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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C8473 AG 1406 -
C8542 EGFR/HER2/CDK9-IN-3 -
C8543 EGFR/HER2/CDK9-IN-1 -
C8544 EGFR/HER2/CDK9-IN-2 -
C8546 EGFR-IN-59 -
C8564 MS39 -
C8565 EGFR-IN-47 -
N2885 Pareruptorin ASummary: An angular pyranocoumarin compound derived from Peucedanum praeruptorum Dunn. -
C8702 RomiplostimSummary: Recombinant “peptibody”-type thrombopoietin receptor (TPO?R, MPL) agonist -
C8752 SEL120-34A hydrochlorideSummary: An ATP-competitive inhibitor of CDK8/CDK19

