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a(CHEBI:resveratrol) increases act(p(HGNC:CAMKK2)) View Subject | View Object

The ‘anti-ageing’ agent resveratrol is thought to indi- rectly recruit AMPK via activation of calcium/calmodulin- dependent protein kinase kinase 2 (CAMKK2), which, acting in synergy with Ca 2+ , exerts its effects via Thr172 phosphorylation 113 . This action, among others (below), is involved in its reduction of Aβ levels in N2a cells and neurons 114 and the elimination of Aβ and Htt in animal models of AD and HD 114,115 . PubMed:30116051

a(CHEBI:resveratrol) decreases p(HGNC:AGER) View Subject | View Object

Interestingly, resver- atrol downregulated RAGE as well as MMP9 — an effect that is related to decreased hippocampal load of Aβ42 (REF.297) . PubMed:30116051

a(CHEBI:resveratrol) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

The ‘anti-ageing’ agent resveratrol is thought to indi- rectly recruit AMPK via activation of calcium/calmodulin- dependent protein kinase kinase 2 (CAMKK2), which, acting in synergy with Ca 2+ , exerts its effects via Thr172 phosphorylation 113 . This action, among others (below), is involved in its reduction of Aβ levels in N2a cells and neurons 114 and the elimination of Aβ and Htt in animal models of AD and HD 114,115 . PubMed:30116051

a(CHEBI:resveratrol) decreases p(HGNC:HTT) View Subject | View Object

The ‘anti-ageing’ agent resveratrol is thought to indi- rectly recruit AMPK via activation of calcium/calmodulin- dependent protein kinase kinase 2 (CAMKK2), which, acting in synergy with Ca 2+ , exerts its effects via Thr172 phosphorylation 113 . This action, among others (below), is involved in its reduction of Aβ levels in N2a cells and neurons 114 and the elimination of Aβ and Htt in animal models of AD and HD 114,115 . PubMed:30116051

a(CHEBI:resveratrol) increases act(p(FPLX:AMPK)) View Subject | View Object

Resveratrol can stimulate SIRT1 via AMPK (see above), and it also possesses an AMPK-independent mode of SIRT1 recruitment that participates in blunting the neurotoxicity of Aβ25–35 fragments in PC12 cells 160 . PubMed:30116051

a(CHEBI:resveratrol) decreases act(p(HGNC:APP, frag("23_35"))) View Subject | View Object

Resveratrol can stimulate SIRT1 via AMPK (see above), and it also possesses an AMPK-independent mode of SIRT1 recruitment that participates in blunting the neurotoxicity of Aβ25–35 fragments in PC12 cells 160 . PubMed:30116051

a(CHEBI:resveratrol) increases r(FPLX:ATG4) View Subject | View Object

The multi-modal agent resveratrol induced the expression of ATG4 and promoted autophagosome formation. PubMed:30116051

a(CHEBI:resveratrol) increases bp(GO:"autophagosome assembly") View Subject | View Object

The multi-modal agent resveratrol induced the expression of ATG4 and promoted autophagosome formation. PubMed:30116051

a(CHEBI:resveratrol) decreases p(HGNC:MMP9) View Subject | View Object

Interestingly, resver- atrol downregulated RAGE as well as MMP9 — an effect that is related to decreased hippocampal load of Aβ42 (REF.297) . PubMed:30116051

a(CHEBI:resveratrol) decreases a(CHEBI:"amyloid-beta polypeptide 42") View Subject | View Object

Interestingly, resver- atrol downregulated RAGE as well as MMP9 — an effect that is related to decreased hippocampal load of Aβ42 (REF.297) . PubMed:30116051

a(CHEBI:resveratrol) directlyIncreases act(p(HGNC:PPP2CA)) View Subject | View Object

Here we show that resveratrol treatment directly interferes with the MID1-α4-PP2A degradation complex by reducing MID1 protein expression in vitro and in vivo. This leads to an increase of microtubule-associated PP2A activity and a time- and dose-dependent dephosphorylation of Tau. Interestingly, we further show that MID1 expression is elevated in AD tissue. PubMed:29062069

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a(CHEBI:resveratrol) directlyDecreases p(HGNC:MID1) View Subject | View Object

Here we show that resveratrol treatment directly interferes with the MID1-α4-PP2A degradation complex by reducing MID1 protein expression in vitro and in vivo. This leads to an increase of microtubule-associated PP2A activity and a time- and dose-dependent dephosphorylation of Tau. Interestingly, we further show that MID1 expression is elevated in AD tissue. PubMed:29062069

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a(CHEBI:resveratrol) increases act(p(HGNC:SIRT1)) View Subject | View Object

The study also found that resveratrol, a putative activator of SIRT1 (Howitz et al., 2003), inhibited Nrf2-dependent transcription, apparently contradicting earlier reports that resveratrol activates Nrf2 (Chen et al., 2005; Ungvari et al., 2010). PubMed:22020111

a(CHEBI:resveratrol) decreases act(p(HGNC:NFE2L2)) View Subject | View Object

The study also found that resveratrol, a putative activator of SIRT1 (Howitz et al., 2003), inhibited Nrf2-dependent transcription, apparently contradicting earlier reports that resveratrol activates Nrf2 (Chen et al., 2005; Ungvari et al., 2010). PubMed:22020111

a(CHEBI:resveratrol) decreases p(FPLX:"IKK_complex", pmod(Ph)) View Subject | View Object

Besides, it decreased the phosphorylation of IKK and IB through LPS stimulation and subse-quently inhibited the activity of NF-B [115]. PubMed:29179999

a(CHEBI:resveratrol) decreases p(HGNC:NFKBIA, pmod(Ph)) View Subject | View Object

Besides, it decreased the phosphorylation of IKK and IB through LPS stimulation and subse-quently inhibited the activity of NF-B [115]. PubMed:29179999

a(CHEBI:resveratrol) decreases a(MESH:Interleukins) View Subject | View Object

Resveratrol crossed the blood-brain barrier (BBB) [111,112] and down-regulated several inflammatory biomarkers such as TNF-, COX2 and interleukins [113,114]. PubMed:29179999

a(CHEBI:resveratrol) decreases p(HGNC:TNF) View Subject | View Object

Resveratrol crossed the blood-brain barrier (BBB) [111,112] and down-regulated several inflammatory biomarkers such as TNF-, COX2 and interleukins [113,114]. PubMed:29179999

a(CHEBI:resveratrol) decreases p(HGNC:PTGS2) View Subject | View Object

Resveratrol crossed the blood-brain barrier (BBB) [111,112] and down-regulated several inflammatory biomarkers such as TNF-, COX2 and interleukins [113,114]. PubMed:29179999

a(CHEBI:resveratrol) decreases p(HGNC:PTGS2) View Subject | View Object

It also lowered the expression of NO and iNOS, and prostaglandin E2 (PGE2) and COX2 in A-activated glial cells. All these effects were attributableto their suppression of nuclear NF-B translocation [116]. PubMed:29179999

a(CHEBI:resveratrol) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Besides, it decreased the phosphorylation of IKK and IB through LPS stimulation and subse-quently inhibited the activity of NF-B [115]. PubMed:29179999

a(CHEBI:resveratrol) decreases p(HGNC:STAT1, pmod(Ph)) View Subject | View Object

Resveratrol disrupted the phosphorylation of signal transducer and activator of transcription factor 1 (STAT1) and STAT3 [115]. PubMed:29179999

a(CHEBI:resveratrol) decreases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

Resveratrol disrupted the phosphorylation of signal transducer and activator of transcription factor 1 (STAT1) and STAT3 [115]. PubMed:29179999

a(CHEBI:resveratrol) decreases a(CHEBI:"nitric oxide") View Subject | View Object

It also lowered the expression of NO and iNOS, and prostaglandin E2 (PGE2) and COX2 in A-activated glial cells. All these effects were attributableto their suppression of nuclear NF-B translocation [116]. PubMed:29179999

a(CHEBI:resveratrol) decreases p(HGNC:NOS2) View Subject | View Object

It also lowered the expression of NO and iNOS, and prostaglandin E2 (PGE2) and COX2 in A-activated glial cells. All these effects were attributableto their suppression of nuclear NF-B translocation [116]. PubMed:29179999

a(CHEBI:resveratrol) decreases a(CHEBI:"prostaglandin E2") View Subject | View Object

It also lowered the expression of NO and iNOS, and prostaglandin E2 (PGE2) and COX2 in A-activated glial cells. All these effects were attributableto their suppression of nuclear NF-B translocation [116]. PubMed:29179999

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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.