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.
- A3339 CYT387 sulfate saltSummary: JAK1/JAK2 inhibitor
- A3397 Erlotinib4 CitationSummary: EGFR tyrosine kinase inhibitor
- A3433 Gefitinib hydrochlorideTarget: EGFRSummary: Potent EGFR inhibitor
- A3482 Icotinib HydrochlorideSummary: EGFR inhibitor,potent and specific
- A3514 JAK2 Inhibitor V, Z3Summary: Jak2 tyrosine kinase inhibitor
- A3515 JANEX-1Summary: JAK3 inhibitor
- A3556 LKB1 (AAK1 dual inhibitor)Target: PimSummary: Pim-1 kinase inhibitor
- A3675 NVP-BSK805Summary: ATP-competitive JAK2 inhibitor
- A3741 Pyridone 6Target: JAKSummary: Pan-JAK inhibitor
- A3781 Ruxolitinib phosphateSummary: JAK1/JAK2 inhibitor