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.
- A4512 Cucurbitacin ITarget: STAT|JAKSummary: STAT3/JAK2 signaling inhibitor
- A5424 FludarabineSummary: DNA synthsis inhibitor
- A2224 Stattic5 CitationTarget: STATSummary: STAT3 inhibitor,small-molecule and potent
- A8317 Fludarabine Phosphate (Fludara)2 CitationTarget: STATSummary: Inhibits STAT1 activation and DNA synthesis
- A8338 NSC 748595 CitationTarget: STATSummary: Stat3 inhibitor
- B4970 HO-38671 CitationTarget: STATSummary: STAT3 inhibitor, selective
- B2283 NiclosamideTarget: STATSummary: Inhibitor of the STAT3 signaling pathway
- A4140 WP1066Target: STAT|JAKSummary: JAK2/STAT3 inhibitor,cell-permeable