenia) View Subject | View Object

Beyond METH, redox-related changes that result from an imbalance between reactive oxygen species (ROS) production and ROS clearance are implicated in schizophrenia PubMed:30061532

Appears in Networks:

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BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.