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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C4105 STAT5 InhibitorSummary: STAT5 inhibitor -
C4533 RO81911 CitationSummary: IFN-α receptor 2 agonist -
C4650 GaliellalactoneSummary: inhibits IL-6-mediated JAK/STAT signal transduction -
B6116 GLPG0634 analogueSummary: JAK1 inhibitor, potent and selective -
B4764 TCS-PIM-1-4aSummary: Pim inhibitor -
B4789 SH-4-541 CitationTarget: STATSummary: STAT inhibitor, potent -
B4836 CPI-360Summary: EZH2 inhibitor -
B4913 Corylifol ASummary: STAT3 inhibitor -
B4970 HO-38671 CitationTarget: STATSummary: STAT3 inhibitor, selective -
B5836 AZ5104Target: EGFRSummary: EGFR inhibitor
