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
- A3012 Ruxolitinib (INCB018424)4 CitationTarget: JAKSummary: JAK inhibitor
- A4135 Tofacitinib (CP-690550) Citrate2 CitationTarget: JAKSummary: Potent JAK inhibitor
- A4136 TG101348 (SAR302503)2 CitationTarget: FLT3|JAK|c-RETSummary: JAK-2 inhibitor,potent and selective
- A4139 AG-4903 CitationTarget: EGFR|JAKSummary: JAK2/EGFR inhibitor
- A3937 XL019Target: JAKSummary: JAK2 inhibitor,potent and selective