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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B8790 Trastuzumab -
N1318 Vitexicarpin -
N1441 Fraxinellone -
N1504 HomoharringtonineTarget: STATSummary: Cytotoxic alkaloid -
N1567 DaphnetinSummary: Protein kinases inhibitor for EGFR/PKA/PKC -
N1622 Panaxadiol -
N1715 Diosgenin -
N1753 Scutellarin -
N1843 CryptotanshinoneSummary: STAT3/AChE inhibitor -
N1852 Chrysophanol

