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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A4092 CUDC-1011 CitationTarget: Histone Deacetylases (HDACs)|EGFR|ErbBSummary: Multitargeted HDAC inhibitor -
A4140 WP1066Target: STAT|JAKSummary: JAK2/STAT3 inhibitor,cell-permeable -
A3967 Lapatinib DitosylateTarget: EGFR|ErbB-2Summary: EGFR/HER2 inhibitor,potent and selective -
C4650 GaliellalactoneSummary: inhibits IL-6-mediated JAK/STAT signal transduction -
A4138 Tofacitinib (CP-690550,Tasocitinib)1 CitationTarget: JAKSummary: Janus kinase inhibitor -
C4105 STAT5 InhibitorSummary: STAT5 inhibitor -
A4137 AZD1480Target: JAKSummary: JAK2 inhibitor,ATP-competitive and novel -
A3482 Icotinib HydrochlorideSummary: EGFR inhibitor,potent and specific -
C3975 5,15-DPPSummary: STAT3 inhibitor -
A4136 TG101348 (SAR302503)2 CitationTarget: FLT3|JAK|c-RETSummary: JAK-2 inhibitor,potent and selective
