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.
- A4140 WP1066Target: STAT|JAKSummary: JAK2/STAT3 inhibitor,cell-permeable
- B4970 HO-38671 CitationTarget: STATSummary: STAT3 inhibitor, selective
- B2283 NiclosamideTarget: STATSummary: Inhibitor of the STAT3 signaling pathway
- A4512 Cucurbitacin ITarget: STAT|JAKSummary: STAT3/JAK2 signaling inhibitor
- A2689 ButeinTarget: Src|STAT|EGFR|Angiotensin-Converting Enzymes (ACEs)|5-Lipoxygenases|PTK|enoyl-acyl-carrier protein reductaseSummary: Protein kinase inhibitor
- A8317 Fludarabine Phosphate (Fludara)2 CitationTarget: STATSummary: Inhibits STAT1 activation and DNA synthesis