The auxiliary β₄ subunit of the cardiac Ca_v1.2 channel plays a poorly understood role in gene transcription. Here, we characterized the regulatory effects of the β₄ subunit in H9c2 rat cardiac cells on the abundances of Ifnb mRNA [which encodes interferon-β (IFN-β)] and of the IFN-β–related genes Ddx58, Ifitm3, Irf7, Stat2, Ifih1, and Mx1, as well as on the abundances of the antiviral proteins DDX58, IRF7, STAT2, and IFITM3. Knocking down the β₄ subunit in H9c2 cells reduced the expression of IFN-β–stimulated genes. In response to inhibition of the kinase JAK1, the abundances of β₄ subunit mRNA and protein were decreased. β₄ subunit abundance was increased, and it translocated to the nucleus, in cells treated with IFN-β, infected with dengue virus (DENV), or transfected with poly(I:C), a synthetic analog of double-stranded RNA. Cells that surrounded the virus-infected cells showed translocation of β₄ subunit proteins to nuclei in response to spreading infection. We showed that the β₄ subunit interacted with the transcriptional regulator IRF7 and that the activity of an Irf7 promoter–driven reporter was increased in cells overexpressing the β₄ subunit. Last, overexpressing β₄ in undifferentiated and differentiated H9c2 cells reduced DENV infection and decreased the abundance of the viral proteins NS1, NS3, and E-protein. DENV infection and poly(I:C) also increased the concentration of intracellular Ca²⁺ in these cells. These findings suggest that the β₄ subunit plays a role in promoting the expression of IFN-related genes, thereby reducing viral infection.

辅助β ₄所述心脏的Ca亚基_v 1.2通道起着基因转录知之甚少作用。在这里，我们表征了β的调节作用₄上的丰度在H9c2心肌大鼠心肌细胞亚基IFNB的mRNA [其编码干扰素β（IFN-β）]和的IFN-β-相关基因DDX58，IFITM3，IRF7，Stat2，Ifih1和Mx1，以及抗病毒蛋白DDX58，IRF7，STAT2和IFITM3的丰度。撞倒β ₄H9c2细胞中的亚基减少了IFN-β刺激基因的表达。响应于抑制激酶JAK1的，β的丰度₄亚基mRNA和蛋白表达降低。β ₄亚基丰度的增加，和它移位到细胞核，与IFN-β处理的细胞，受登革热病毒感染（DENV），或与聚转染（I：C），双链RNA的合成类似物。细胞包围的病毒感染的细胞表现出β的易位_4个亚基蛋白到细胞核响应于传播感染。我们发现，在β ₄亚单位互动与转录调节IRF7和一个活性IRF7启动子驱动的报道是在过量表达β增加_4个亚基。最后，过表达β ₄在未分化和分化H9c2细胞降低DENV感染，降低了病毒蛋白NS1，NS3，和E蛋白的丰度。DENV感染和poly（I：C）也增加了这些细胞中细胞内Ca ²⁺的浓度。这些结果表明，该β ₄亚基在促进的IFN相关基因表达的作用，从而减少了病毒感染。