Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Appears in Networks 6

In-Edges 13

a(CHEBI:"amyloid-beta") increases act(p(HGNC:MAPK14)) View Subject | View Object

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

a(PUBCHEM:10341154) association p(HGNC:MAPK14) View Subject | View Object

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

a(PUBCHEM:11570805) association p(HGNC:MAPK14) View Subject | View Object

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

a(PUBCHEM:156422) association p(HGNC:MAPK14) View Subject | View Object

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

a(CHEBI:"N(5)-ethyl-L-glutamine") decreases act(p(HGNC:MAPK14)) View Subject | View Object

Besides, extracellular signal-regulated kinase (ERK), p38 MAPK and NF-B pathway were disrupted byL-theanine [128]. PubMed:29179999

a(CHEBI:berberine) decreases act(p(HGNC:MAPK14)) View Subject | View Object

Berberine inhibited the p38,ERK and Akt signaling pathways, which were stimulated by A PubMed:29179999

a(PUBCHEM:14193399) decreases act(p(HGNC:MAPK14)) 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

a(PUBCHEM:440312) decreases act(p(HGNC:MAPK14)) 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

a(CHEBI:"SB-239063") decreases act(p(HGNC:MAPK14)) View Subject | View Object

Treatment with p38 inhibitor, SB239063, prevents downstream phosphorylation of IκBα and p65 translocation to the nucleus in the ventral midbrain. PubMed:27288790

a(CHEBI:"anthra[1,9-cd]pyrazol-6(2H)-one") increases act(p(HGNC:MAPK14)) View Subject | View Object

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

a(PUBCHEM:439378) decreases p(HGNC:MAPK14) View Subject | View Object

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

Out-Edges 10

p(HGNC:MAPK14) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

All five SAP kinases generated the AT270 epitope, indicative of phosphorylation of T181 in tau. PubMed:11943212

Appears in Networks:

act(p(HGNC:MAPK14)) increases a(HBP:"Tau aggregates") View Subject | View Object

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

p(HGNC:MAPK14) association a(PUBCHEM:11570805) View Subject | View Object

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

p(HGNC:MAPK14) association a(PUBCHEM:156422) View Subject | View Object

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

p(HGNC:MAPK14) association a(PUBCHEM:10341154) View Subject | View Object

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

p(HGNC:MAPK14) increases act(p(FPLX:NFkappaB)) View Subject | View Object

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

act(p(HGNC:MAPK14)) increases p(HGNC:NFKBIA, pmod(Ph)) View Subject | View Object

Treatment with p38 inhibitor, SB239063, prevents downstream phosphorylation of IκBα and p65 translocation to the nucleus in the ventral midbrain. PubMed:27288790

act(p(HGNC:MAPK14)) increases p(HGNC:NFKBIA, pmod(Ph)) View Subject | View Object

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

act(p(HGNC:MAPK14)) increases tloc(p(HGNC:RELA), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Treatment with p38 inhibitor, SB239063, prevents downstream phosphorylation of IκBα and p65 translocation to the nucleus in the ventral midbrain. PubMed:27288790

About

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.