p(HGNC:MAPK14)
Consequently, there is mounting evidence that Abeta affects cholinergic signaling independent of its cytotoxic action. For example, Abeta blocks long-term potentiation, a cellular correlate of learning, through activation of JNK and p38MAPK (Wang et al., 2004). PubMed:19293145
Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040
Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040
Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040
Besides, extracellular signal-regulated kinase (ERK), p38 MAPK and NF-B pathway were disrupted byL-theanine [128]. PubMed:29179999
Berberine inhibited the p38,ERK and Akt signaling pathways, which were stimulated by A PubMed:29179999
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
Besides, it significantly decreased the generation of ROS and affected LPS-induced activation of MAPK, including p38 and NF-B signaling[243]. PubMed:29179999
Treatment with p38 inhibitor, SB239063, prevents downstream phosphorylation of IκBα and p65 translocation to the nucleus in the ventral midbrain. PubMed:27288790
In contrast, SP600125 treatment, a JNK inhibitor, increases the p38 MAPK depen- dent phosphorylation of p65 NF-κB subunit in the nucleus [47]. PubMed:27288790
L-Theanine, an amino acid in green tea, reduced Aβ 42 levels in the cortex and hippocampus of the brain, which is mediated by suppres- sion of ERK/p38 and NF-κB as well as the reduction of macromolecular oxidative damage [81]. PubMed:27288790
All five SAP kinases generated the AT270 epitope, indicative of phosphorylation of T181 in tau. PubMed:11943212
The dose response screening identified compounds related to the inhibition of 3 major targets led to inhibition of Tau aggregation: p38 MAPK (7 out of 8 compounds in the initial library), VEGFR1/2 (3 of 8) and TGF (3 of 10). PubMed:30640040
Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040
Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040
Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040
Pharmacologic inhibition of ERK and p38 MAPK and dominant- negative mutation of both enzymes suppressed Aβ-induced NF-κB transactivation thus neurotoxicity by Aβ [45,46]. PubMed:27288790
Treatment with p38 inhibitor, SB239063, prevents downstream phosphorylation of IκBα and p65 translocation to the nucleus in the ventral midbrain. PubMed:27288790
In contrast, SP600125 treatment, a JNK inhibitor, increases the p38 MAPK depen- dent phosphorylation of p65 NF-κB subunit in the nucleus [47]. PubMed:27288790
Treatment with p38 inhibitor, SB239063, prevents downstream phosphorylation of IκBα and p65 translocation to the nucleus in the ventral midbrain. PubMed:27288790
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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.