BLK
Gene Ontology Biological Process
- B cell receptor signaling pathway [IDA]
- T cell differentiation [IBA]
- cellular response to peptide hormone stimulus [IBA]
- innate immune response [IBA]
- intracellular signal transduction [TAS]
- peptidyl-tyrosine autophosphorylation [IBA]
- positive regulation of insulin secretion [IMP]
- regulation of cell proliferation [IBA]
- transmembrane receptor protein tyrosine kinase signaling pathway [IBA]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
SOCS1
Gene Ontology Biological Process
- JAK-STAT cascade [TAS]
- JAK-STAT cascade involved in growth hormone signaling pathway [TAS]
- cytokine-mediated signaling pathway [IBA, ISS, TAS]
- interferon-gamma-mediated signaling pathway [TAS]
- negative regulation of JAK-STAT cascade [IBA, ISS, NAS]
- negative regulation of insulin receptor signaling pathway [IBA, ISS]
- negative regulation of protein kinase activity [TAS]
- negative regulation of tyrosine phosphorylation of Stat3 protein [ISS]
- regulation of interferon-gamma-mediated signaling pathway [TAS]
- regulation of protein phosphorylation [ISS]
- regulation of type I interferon-mediated signaling pathway [TAS]
- type I interferon signaling pathway [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
Phosphorylation of SOCS1 Inhibits the SOCS1-p53 Tumor Suppressor Axis.
Expression of the suppressor of cytokine signaling-1 (SOCS1) is inactivated in hematopoietic and solid cancers by promoter methylation, miRNA-mediated silencing, and mutations. Paradoxically, SOCS1 is also overexpressed in many human cancers. We report here that the ability of SOCS1 to interact with p53 and regulate cellular senescence depends on a structural motif that includes tyrosine (Y)80 in the SH2 domain ... [more]
Throughput
- Low Throughput
Additional Notes
- in vitro phosphorylation with LCK, LYN or BLK as kinase and SOCS1 as substrate
Curated By
- BioGRID