https://www.selleckchem.com/products/3bdo.html
Here, we demonstrated that the influenza A/Hong Kong/54/98 (H1N1)- or H9N2/G1 virus-induced CXCL10 expressions can be significantly attenuated by knocking down the MXD1 expression in primary human blood macrophages. Indeed, only the MXD1 expression was up-regulated by both H1N1 and H9N2/G1 viruses, but not other MYC/MAX/MXD1 members. The MXD1 expression and the CXCL10 hyperinduction were dependent on MEK1/2 activation. By using EMSAs, we revealed that MXD1 directly binds to the CXCL10 promoter-derived oligonucleotides upon infection of bot
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