TSC22D3
Gene Ontology Biological Process
JUN
Gene Ontology Biological Process
- Fc-epsilon receptor signaling pathway [TAS]
- MyD88-dependent toll-like receptor signaling pathway [TAS]
- MyD88-independent toll-like receptor signaling pathway [TAS]
- SMAD protein import into nucleus [IDA]
- SMAD protein signal transduction [IDA]
- TRIF-dependent toll-like receptor signaling pathway [TAS]
- innate immune response [TAS]
- negative regulation by host of viral transcription [IDA]
- negative regulation of DNA binding [IDA]
- negative regulation of transcription from RNA polymerase II promoter in response to endoplasmic reticulum stress [IMP]
- negative regulation of transcription, DNA-templated [IDA]
- positive regulation by host of viral transcription [IDA]
- positive regulation of Rho GTPase activity [IDA]
- positive regulation of transcription from RNA polymerase II promoter [IC, IDA]
- positive regulation of transcription, DNA-templated [IDA]
- regulation of sequence-specific DNA binding transcription factor activity [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]
- transforming growth factor beta receptor signaling pathway [IDA]
Gene Ontology Molecular Function- DNA binding [TAS]
- R-SMAD binding [IPI]
- RNA polymerase II activating transcription factor binding [IPI]
- RNA polymerase II distal enhancer sequence-specific DNA binding [IDA]
- RNA polymerase II distal enhancer sequence-specific DNA binding transcription factor activity [IC, IDA]
- RNA polymerase II transcription factor binding transcription factor activity involved in positive regulation of transcription [IC]
- Rho GTPase activator activity [IDA]
- cAMP response element binding [IDA]
- enzyme binding [IPI]
- poly(A) RNA binding [IDA]
- protein binding [IPI]
- sequence-specific DNA binding RNA polymerase II transcription factor activity [IC]
- sequence-specific DNA binding transcription factor activity [IDA]
- transcription coactivator activity [IDA]
- transcription factor binding [IPI]
- transcription regulatory region DNA binding [IDA]
- DNA binding [TAS]
- R-SMAD binding [IPI]
- RNA polymerase II activating transcription factor binding [IPI]
- RNA polymerase II distal enhancer sequence-specific DNA binding [IDA]
- RNA polymerase II distal enhancer sequence-specific DNA binding transcription factor activity [IC, IDA]
- RNA polymerase II transcription factor binding transcription factor activity involved in positive regulation of transcription [IC]
- Rho GTPase activator activity [IDA]
- cAMP response element binding [IDA]
- enzyme binding [IPI]
- poly(A) RNA binding [IDA]
- protein binding [IPI]
- sequence-specific DNA binding RNA polymerase II transcription factor activity [IC]
- sequence-specific DNA binding transcription factor activity [IDA]
- transcription coactivator activity [IDA]
- transcription factor binding [IPI]
- transcription regulatory region DNA binding [IDA]
Gene Ontology Cellular Component
Reconstituted Complex
An interaction is inferred between proteins in vitro. This can include proteins in recombinant form or proteins isolated directly from cells with recombinant or purified bait. For example, GST pull-down assays where a GST-tagged protein is first isolated and then used to fish interactors from cell lysates are considered reconstituted complexes (e.g. PUBMED: 14657240, Fig. 4A or PUBMED: 14761940, Fig. 5). This can also include gel-shifts, surface plasmon resonance, isothermal titration calorimetry (ITC) and bio-layer interferometry (BLI) experiments. The bait-hit directionality may not be clear for 2 interacting proteins. In these cases the directionality is up to the discretion of the curator.
Publication
Inhibition of AP-1 by the glucocorticoid-inducible protein GILZ.
The immunosuppressive effects of glucocorticoids arise largely by inhibition of cytokine gene expression, which has been ascribed to interference between the glucocorticoid receptor and transcription factors such as AP-1 and NF-kappa B as well as by competition for common coactivators. Here we show that glucocorticoid-induced inhibition of interleukin-2 mRNA expression in activated normal T cells required new protein synthesis, suggesting ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID