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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B4836 CPI-360Summary: EZH2 inhibitor -
A8998 SI-2 hydrochloride -
A8779 WM-8014Summary: Inhibitor for KAT6A (MOZ) and KAT6B (MORF/QKF), anticancer -
C8406 LomedeucitinibSummary: Lomedeucitinib (BMS-986322) acts by targeting receptor tyrosine protein kinases. -
B6115 RG 13022Summary: EGFR tyrosine kinase inhibitor -
B5962 AZD3759Summary: EGFR inhibitor,oral active -
B5836 AZ5104Target: EGFRSummary: EGFR inhibitor -
B6116 GLPG0634 analogueSummary: JAK1 inhibitor, potent and selective -
B1496 IcotinibSummary: EGFR tyrosine kinase inhibitor -
B1495 OSI-420 free baseSummary: EGFR inhibitor
