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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A3937 XL019Target: JAKSummary: JAK2 inhibitor,potent and selective -
A8779 WM-80141 CitationSummary: Inhibitor for KAT6A (MOZ) and KAT6B (MORF/QKF), anticancer -
A7026 HOOBt -
C6459 Balsalazide disodium dihydrateSummary: A prodrug of aminosalicylic acid that exerts local anti-inflammatory effects in the colon -
B6115 RG 13022Summary: EGFR tyrosine kinase inhibitor -
B6175 STA-21Summary: STAT3 inhibitor -
B7802 APTSTAT3-9RSummary: STAT3 inhibitor -
C3975 5,15-DPPSummary: STAT3 inhibitor -
C4105 STAT5 InhibitorSummary: STAT5 inhibitor -
C4533 RO81911 CitationSummary: IFN-α receptor 2 agonist

