MAPK10
Gene Ontology Biological Process
- Fc-epsilon receptor signaling pathway [TAS]
- JNK cascade [ISS, TAS]
- JUN phosphorylation [ISS, TAS]
- MyD88-dependent toll-like receptor signaling pathway [TAS]
- MyD88-independent toll-like receptor signaling pathway [TAS]
- TRIF-dependent toll-like receptor signaling pathway [TAS]
- activation of MAPK activity [TAS]
- innate immune response [TAS]
- regulation of sequence-specific DNA binding transcription factor activity [TAS]
- signal transduction [TAS]
- stress-activated MAPK cascade [TAS]
- toll-like receptor 10 signaling pathway [TAS]
- toll-like receptor 2 signaling pathway [TAS]
- toll-like receptor 3 signaling pathway [TAS]
- toll-like receptor 4 signaling pathway [TAS]
- toll-like receptor 5 signaling pathway [TAS]
- toll-like receptor 9 signaling pathway [TAS]
- toll-like receptor TLR1:TLR2 signaling pathway [TAS]
- toll-like receptor TLR6:TLR2 signaling pathway [TAS]
- toll-like receptor signaling pathway [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
KIF5A
Gene Ontology Biological Process
- ATP catabolic process [IBA]
- antigen processing and presentation of exogenous peptide antigen via MHC class II [TAS]
- axon guidance [IBA]
- blood coagulation [TAS]
- cytoskeleton-dependent intracellular transport [IBA]
- metabolic process [IBA, TAS]
- microtubule-based movement [IBA, TAS]
- protein localization [IBA]
- synaptic transmission [TAS]
Gene Ontology Molecular Function
Biochemical Activity (Phosphorylation)
An interaction is inferred from the biochemical effect of one protein upon another, for example, GTP-GDP exchange activity or phosphorylation of a substrate by a kinase. The bait protein executes the activity on the substrate hit protein. A Modification value is recorded for interactions of this type with the possible values Phosphorylation, Ubiquitination, Sumoylation, Dephosphorylation, Methylation, Prenylation, Acetylation, Deubiquitination, Proteolytic Processing, Glucosylation, Nedd(Rub1)ylation, Deacetylation, No Modification, Demethylation.
Publication
Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin.
Selected vulnerability of neurons in Huntington's disease suggests that alterations occur in a cellular process that is particularly critical for neuronal function. Supporting this idea, pathogenic Htt (polyQ-Htt) inhibits fast axonal transport (FAT) in various cellular and animal models of Huntington's disease (mouse and squid), but the molecular basis of this effect remains unknown. We found that polyQ-Htt inhibited FAT ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID