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.
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B1496 IcotinibSummary: EGFR tyrosine kinase inhibitor -
B1104 AZD-92911 CitationTarget: EGFRSummary: Mutated forms EGFR inhibitor -
B1105 AZD-9291 mesylateSummary: third generation EGFRm inhibitor, oral and irreversible -
B1130 GLPG06341 CitationTarget: JAKSummary: JAK1 inhibitor -
B2283 NiclosamideTarget: STATSummary: Inhibitor of the STAT3 signaling pathway -
B1799 NifuroxazideTarget: STATSummary: STAT inhibitor -
B1759 FlubendazoleSummary: Autophagy activator -
N1318 Vitexicarpin -
N1441 Fraxinellone -
N1504 HomoharringtonineTarget: STATSummary: Cytotoxic alkaloid

