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.
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A8375 AZD8931 (Sapitinib)Target: EGFR|ErbBSummary: ErbB inhibitor -
A4512 Cucurbitacin ITarget: STAT|JAKSummary: STAT3/JAK2 signaling inhibitor -
A8367 AST-1306Summary: EGFR/HER2 inhibitor -
A4511 CercosporamideTarget: JAK|MNKSummary: Mnk2 and JAK3 inhibitor -
A8366 ARRY-380Target: HER2Summary: Tyrosine kinase HER2 and p95-HER2 inhibitor -
A4510 1,2,3,4,5,6-HexabromocyclohexaneSummary: JAK2 tyrosine kinase inhibitor -
A8365 Varlitinib (ARRY334543)Summary: ErbB inhibitor -
A8357 AG-1478Target: EGFRSummary: EGFR inhibitor,potent and selective -
A4152 BMS-911543Target: JAKSummary: JAK2 inhibitor,selective small molecule -
A8322 Neratinib (HKI-272)3 CitationTarget: EGFRSummary: HER2/EGFR inhibitor,potent and irreversible
