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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B8790 Trastuzumab -
A8998 SI-2 hydrochloride -
C8406 LomedeucitinibSummary: Lomedeucitinib (BMS-986322) acts by targeting receptor tyrosine protein kinases. -
A9916 Fedratinib hydrochloride hydrateSummary: A JAK2 inhibitor -
BA7032 MoringinSummary: Moringin is a potent and selective natural agonist of ion channels. -
BA7641 MyricanoneSummary: A compound isolated from the bark of the tree. -
BA4122 GivinostatSummary: Inhibitors. -
BA8685 PhellopterinSummary: Phellopterin is a natural product. -
BA5012 TropisetronSummary: Tropisetron (SDZ-ICS-930freebase) is a 5-HT3 receptor antagonist. -
BA2881 AG-825Summary: AG-825 is a selective, ATP-competitive, inhibitor of tyrosine phosphorylation.

