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https://www.selleckchem.com/products/c-176-sting-inhibitor.html It was found that SNHG5 could bind miR-489-3p, and the relative expression of SNHG5 was negatively correlated with miR-489-3p. Further results suggested that SOX4 might be the target gene of miR-489-3p. Finally, our experimental data indicated that knockdown of SNHG5 could reduce the tumor volume and down-regulated SOX4 levels in vivo. CONCLUSIONS Our results demonstrated that SNHG5 affected the expression of SOX4 through binding miR-489-3p to regulate proliferation and apoptosis of AML, which might act as a prospective prognostic biological marker and a promising therapeutic target for AML.Diphtheria toxin (DT) efficiently inhibits protein synthesis in human cells, resulting in severe disease diphtheria. The sensitivity towards DT varies between mammalian species. Mice and rats are resistant to DT. However, the reason underlying this insensitivity is controversially discussed and not well understood. Therefore, we investigated the steps of DT uptake, i.e. receptor binding and internalization into mouse J774A.1 macrophages and primary rat fibroblasts. We exploited the non-toxic DT-mutant cross-reacting material 197 (CRM197) and three additional receptor binding-deficient mutants (250 nM each) to investigate binding to cell surface and internalization into murine cells via flow cytometry and stimulated emission depletion (STED) super-resolution optical microscopy. Dual-color STED imaging unveiled CRM197 interacting with the murine precursor of the heparin-binding epidermal growth factor-like growth factor (HB-EGF). Moreover, we identified CRM197's transmembrane domain as an additional HB-EGF binding site, which is also involved in the receptor-mediated internalization into murine cells. However, we do not find evidence for translocation of the catalytically active subunit (DTA) into the cytosol when 250 nM DT were applied. In conclusion, we provide evidence that the resistance of murine cells to DT is ca

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