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.
-
C8752 SEL120-34A hydrochlorideSummary: An ATP-competitive inhibitor of CDK8/CDK19 -
B8534 BP-1-102Summary: An orally active, potent and selective STAT3 inhibitor -
C4252 ML115Summary: A selective STAT3 agonist for research on cell proliferation and differentiation. -
C8406 LomedeucitinibSummary: Lomedeucitinib (BMS-986322) acts by targeting receptor tyrosine protein kinases. -
A9916 Fedratinib hydrochloride hydrateSummary: A JAK2 inhibitor -
C8473 AG 1406 -
BA2725 C188-9Summary: C188-9 (TTI-101) is an inhibitor. -
BA2752 AC-4-130Summary: AC-4-130 is a potent structural domain inhibitor. -
BA2753 SD-36Summary: SD-36 is an effective degradant (=~50nM) with high selectivity compared to other members. -
BA2797 STAT3-IN-1Summary: STAT3-IN-1 is a potent, selective, and orally effective inhibitor with values of 1.82 μM and 2.14 μM in HT29 and MDA-MB231 cells, respectively.
