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HTATSF1 is important for HSV-1- or SeV-triggered phosphorylation of downstream signaling components. (A) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, <t>IRF3,</t> and STAT1 in THP-1 cells. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies. (B) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in BMDMs. Lyz2 -Cre; Htatsf1 fl/fl and Htatsf1 fl/fl BMDM cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies.
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HTATSF1 is important for HSV-1- or SeV-triggered phosphorylation of downstream signaling components. (A) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, <t>IRF3,</t> and STAT1 in THP-1 cells. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies. (B) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in BMDMs. Lyz2 -Cre; Htatsf1 fl/fl and Htatsf1 fl/fl BMDM cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies.
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HTATSF1 is important for HSV-1- or SeV-triggered phosphorylation of downstream signaling components. (A) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in THP-1 cells. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies. (B) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in BMDMs. Lyz2 -Cre; Htatsf1 fl/fl and Htatsf1 fl/fl BMDM cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies.

Journal: Cell Insight

Article Title: HTATSF1 regulates innate antiviral immune response by orchestrating TRAF3-IRF3 and TRAF6-NF-κB pathways

doi: 10.1016/j.cellin.2025.100294

Figure Lengend Snippet: HTATSF1 is important for HSV-1- or SeV-triggered phosphorylation of downstream signaling components. (A) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in THP-1 cells. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies. (B) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in BMDMs. Lyz2 -Cre; Htatsf1 fl/fl and Htatsf1 fl/fl BMDM cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies.

Article Snippet: Antibodies against HA (TA180128) (OriGene); Flag (F3165) and β-actin (A2228) (Sigma); p-TBK1 S172 (ab109272), TBK1 (ab40676), p-IRF3 S386 (ab76493), TAK1 (ab109526), TRAF6 (ab33915), p65 (ab7970), ubiquitin (ab7254), K48-linkage specific polyubiquitin (ab140601) and K63-linkage specific polyubiquitin (ab179434) (Abcam); IRF3 (sc-33641) and STAT1 (SC-417) (Santa Cruz Biotechnology); Myc (5605), p-IRF3 S396 (4947), p-STAT1 Y701 (9167), TRAF3 (4729), p-TAK1 T184/187 (4508), p-IκBα S32/36 (9246), IκBα (9242), p-IKKα/β S176/177 (2078), IKKβ (2370), and p-p65 S536 (3033) (Cell Signaling Technology), HTATSF1 (20805-1-AP) and HECTD3 (11487-1-AP) (Proteintech) were purchased from the indicated companies.

Techniques: Phospho-proteomics, Control, Infection, Western Blot