C-178 is a potent and selective inhibitor against murine, but not human, stimulator of interferon genes (STING) via covalent modifiation of mSTING Cys91. C-178 inhibits mSTING-mediated IFNβ reporter activity (IC50 <500 nM) without affecting RIG-I, and blocks (0.5 μM) downstream TBK1 phosphorylation induction by STING agonist CMA (1.4 h) in mSTING-expressing HEK293T cells.
Potent and selective, Cys91-targeting covalent inhibitor against murine, but not human, STING.
DNA transfection is often the bottleneck of research and gene therapy practices. To explore the mechanism regulating transgene expression, we investigated the role of the cGAS-STING signaling pathway, which induces type-I interferons in response to DNA. We confirmed that deletion
Aberrant activation of innate immune pathways is associated with a variety of diseases. Progress in understanding the molecular mechanisms of innate immune pathways has led to the promise of targeted therapeutic approaches, but the development of drugs that act specifically
Dysregulated sensing of self-nucleic acid is a leading cause of autoimmunity in multifactorial and monogenic diseases. Mutations in Wiskott-Aldrich syndrome protein (WASp), a key regulator of cytoskeletal dynamics in immune cells, cause autoimmune manifestations and increased production of type I
Coat protein complex I (COP-I) mediates the retrograde transport from the Golgi apparatus to the endoplasmic reticulum (ER). Mutation of the COPA gene, encoding one of the COP-I subunits (α-COP), causes an immune dysregulatory disease known as COPA syndrome. The
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