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.
- A3962 AZD1208Target: PimSummary: PIM kinase inhibitor
- A4510 1,2,3,4,5,6-HexabromocyclohexaneSummary: JAK2 tyrosine kinase inhibitor
- A4511 CercosporamideTarget: JAK|MNKSummary: Mnk2 and JAK3 inhibitor
- A4512 Cucurbitacin ITarget: STAT|JAKSummary: STAT3/JAK2 signaling inhibitor
- A4513 Lestaurtinib1 CitationSummary: JAK2/FLT3/TrkA inhibitor
- A4515 SD 1008Summary: Inhibitor of JAK2/STAT3 signaling pathway,apoptosis inducer
- A4516 TCS 21311Summary: JAK3 inhibitor
- A4517 ZM 449829Summary: JAK3 inhibitor
- A4519 PIM-1 Inhibitor 2Summary: Potent Pim-1 kinase inhibitor
- A4520 R8-T198wtSummary: Pim-1 kinase inhibitor