MAPK11
Gene Ontology Biological Process
- MyD88-dependent toll-like receptor signaling pathway [TAS]
- MyD88-independent toll-like receptor signaling pathway [TAS]
- RNA metabolic process [TAS]
- Ras protein signal transduction [TAS]
- TRIF-dependent toll-like receptor signaling pathway [TAS]
- activation of MAPK activity [TAS]
- gene expression [TAS]
- innate immune response [TAS]
- intracellular signal transduction [IDA]
- mRNA metabolic process [TAS]
- muscle cell differentiation [TAS]
- neurotrophin TRK receptor signaling pathway [TAS]
- positive regulation of muscle cell differentiation [TAS]
- regulation of sequence-specific DNA binding transcription factor activity [TAS]
- response to stress [IDA]
- 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
- cytosol [TAS]
- nucleoplasm [TAS]
MBP
Gene Ontology Biological Process
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
The mitochondrial protease HtrA2 is regulated by Parkinson's disease-associated kinase PINK1.
In mice, targeted deletion of the serine protease HtrA2 (also known as Omi) causes mitochondrial dysfunction leading to a neurodegenerative disorder with parkinsonian features. In humans, point mutations in HtrA2 are a susceptibility factor for Parkinson's disease (PARK13 locus). Mutations in PINK1, a putative mitochondrial protein kinase, are associated with the PARK6 autosomal recessive locus for susceptibility to early-onset Parkinson's ... [more]
Throughput
- Low Throughput
Additional Notes
- figure S2.
Curated By
- BioGRID