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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A3514 JAK2 Inhibitor V, Z3Summary: Jak2 tyrosine kinase inhibitor -
A3515 JANEX-1Summary: JAK3 inhibitor -
A3556 LKB1 (AAK1 dual inhibitor)Target: PimSummary: Pim-1 kinase inhibitor -
A3675 NVP-BSK805Summary: ATP-competitive JAK2 inhibitor -
A3741 Pyridone 6Target: JAKSummary: Pan-JAK inhibitor -
A3781 Ruxolitinib phosphateSummary: JAK1/JAK2 inhibitor -
A3794 SB1317Summary: CDK,JAK and FLT inhibitor -
A3936 WHI-P97Summary: Janus kinase (JAK)-3 inhibitor -
A3937 XL019Target: JAKSummary: JAK2 inhibitor,potent and selective -
A7026 HOOBt

