JAK/STAT Signaling
Various ligands including cytokines (e.g. interferons and interleukins), hormones (e.g. erythropoietin and growth hormone) and their cell surface receptors activate JAK proteins, which autophosphorylate, and then phosphorylate the receptor. Subsequently, JAKs phosphorylate a specific tyrosine residue on the STAT protein, promoting dimerization via SH2 domains. The activated STATs form homo-/heterodimers and translocate to the nucleus to trigger target gene transcription. In addition, suppressors of cytokine signaling (SOCS) family inhibit receptor signaling via homologous or heterologous feedback regulation. Dysregulation in JAK/STAT signaling is associated with diseases such as atherosclerosis, immunodeficiencies and cancer.
- C4650 GaliellalactoneSummary: inhibits IL-6-mediated JAK/STAT signal transduction
- C4533 RO8191Summary: IFN-α receptor 2 agonist
- C4105 STAT5 InhibitorSummary: STAT5 inhibitor
- C3975 5,15-DPPSummary: STAT3 inhibitor
- B7802 APTSTAT3-9RSummary: STAT3 inhibitor
- B6175 STA-21Summary: STAT3 inhibitor
- B6115 RG 13022Summary: EGFR tyrosine kinase inhibitor
- B5999 FLLL32Summary: STAT3 inhibitor
- B5962 AZD3759Summary: EGFR inhibitor,oral active
- B5836 AZ5104Target: EGFRSummary: EGFR inhibitor