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.
- A4192 SGI-1776 free base3 CitationSummary: Pim kinase inhibitor,ATP-competitive
- A4193 SMI-4aTarget: PimSummary: Potent Pim inhibitor
- A3337 CX-6258Summary: Pan-Pim kinases Inhibitor
- A3556 LKB1 (AAK1 dual inhibitor)Target: PimSummary: Pim-1 kinase inhibitor
- B4764 TCS-PIM-1-4aSummary: Pim inhibitor
- A3962 AZD1208Target: PimSummary: PIM kinase inhibitor
- A4519 PIM-1 Inhibitor 2Summary: Potent Pim-1 kinase inhibitor
- A4520 R8-T198wtSummary: Pim-1 kinase inhibitor
- A4521 TCS PIM-1 1Summary: Pim-1 kinase inhibitor,ATP-competitve