a(CHEBI:resveratrol)
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
Interestingly, resver- atrol downregulated RAGE as well as MMP9 — an effect that is related to decreased hippocampal load of Aβ42 (REF.297) . PubMed:30116051
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
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
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
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
The multi-modal agent resveratrol induced the expression of ATG4 and promoted autophagosome formation. PubMed:30116051
The multi-modal agent resveratrol induced the expression of ATG4 and promoted autophagosome formation. PubMed:30116051
Interestingly, resver- atrol downregulated RAGE as well as MMP9 — an effect that is related to decreased hippocampal load of Aβ42 (REF.297) . PubMed:30116051
Interestingly, resver- atrol downregulated RAGE as well as MMP9 — an effect that is related to decreased hippocampal load of Aβ42 (REF.297) . PubMed:30116051
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
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
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
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
Besides, it decreased the phosphorylation of IKK and IB through LPS stimulation and subse-quently inhibited the activity of NF-B [115]. PubMed:29179999
Besides, it decreased the phosphorylation of IKK and IB through LPS stimulation and subse-quently inhibited the activity of NF-B [115]. PubMed:29179999
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
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
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
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
Besides, it decreased the phosphorylation of IKK and IB through LPS stimulation and subse-quently inhibited the activity of NF-B [115]. PubMed:29179999
Resveratrol disrupted the phosphorylation of signal transducer and activator of transcription factor 1 (STAT1) and STAT3 [115]. PubMed:29179999
Resveratrol disrupted the phosphorylation of signal transducer and activator of transcription factor 1 (STAT1) and STAT3 [115]. PubMed:29179999
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
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
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.