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Entity

Name
ERK1 and ERK2 cascade
Namespace
go
Namespace Version
20181221
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/73688d6dc24e309fca59a1340dc9ee971e9f3baa/external/go-names.belns

Appears in Networks 8

In-Edges 9

a(CHEBI:"amyloid-beta") association bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

Intraneuronal Abeta can also impair amygdala-dependent emotional responses by affecting the ERK/MAPK signaling pathway [153] PubMed:21214928

act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) regulates bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

Mechanistically, nicotine, acting through nAChRs, decreases keratinocyte migration (188, 189) and modifies the activity of PI3K/Akt, ERK, MEK, and JAK signaling pathways. PubMed:19126755

Appears in Networks:
Annotations
MeSH
Keratinocytes
Text Location
Review

a(CHEBI:nicotine) increases bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

Furthermore, nicotinic activation of ERK-1/2 promotes survival of cultured murine spinal cord neurons, and the blocking of ERK-1 prevents nicotine’s antiapoptotic action (Toborek et al., 2007). Likewise, the alpha7-specific agonist A-582941 induces phosphorylation of ERK-1/2 in PC12 cells and in mouse brain, and this is completely blocked by the mitogen-activated protein kinase 1 inhibitor SL327 (Bitner et al., 2007). PubMed:19293145

complex(a(CHEBI:nicotine), p(HGNC:CHRNA7)) increases bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

In studies on SH-SY5Y cells and cultured rat hippocampal neurons, nicotine, acting through alpha7 nAChRs, results in the activation of ERK-1/2 pathways dependent upon calcium and protein kinase A (Dajas-Bailador et al., 2002b). In addition, the alpha7-specific agonist GTS-21 promotes ERK-1/2 phosphorylation, but not that of c-jun N-terminal kinase (JNK) or p38 (Ren et al., 2005). PubMed:19293145

act(p(HGNC:CHRM1)) increases bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

Some studies suggest that M1 mAChR stimulation also leads to activation of ERK1/2, which can modulate alpha-secretase activity and APP processing[67, 73], PubMed:24590577

act(p(HGNC:CHRM1)) causesNoChange bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

though there are contradictory findings showing that the alpha-secretase-mediated APP processing via M1 mAChR stimulation is not modulated by the ERK1/MEK cascade[71]. On the other hand, loss of M1 mAChR increases amyloidogenic APP processing in neurons and promotes brain Abeta plaque pathology in a mouse model of AD PubMed:24590577

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

In this system enhancement of Akt phosphorylation and activation of ERK pathway was observed following alpha7 agonist treatment, suggesting that Abeta inhibits the neuroprotective effect of alpha7 nAChR activation (Zhi et al., 2014) PubMed:25514383

p(HBP:HBP00045, var("p.Ala152Thr")) increases bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

Taken together, these findings strongly suggest that 4R tau-A152T activates the ERK pathway more strongly, which in turn increases the level and activity of secreted MMP-9. 4R tau-A152T expression (Figures 4E and 4F) but not inhibition of ERK activity (Figures 4B and 4C) also increases the total activity of secreted MMP-2, suggesting that tau-A152T increases the level and activity of secreted MMP-2, likely through an ERK-independent pathway PubMed:27594586

a(CHEBI:simvastatin) increases bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

Simvastatin and atorvastatin enhance extracellular Aβ degradation via increasing NEP secretion from astrocytes by activating MAPK/Erk1/2 (Yamamoto et al. 2016) PubMed:29626319

Out-Edges 7

bp(GO:"ERK1 and ERK2 cascade") association a(CHEBI:"amyloid-beta") View Subject | View Object

Intraneuronal Abeta can also impair amygdala-dependent emotional responses by affecting the ERK/MAPK signaling pathway [153] PubMed:21214928

bp(GO:"ERK1 and ERK2 cascade") increases act(a(CHEBI:nicotine)) View Subject | View Object

Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755

Appears in Networks:
Annotations
MeSH
Skin
Text Location
Review

bp(GO:"ERK1 and ERK2 cascade") increases bp(GO:"apoptotic process") View Subject | View Object

Furthermore, nicotinic activation of ERK-1/2 promotes survival of cultured murine spinal cord neurons, and the blocking of ERK-1 prevents nicotine’s antiapoptotic action (Toborek et al., 2007). Likewise, the alpha7-specific agonist A-582941 induces phosphorylation of ERK-1/2 in PC12 cells and in mouse brain, and this is completely blocked by the mitogen-activated protein kinase 1 inhibitor SL327 (Bitner et al., 2007). PubMed:19293145

bp(GO:"ERK1 and ERK2 cascade") regulates act(p(HGNC:ADAM10)) View Subject | View Object

Some studies suggest that M1 mAChR stimulation also leads to activation of ERK1/2, which can modulate alpha-secretase activity and APP processing[67, 73], PubMed:24590577

bp(GO:"ERK1 and ERK2 cascade") regulates bp(HBP:"APP processing") View Subject | View Object

Some studies suggest that M1 mAChR stimulation also leads to activation of ERK1/2, which can modulate alpha-secretase activity and APP processing[67, 73], PubMed:24590577

bp(GO:"ERK1 and ERK2 cascade") regulates p(HGNC:MMP9) View Subject | View Object

Correspondingly, the level and activity of secreted MMP-9 was greatly suppressed in both tau-A152T and MAPT IVS10+16 patient neurons (Figures 4B and 4C), suggesting that MMP-9 expression is regulated by the ERK signaling pathway in cortical neurons PubMed:27594586

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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.