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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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. -
A8980 Avitinib maleateSummary: A third-generation EGFR and BTK dual-target irreversible inhibitor with oral activity. -
B8611 AstaxanthinSummary: A carotenoid with antioxidant, anti-inflammatory, anticancer, and feed coloring effects. -
C3359 Glycochenodeoxycholic Acid (sodium salt)Summary: A bile acid metabolism modulator for research on cholestasis, liver cancer, and PSC.

