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p(HGNC:MAPK8)

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

Entity

Name
MAPK8
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 4

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Tau degradation: the ubiquitin-proteasome system versus the autophagy-lysosome system. v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 5

a(CHEBI:"amyloid-beta") increases act(p(HGNC:MAPK8)) 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

Appears in Networks:

composite(p(HGNC:MAPK14), p(HGNC:MAPK8)) hasComponent p(HGNC:MAPK8) View Subject | View Object

Appears in Networks:

p(HGNC:MAPK8, pmod(Ph)) increases act(p(HGNC:MAPK8)) View Subject | View Object

Collectively, these studies demonstrate that the soluble, astroglial-derived S100B protein interacts with RAGE leading to the JNK phosphorylation and the pJNK-dependent up-regulation of c-Jun, a component of the AP-1 complex. PubMed:18494933

Appears in Networks:

complex(p(HGNC:MAPK1), p(HGNC:MAPK14), p(HGNC:MAPK8)) hasComponent p(HGNC:MAPK8) View Subject | View Object

Appears in Networks:

p(HGNC:FTH1) decreases p(HGNC:MAPK8) View Subject | View Object

The antioxidant property of FtH blocks TNF-induced JNK activation, reducing cell death (Pham et al., 2004; Kamata et al., 2005; Gozzelino et al., 2012). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Cerebral Hemorrhage
Text Location
Review

Out-Edges 7

p(HGNC:MAPK8) hasVariant p(HGNC:MAPK8, pmod(Ph)) View Subject | View Object

Appears in Networks:

p(HGNC:MAPK8) increases bp(GO:autophagy) View Subject | View Object

For instance, c-Jun NH 2-terminal kinase 1 (JNK1) may induce autophagy by phosphorylating Bcl-2 or Bim and abolishing their inhibitory effects on autophagy (Luo et al., 2012; Wei et al., 2008). PubMed:23528736

Appears in Networks:

p(HGNC:MAPK8) increases p(HGNC:BCL2, pmod(Ph)) View Subject | View Object

For instance, c-Jun NH 2-terminal kinase 1 (JNK1) may induce autophagy by phosphorylating Bcl-2 or Bim and abolishing their inhibitory effects on autophagy (Luo et al., 2012; Wei et al., 2008). PubMed:23528736

Appears in Networks:

p(HGNC:MAPK8) increases p(HGNC:BCL2L11, pmod(Ph)) View Subject | View Object

For instance, c-Jun NH 2-terminal kinase 1 (JNK1) may induce autophagy by phosphorylating Bcl-2 or Bim and abolishing their inhibitory effects on autophagy (Luo et al., 2012; Wei et al., 2008). PubMed:23528736

Appears in Networks:

act(p(HGNC:MAPK8)) increases p(HGNC:JUN) View Subject | View Object

Collectively, these studies demonstrate that the soluble, astroglial-derived S100B protein interacts with RAGE leading to the JNK phosphorylation and the pJNK-dependent up-regulation of c-Jun, a component of the AP-1 complex. PubMed:18494933

Appears in Networks:

p(HGNC:MAPK8) 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:

p(HGNC:MAPK8) increases a(MESH:"Reactive Oxygen Species") View Subject | View Object

WhileMAPK8 increases ROS generation, TNF induces RIP1–RIP3 necrosome which triggers necroptosis. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

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.