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ncoa4 9a  (TargetMol)


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    TargetMol ncoa4 9a
    Lipid peroxidation resulting from IAV hemagglutinin impairs MAVS‐mediated antiviral immunity. A) The IFNβ promoter activity induced by MAVS in HEK293T WT cells or <t>NCOA4</t> KO cells, with or without transfection of PR8 HA. HEK293 WT or KO cells were transfected with vector or PR8 HA and MAVS, followed by IFNβ promoter activity determined by luciferase assay. B–D) The effects of PR8 HA on MAVS‐induced IFNβ promoter activity with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h post‐transfection, the cells were treated <t>with</t> <t>NCOA4‐9a</t> (2.5 µ m ), DFO (100 µ m ), or Fer‐1 (5 µ m ) for 24 h. The IFNβ promoter activity was detected by luciferase assay. E) Western blotting analysis was performed to investigate the impact of PR8 HA on MAVS aggregates. HEK293T cells were co‐transfected with vector or HA‐HA PR8 and Flag‐MAVS in HEK293T cells, and cell lysates were harvested at 24 h for SDS‐PAGE and SDD‐AGE, followed by western blotting analysis. F) Western blotting analysis of the effect of PR8 HA for MAVS aggregates in NCOA4 KO cells. In HEK293T WT or NCOA4 KO cells, vector or HA‐HA PR8 and Flag‐MAVS were co‐transfected separately, and cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. G‐I) The effects of PR8 HA on MAVS aggregates with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h of transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ) or Fer‐1 (5 µ m ) for 24 h. Cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. J) 4‐HNE levels were analyzed by western blotting in HEK293T cells transfected with 1, 2, and 4 µg of PR8 HA. K‐M) HEK293T cells were transfected with Flag‐MAVS, followed by treatment with 0, 5, 10 and 20 µ m 4‐HNE for 12 h. Cell lysates were harvested for analysis. K) The IFNβ promoter activity induced by 4‐HNE on MAVS was determined by luciferase assay. L) The effects of 4‐HNE on MAVS aggregates were analyzed by western blotting. M) The ρ‐IRF3 level induced by 4‐HNE on MAVS was analyzed by western blotting. Data were shown as mean ± SEM ( n = 3) from triplicate independent experiments, and significance was analyzed by two‐tailed Student's t‐test. (** p < 0.01; *** p < 0.001; ns, no significant).
    Ncoa4 9a, supplied by TargetMol, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ncoa4 9a/product/TargetMol
    Average 92 stars, based on 1 article reviews
    ncoa4 9a - by Bioz Stars, 2026-04
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    1) Product Images from "The Hemagglutinin of Influenza A Virus Induces Ferroptosis to Facilitate Viral Replication"

    Article Title: The Hemagglutinin of Influenza A Virus Induces Ferroptosis to Facilitate Viral Replication

    Journal: Advanced Science

    doi: 10.1002/advs.202404365

    Lipid peroxidation resulting from IAV hemagglutinin impairs MAVS‐mediated antiviral immunity. A) The IFNβ promoter activity induced by MAVS in HEK293T WT cells or NCOA4 KO cells, with or without transfection of PR8 HA. HEK293 WT or KO cells were transfected with vector or PR8 HA and MAVS, followed by IFNβ promoter activity determined by luciferase assay. B–D) The effects of PR8 HA on MAVS‐induced IFNβ promoter activity with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h post‐transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ), or Fer‐1 (5 µ m ) for 24 h. The IFNβ promoter activity was detected by luciferase assay. E) Western blotting analysis was performed to investigate the impact of PR8 HA on MAVS aggregates. HEK293T cells were co‐transfected with vector or HA‐HA PR8 and Flag‐MAVS in HEK293T cells, and cell lysates were harvested at 24 h for SDS‐PAGE and SDD‐AGE, followed by western blotting analysis. F) Western blotting analysis of the effect of PR8 HA for MAVS aggregates in NCOA4 KO cells. In HEK293T WT or NCOA4 KO cells, vector or HA‐HA PR8 and Flag‐MAVS were co‐transfected separately, and cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. G‐I) The effects of PR8 HA on MAVS aggregates with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h of transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ) or Fer‐1 (5 µ m ) for 24 h. Cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. J) 4‐HNE levels were analyzed by western blotting in HEK293T cells transfected with 1, 2, and 4 µg of PR8 HA. K‐M) HEK293T cells were transfected with Flag‐MAVS, followed by treatment with 0, 5, 10 and 20 µ m 4‐HNE for 12 h. Cell lysates were harvested for analysis. K) The IFNβ promoter activity induced by 4‐HNE on MAVS was determined by luciferase assay. L) The effects of 4‐HNE on MAVS aggregates were analyzed by western blotting. M) The ρ‐IRF3 level induced by 4‐HNE on MAVS was analyzed by western blotting. Data were shown as mean ± SEM ( n = 3) from triplicate independent experiments, and significance was analyzed by two‐tailed Student's t‐test. (** p < 0.01; *** p < 0.001; ns, no significant).
    Figure Legend Snippet: Lipid peroxidation resulting from IAV hemagglutinin impairs MAVS‐mediated antiviral immunity. A) The IFNβ promoter activity induced by MAVS in HEK293T WT cells or NCOA4 KO cells, with or without transfection of PR8 HA. HEK293 WT or KO cells were transfected with vector or PR8 HA and MAVS, followed by IFNβ promoter activity determined by luciferase assay. B–D) The effects of PR8 HA on MAVS‐induced IFNβ promoter activity with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h post‐transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ), or Fer‐1 (5 µ m ) for 24 h. The IFNβ promoter activity was detected by luciferase assay. E) Western blotting analysis was performed to investigate the impact of PR8 HA on MAVS aggregates. HEK293T cells were co‐transfected with vector or HA‐HA PR8 and Flag‐MAVS in HEK293T cells, and cell lysates were harvested at 24 h for SDS‐PAGE and SDD‐AGE, followed by western blotting analysis. F) Western blotting analysis of the effect of PR8 HA for MAVS aggregates in NCOA4 KO cells. In HEK293T WT or NCOA4 KO cells, vector or HA‐HA PR8 and Flag‐MAVS were co‐transfected separately, and cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. G‐I) The effects of PR8 HA on MAVS aggregates with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h of transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ) or Fer‐1 (5 µ m ) for 24 h. Cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. J) 4‐HNE levels were analyzed by western blotting in HEK293T cells transfected with 1, 2, and 4 µg of PR8 HA. K‐M) HEK293T cells were transfected with Flag‐MAVS, followed by treatment with 0, 5, 10 and 20 µ m 4‐HNE for 12 h. Cell lysates were harvested for analysis. K) The IFNβ promoter activity induced by 4‐HNE on MAVS was determined by luciferase assay. L) The effects of 4‐HNE on MAVS aggregates were analyzed by western blotting. M) The ρ‐IRF3 level induced by 4‐HNE on MAVS was analyzed by western blotting. Data were shown as mean ± SEM ( n = 3) from triplicate independent experiments, and significance was analyzed by two‐tailed Student's t‐test. (** p < 0.01; *** p < 0.001; ns, no significant).

    Techniques Used: Activity Assay, Transfection, Plasmid Preparation, Luciferase, Inhibition, Western Blot, SDS Page, Two Tailed Test



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    ncoa4 9a  (TargetMol)
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    TargetMol ncoa4 9a
    Lipid peroxidation resulting from IAV hemagglutinin impairs MAVS‐mediated antiviral immunity. A) The IFNβ promoter activity induced by MAVS in HEK293T WT cells or <t>NCOA4</t> KO cells, with or without transfection of PR8 HA. HEK293 WT or KO cells were transfected with vector or PR8 HA and MAVS, followed by IFNβ promoter activity determined by luciferase assay. B–D) The effects of PR8 HA on MAVS‐induced IFNβ promoter activity with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h post‐transfection, the cells were treated <t>with</t> <t>NCOA4‐9a</t> (2.5 µ m ), DFO (100 µ m ), or Fer‐1 (5 µ m ) for 24 h. The IFNβ promoter activity was detected by luciferase assay. E) Western blotting analysis was performed to investigate the impact of PR8 HA on MAVS aggregates. HEK293T cells were co‐transfected with vector or HA‐HA PR8 and Flag‐MAVS in HEK293T cells, and cell lysates were harvested at 24 h for SDS‐PAGE and SDD‐AGE, followed by western blotting analysis. F) Western blotting analysis of the effect of PR8 HA for MAVS aggregates in NCOA4 KO cells. In HEK293T WT or NCOA4 KO cells, vector or HA‐HA PR8 and Flag‐MAVS were co‐transfected separately, and cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. G‐I) The effects of PR8 HA on MAVS aggregates with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h of transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ) or Fer‐1 (5 µ m ) for 24 h. Cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. J) 4‐HNE levels were analyzed by western blotting in HEK293T cells transfected with 1, 2, and 4 µg of PR8 HA. K‐M) HEK293T cells were transfected with Flag‐MAVS, followed by treatment with 0, 5, 10 and 20 µ m 4‐HNE for 12 h. Cell lysates were harvested for analysis. K) The IFNβ promoter activity induced by 4‐HNE on MAVS was determined by luciferase assay. L) The effects of 4‐HNE on MAVS aggregates were analyzed by western blotting. M) The ρ‐IRF3 level induced by 4‐HNE on MAVS was analyzed by western blotting. Data were shown as mean ± SEM ( n = 3) from triplicate independent experiments, and significance was analyzed by two‐tailed Student's t‐test. (** p < 0.01; *** p < 0.001; ns, no significant).
    Ncoa4 9a, supplied by TargetMol, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ncoa4 9a/product/TargetMol
    Average 92 stars, based on 1 article reviews
    ncoa4 9a - by Bioz Stars, 2026-04
    92/100 stars
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    Lipid peroxidation resulting from IAV hemagglutinin impairs MAVS‐mediated antiviral immunity. A) The IFNβ promoter activity induced by MAVS in HEK293T WT cells or NCOA4 KO cells, with or without transfection of PR8 HA. HEK293 WT or KO cells were transfected with vector or PR8 HA and MAVS, followed by IFNβ promoter activity determined by luciferase assay. B–D) The effects of PR8 HA on MAVS‐induced IFNβ promoter activity with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h post‐transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ), or Fer‐1 (5 µ m ) for 24 h. The IFNβ promoter activity was detected by luciferase assay. E) Western blotting analysis was performed to investigate the impact of PR8 HA on MAVS aggregates. HEK293T cells were co‐transfected with vector or HA‐HA PR8 and Flag‐MAVS in HEK293T cells, and cell lysates were harvested at 24 h for SDS‐PAGE and SDD‐AGE, followed by western blotting analysis. F) Western blotting analysis of the effect of PR8 HA for MAVS aggregates in NCOA4 KO cells. In HEK293T WT or NCOA4 KO cells, vector or HA‐HA PR8 and Flag‐MAVS were co‐transfected separately, and cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. G‐I) The effects of PR8 HA on MAVS aggregates with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h of transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ) or Fer‐1 (5 µ m ) for 24 h. Cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. J) 4‐HNE levels were analyzed by western blotting in HEK293T cells transfected with 1, 2, and 4 µg of PR8 HA. K‐M) HEK293T cells were transfected with Flag‐MAVS, followed by treatment with 0, 5, 10 and 20 µ m 4‐HNE for 12 h. Cell lysates were harvested for analysis. K) The IFNβ promoter activity induced by 4‐HNE on MAVS was determined by luciferase assay. L) The effects of 4‐HNE on MAVS aggregates were analyzed by western blotting. M) The ρ‐IRF3 level induced by 4‐HNE on MAVS was analyzed by western blotting. Data were shown as mean ± SEM ( n = 3) from triplicate independent experiments, and significance was analyzed by two‐tailed Student's t‐test. (** p < 0.01; *** p < 0.001; ns, no significant).

    Journal: Advanced Science

    Article Title: The Hemagglutinin of Influenza A Virus Induces Ferroptosis to Facilitate Viral Replication

    doi: 10.1002/advs.202404365

    Figure Lengend Snippet: Lipid peroxidation resulting from IAV hemagglutinin impairs MAVS‐mediated antiviral immunity. A) The IFNβ promoter activity induced by MAVS in HEK293T WT cells or NCOA4 KO cells, with or without transfection of PR8 HA. HEK293 WT or KO cells were transfected with vector or PR8 HA and MAVS, followed by IFNβ promoter activity determined by luciferase assay. B–D) The effects of PR8 HA on MAVS‐induced IFNβ promoter activity with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h post‐transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ), or Fer‐1 (5 µ m ) for 24 h. The IFNβ promoter activity was detected by luciferase assay. E) Western blotting analysis was performed to investigate the impact of PR8 HA on MAVS aggregates. HEK293T cells were co‐transfected with vector or HA‐HA PR8 and Flag‐MAVS in HEK293T cells, and cell lysates were harvested at 24 h for SDS‐PAGE and SDD‐AGE, followed by western blotting analysis. F) Western blotting analysis of the effect of PR8 HA for MAVS aggregates in NCOA4 KO cells. In HEK293T WT or NCOA4 KO cells, vector or HA‐HA PR8 and Flag‐MAVS were co‐transfected separately, and cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. G‐I) The effects of PR8 HA on MAVS aggregates with and without lipid peroxidation inhibition. HEK293T cells were transfected with either vector or PR8 HA and MAVS. After 6 h of transfection, the cells were treated with NCOA4‐9a (2.5 µ m ), DFO (100 µ m ) or Fer‐1 (5 µ m ) for 24 h. Cell lysates were harvested at 24 h post‐transfection for SDD‐AGE vs SDS‐PAGE, followed by western blotting analysis. J) 4‐HNE levels were analyzed by western blotting in HEK293T cells transfected with 1, 2, and 4 µg of PR8 HA. K‐M) HEK293T cells were transfected with Flag‐MAVS, followed by treatment with 0, 5, 10 and 20 µ m 4‐HNE for 12 h. Cell lysates were harvested for analysis. K) The IFNβ promoter activity induced by 4‐HNE on MAVS was determined by luciferase assay. L) The effects of 4‐HNE on MAVS aggregates were analyzed by western blotting. M) The ρ‐IRF3 level induced by 4‐HNE on MAVS was analyzed by western blotting. Data were shown as mean ± SEM ( n = 3) from triplicate independent experiments, and significance was analyzed by two‐tailed Student's t‐test. (** p < 0.01; *** p < 0.001; ns, no significant).

    Article Snippet: The inhibitors and stimulators used in this study were as follows: RSL3 (HY‐100218A), Ferrostatin‐1 (Fer‐1, HY‐100579), Liproxstatin‐1 (Lip‐1, HY‐12726), Deferoxamine mesylate (DFO, HY‐B0988), Chloroquine (CQ, HY‐17589A), and Polyinosinic‐polycytidylic acid (Poly (I:C), HY‐107202) were MCE; NCOA4‐9a (2650557‐72‐3), and 4‐Hydroxynonenal (4‐HNE, 75899‐68‐2) were from TargetMol.

    Techniques: Activity Assay, Transfection, Plasmid Preparation, Luciferase, Inhibition, Western Blot, SDS Page, Two Tailed Test