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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A8365 Varlitinib (ARRY334543)Summary: ErbB inhibitor -
A8366 ARRY-380Target: HER2Summary: Tyrosine kinase HER2 and p95-HER2 inhibitor -
A8367 AST-1306Summary: EGFR/HER2 inhibitor -
A8375 AZD8931 (Sapitinib)Target: EGFR|ErbBSummary: ErbB inhibitor -
B3227 CNX-2006Summary: mutant-EGFR inhibitor, selective and irreversible -
B1495 OSI-420 free baseSummary: EGFR inhibitor -
B1020 AST-1306 TsOHSummary: ErbB2 and EGFR inhibitor -
B3460 BalsalazideSummary: anti-inflammatory drug -
A8197 Compound 561 CitationTarget: EGFRSummary: REGFR inhibitor -
A8199 PD153035 hydrochloride1 CitationTarget: EGFRSummary: Potent EGFR inhibitor

