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Entity

Name
microglial cell activation
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 8

In-Edges 18

a(HBP:HBP00074) increases bp(GO:"microglial cell activation") View Subject | View Object

Furthermore, it was demonstrated that AβO may not only injure the neurites of brain neurons, but also activate microglia and astrocyte response (Sondag et al. 2009). PubMed:29196815

a(HBP:HBP00075) increases bp(GO:"microglial cell activation") View Subject | View Object

LMW oligomers led to a decrease in the neuronal levels of β2ARs, activated brain microglia, and induced impaired hippocampal LTP in mice in vivo (Yang et al. 2017). PubMed:29196815

p(MGI:App, var("p.Lys670Asn"), var("p.Met671Leu"), var("p.Thr714Ile"), var("p.Val717Ile")) causesNoChange bp(GO:"microglial cell activation") View Subject | View Object

We did not detect any glia or microglia activation in WT-APP (Fig. 3C and F) compared with WT-GFP (Fig. 3B and E), meaning that the neuroinflammation does not play a role in the memory deficit we observed PubMed:27522251

a(HBP:HBP00038) increases bp(GO:"microglial cell activation") View Subject | View Object

The deposition of fibrillar Ab in the AD brain results in the recruitment of microglia to the plaques owing to their expression of CCL2, which acts to attract microglia [82]. PubMed:21718217

a(HBP:HBP00089) association bp(GO:"microglial cell activation") View Subject | View Object

The development of dense-core amyloid plaques is associated with a robust immune response mediated by microglial cells. PubMed:21718217

a(HBP:HBP00089) positiveCorrelation bp(GO:"microglial cell activation") View Subject | View Object

The appearance of amyloid deposition in the AD brain coincides with a dramatic phenotypic activation of microglial cells in the surrounding area. PubMed:21718217

act(p(FPLX:PPAR)) decreases bp(GO:"microglial cell activation") View Subject | View Object

Indeed, treatment of AD mouse models with LXR or PPAR agonists has resulted in the suppression of microglial activation [44,45,47,59,63]. PubMed:21718217

act(p(HGNC:NR1H3)) decreases bp(GO:"microglial cell activation") View Subject | View Object

Indeed, treatment of AD mouse models with LXR or PPAR agonists has resulted in the suppression of microglial activation [44,45,47,59,63]. PubMed:21718217

p(HGNC:CCL2) increases bp(GO:"microglial cell activation") View Subject | View Object

The deposition of fibrillar Ab in the AD brain results in the recruitment of microglia to the plaques owing to their expression of CCL2, which acts to attract microglia [82]. PubMed:21718217

a(HBP:HBP00092) increases bp(GO:"microglial cell activation") View Subject | View Object

a report by Hoffmann et al. showed that fibrillar a-syn induced a more pronounced inflammatory response in microglial cells [61]. PubMed:28803412

Annotations
Confidence
Medium
MeSH
Microglia

a(HBP:HBP00093) increases bp(GO:"microglial cell activation") View Subject | View Object

However, in a different report, oligomers were shown to activate proinflammatory signals in microglial cells in vitro and in vivo, and this was prevented by addition of a MAP kinase inhibitor [161]. PubMed:28803412

Annotations
Confidence
High
MeSH
Microglia

p(HGNC:IL18) increases bp(GO:"microglial cell activation") View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

p(HGNC:IL1B) increases bp(GO:"microglial cell activation") View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

a(CHEBI:Anatabine) decreases bp(GO:"microglial cell activation") View Subject | View Object

Interestingly, Tg PS1/APPswe mice treated with anata- bine at a dosage of 20 mg/Kg/Day, but not 10mg/Kg/day showed a significant reduction in Iba- 1 burden in the hippocampus compared to untreated Tg PS1/APPswe mice (Fig 5A and 5B), suggesting that anatabine suppresses microgliosis in the brain of Tg PS1/APPswe mice. PubMed:26010758

p(HGNC:AIF1) positiveCorrelation bp(GO:"microglial cell activation") View Subject | View Object

A significant increase in Iba-1 bur- den was observed in the cortex and hippocampus of Tg PS1/APPswe mice compared to their control wild-type littermates, suggesting increased Iba-1 immunopositive microglia in the brain of Tg PS1/APPswe mice (Fig 5A). PubMed:26010758

act(p(HGNC:SYK)) positiveCorrelation bp(GO:"microglial cell activation") View Subject | View Object

To investigate whether pathological Syk activation oc- curs in the brain of AD mouse models, we analyzed the brains of 116-week-old wild-type, Tg APPsw and Tg PS1/APPsw mice using high-resolution confocal micros- copy and immunofluorescence. All transgenic mice (Fig. 1b-e) exhibit an increased Iba-1 and GFAP reactiv- ity compared to wild-type littermates (Fig. 1a). Moreo- ver,wild-type some of the activated amoeboid microglia that are observed in transgenic mice are also strongly positive for pSyk (Fig. 1b-d). PubMed:28877763

path(MESH:"Alzheimer Disease") increases bp(GO:"microglial cell activation") View Subject | View Object

To investigate whether pathological Syk activation oc- curs in the brain of AD mouse models, we analyzed the brains of 116-week-old wild-type, Tg APPsw and Tg PS1/APPsw mice using high-resolution confocal micros- copy and immunofluorescence. All transgenic mice (Fig. 1b-e) exhibit an increased Iba-1 and GFAP reactiv- ity compared to wild-type littermates (Fig. 1a). Moreo- ver,wild-type some of the activated amoeboid microglia that are observed in transgenic mice are also strongly positive for pSyk (Fig. 1b-d). PubMed:28877763

a(CHEBI:"alpha-tocopherol") decreases bp(GO:"microglial cell activation") View Subject | View Object

Furthermore, it disrupted the activity of NF-B, and thus, caused the suppression of NO synthase and inflammatory regulators such as IL-6 and IL-1, and the reduction of microglial activation [37] PubMed:29179999

Out-Edges 8

bp(GO:"microglial cell activation") association a(HBP:HBP00089) View Subject | View Object

The development of dense-core amyloid plaques is associated with a robust immune response mediated by microglial cells. PubMed:21718217

bp(GO:"microglial cell activation") positiveCorrelation a(HBP:HBP00089) View Subject | View Object

The appearance of amyloid deposition in the AD brain coincides with a dramatic phenotypic activation of microglial cells in the surrounding area. PubMed:21718217

bp(GO:"microglial cell activation") increases sec(p(HGNC:IL1B)) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

bp(GO:"microglial cell activation") increases sec(p(HGNC:IL6)) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

bp(GO:"microglial cell activation") increases sec(p(HGNC:IL18)) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

bp(GO:"microglial cell activation") increases sec(p(HGNC:NOS2)) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

bp(GO:"microglial cell activation") positiveCorrelation p(HGNC:AIF1) View Subject | View Object

A significant increase in Iba-1 bur- den was observed in the cortex and hippocampus of Tg PS1/APPswe mice compared to their control wild-type littermates, suggesting increased Iba-1 immunopositive microglia in the brain of Tg PS1/APPswe mice (Fig 5A). PubMed:26010758

bp(GO:"microglial cell activation") positiveCorrelation act(p(HGNC:SYK)) View Subject | View Object

To investigate whether pathological Syk activation oc- curs in the brain of AD mouse models, we analyzed the brains of 116-week-old wild-type, Tg APPsw and Tg PS1/APPsw mice using high-resolution confocal micros- copy and immunofluorescence. All transgenic mice (Fig. 1b-e) exhibit an increased Iba-1 and GFAP reactiv- ity compared to wild-type littermates (Fig. 1a). Moreo- ver,wild-type some of the activated amoeboid microglia that are observed in transgenic mice are also strongly positive for pSyk (Fig. 1b-d). PubMed:28877763

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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.