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.
- A4511 CercosporamideTarget: JAK|MNKSummary: Mnk2 and JAK3 inhibitor
- A4512 Cucurbitacin ITarget: STAT|JAKSummary: STAT3/JAK2 signaling inhibitor
- B1130 GLPG06341 CitationTarget: JAKSummary: JAK1 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
- A4137 AZD1480Target: JAKSummary: JAK2 inhibitor,ATP-competitive and novel
- A4138 Tofacitinib (CP-690550,Tasocitinib)1 CitationTarget: JAKSummary: Janus kinase inhibitor
- A4139 AG-4903 CitationTarget: EGFR|JAKSummary: JAK2/EGFR inhibitor
- A4140 WP1066Target: STAT|JAKSummary: JAK2/STAT3 inhibitor,cell-permeable