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Genechem edar knockdown lentiviral plasmids

Vinburnine promotes <t>IR‐EDAR‐NFκB‐induced</t> apoptosis and pyroptosis. A) Reactome analysis of upregulated differential genes after 5µ m Vin / 2Gy IR treatment for 48h. B) Heatmap of differential gene expression in transcriptomics. C) qPCR of EDAR mRNA in NPC cells treated with 5µ m Vin / 2Gy IR for 48h ( n = 3). D) Protein expression of EDAR in the cell membrane/cytoplasm after being treated with 5µ m Vin / 2Gy IR for 48h. E) Western blotting detected the protein expression levels of the NFκB pathway (p65/p50) and pyroptosis index (GSDME/N‐GSDME/ Cleaved‐Caspase3) after 5µ m Vin / 2Gy IR treatment for 48h. Upon activation of the NFκB signaling pathway, its downstream signal, Caspase3, undergoes cleavage. This cleavage then cuts GSDME to form N‐GSDME, ultimately resulting in the pyroptosis of the cells. F) The binding of p65 to the EDAR promoter in the treated SUNE1 cells was detected by ChIP assay. G) The CB‐Dock2 website predicts the structural complex of vinburnine bound with the EDAR protein. Vinburnine is colored green; EDAR is colored grey and yellow. H) SPR technology proved that EDAR is the target of vinburnine. I) The Co‐IP experiment confirmed that after treatment with 5µ m Vin+2Gy IR, EDAR formed more protein complexes with EDARADD/TRAF6. Multiple samples were presented using mean ± standard deviation (SD). C) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. F) Statistical analysis with One‐way ANOVA was used to analyze the statistical differences among multiple groups. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Edar Knockdown Lentiviral Plasmids, supplied by Genechem, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/edar+knockdown+lentiviral+plasmids/edar+knockdown+lentiviral+plasmids/pmc12697895-220-0-4
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edar knockdown lentiviral plasmids - by Bioz Stars, 2026-09

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1) Product Images from "Vinburnine Sensitizes Radiotherapy Efficacy in Nasopharyngeal Carcinoma by Triggering Pyroptosis and Immune Responses via Activation of EDAR‐NFκB Pathway"

Article Title: Vinburnine Sensitizes Radiotherapy Efficacy in Nasopharyngeal Carcinoma by Triggering Pyroptosis and Immune Responses via Activation of EDAR‐NFκB Pathway

Journal: Advanced Science

doi: 10.1002/advs.202506139

Vinburnine promotes IR‐EDAR‐NFκB‐induced apoptosis and pyroptosis. A) Reactome analysis of upregulated differential genes after 5µ m Vin / 2Gy IR treatment for 48h. B) Heatmap of differential gene expression in transcriptomics. C) qPCR of EDAR mRNA in NPC cells treated with 5µ m Vin / 2Gy IR for 48h ( n = 3). D) Protein expression of EDAR in the cell membrane/cytoplasm after being treated with 5µ m Vin / 2Gy IR for 48h. E) Western blotting detected the protein expression levels of the NFκB pathway (p65/p50) and pyroptosis index (GSDME/N‐GSDME/ Cleaved‐Caspase3) after 5µ m Vin / 2Gy IR treatment for 48h. Upon activation of the NFκB signaling pathway, its downstream signal, Caspase3, undergoes cleavage. This cleavage then cuts GSDME to form N‐GSDME, ultimately resulting in the pyroptosis of the cells. F) The binding of p65 to the EDAR promoter in the treated SUNE1 cells was detected by ChIP assay. G) The CB‐Dock2 website predicts the structural complex of vinburnine bound with the EDAR protein. Vinburnine is colored green; EDAR is colored grey and yellow. H) SPR technology proved that EDAR is the target of vinburnine. I) The Co‐IP experiment confirmed that after treatment with 5µ m Vin+2Gy IR, EDAR formed more protein complexes with EDARADD/TRAF6. Multiple samples were presented using mean ± standard deviation (SD). C) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. F) Statistical analysis with One‐way ANOVA was used to analyze the statistical differences among multiple groups. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Figure Legend Snippet: Vinburnine promotes IR‐EDAR‐NFκB‐induced apoptosis and pyroptosis. A) Reactome analysis of upregulated differential genes after 5µ m Vin / 2Gy IR treatment for 48h. B) Heatmap of differential gene expression in transcriptomics. C) qPCR of EDAR mRNA in NPC cells treated with 5µ m Vin / 2Gy IR for 48h ( n = 3). D) Protein expression of EDAR in the cell membrane/cytoplasm after being treated with 5µ m Vin / 2Gy IR for 48h. E) Western blotting detected the protein expression levels of the NFκB pathway (p65/p50) and pyroptosis index (GSDME/N‐GSDME/ Cleaved‐Caspase3) after 5µ m Vin / 2Gy IR treatment for 48h. Upon activation of the NFκB signaling pathway, its downstream signal, Caspase3, undergoes cleavage. This cleavage then cuts GSDME to form N‐GSDME, ultimately resulting in the pyroptosis of the cells. F) The binding of p65 to the EDAR promoter in the treated SUNE1 cells was detected by ChIP assay. G) The CB‐Dock2 website predicts the structural complex of vinburnine bound with the EDAR protein. Vinburnine is colored green; EDAR is colored grey and yellow. H) SPR technology proved that EDAR is the target of vinburnine. I) The Co‐IP experiment confirmed that after treatment with 5µ m Vin+2Gy IR, EDAR formed more protein complexes with EDARADD/TRAF6. Multiple samples were presented using mean ± standard deviation (SD). C) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. F) Statistical analysis with One‐way ANOVA was used to analyze the statistical differences among multiple groups. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Techniques Used: Gene Expression, Expressing, Membrane, Western Blot, Activation Assay, Binding Assay, Co-Immunoprecipitation Assay, Standard Deviation

Knocking down EDAR suppresses the radiosensitization effect of vinburnine. A) The cytotoxic effect of 5uM Vin/2Gy IR on EDAR‐knockdown cells was assessed using the CCK‐8 assay ( n = 5). B) Following EDAR knockdown, cells were treated with 5uM Vin/2Gy IR. Colony formation was evaluated by crystal violet staining (left) and the number of colonies was quantified (right) ( n = 3). C–E) Flow cytometry detected the apoptosis/ROS levels/mitochondrial membrane potential of the Vin±IR‐treated cells after EDAR knockdown ( n = 3). F) After EDAR knockdown, western blotting detected the protein expression (p65/p50/GSDME/N‐GSDME/Cleaved‐Caspase3) in the treated group. Multiple samples were presented using mean ± standard deviation (SD). A–E) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Figure Legend Snippet: Knocking down EDAR suppresses the radiosensitization effect of vinburnine. A) The cytotoxic effect of 5uM Vin/2Gy IR on EDAR‐knockdown cells was assessed using the CCK‐8 assay ( n = 5). B) Following EDAR knockdown, cells were treated with 5uM Vin/2Gy IR. Colony formation was evaluated by crystal violet staining (left) and the number of colonies was quantified (right) ( n = 3). C–E) Flow cytometry detected the apoptosis/ROS levels/mitochondrial membrane potential of the Vin±IR‐treated cells after EDAR knockdown ( n = 3). F) After EDAR knockdown, western blotting detected the protein expression (p65/p50/GSDME/N‐GSDME/Cleaved‐Caspase3) in the treated group. Multiple samples were presented using mean ± standard deviation (SD). A–E) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Techniques Used: Knockdown, CCK-8 Assay, Staining, Flow Cytometry, Membrane, Western Blot, Expressing, Standard Deviation

Vin+IR activates T cell immunity through the EDAR‐NFκB‐CCL5/CX3CL1 pathway. A) The mRNA expression of CCL5 and CX3CL1 in SUNE1 after 5µ m Vin/ 2Gy IR treatment ( n = 3). B) Diagram of human T cell‐related experiments. C). After 24h of 5µ m Vin / 2Gy IR treatment, 1×10^4 SUNE1 was co‐cultured with 2.5×10^4 T cells for 48h. The suspended T cells were washed away with PBS, and the viability of tumor cells was detected by CCK8 ( n = 5). D) T‐cell chemotaxis assay. The supernatant from SUNE1 cells treated with Vin/IR was collected and placed in the lower chamber of the transwell. T cells were then placed in the upper chamber of the transwell. After 48h, the liquid from the lower chamber was collected for T‐cell counting ( n = 3). E) T cells were co‐cultured with treated SUNE1 cell supernatant for 48h, and CD45 + CD3 + CD8 + GZMB + T cells were detected by flow cytometry ( n = 3). F) The ChIP assay was conducted to detect the binding of p65 to the CCL5 and CX3CL1 promoters following treatment with 5µ m Vin / 2Gy IR for 48h ( n = 3). G) Following sh‐EDAR or NFκBi pretreatment, the mRNA expression of CCL5 and CX3CL1 in Vin/IR‐treated SUNE1 was detected using qRT‐PCR ( n = 3). H–J) After sh‐EDAR or NFκBi pretreatment, the proliferation of SUNE1 cells treated with 5µ m Vin / 2Gy IR and co‐cultured with T cells, the number of chemotactic T cells in the supernatant of Vin/IR‐treated SUNE1 cells, and the proportion of CD45 + CD3 + CD8 + GZMB + T cells were measured ( n = 3). K) EDAR and CD8 multiplex immunofluorescence staining was performed on nasopharyngeal carcinoma tissue microarrays. Comparison of mean fluorescence intensity of EDAR in tissues with recurrence ( n = 39) and without recurrence ( n = 45) in NPC patients. L) Correlation between EDAR and CD8 expression in human NPC tissues ( n = 84). M) The patients were divided into EDAR low‐expression ( n = 21) and EDAR high‐expression ( n = 21) groups based on the quartile method. Survival analysis evaluated the association between EDAR expression levels and patient survival. Multiple samples were presented using mean ± standard deviation (SD). A, D–F) Statistical analysis with One‐way ANOVA was used to analyze the statistical differences among multiple groups. C, G–J) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. K) The Mann‐Whitney test was used to analyze the expression of EDAR in patients with recurrence and those without recurrence. L) The correlation between EDAR and CD8 expression in tissue microarrays was analyzed using Pearson's and simple linear regression. M) Survival analysis (Kaplan‐Meier) was utilized to examine the correlation between EDAR expression and the prognosis of patients diagnosed with nasopharyngeal carcinoma. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Figure Legend Snippet: Vin+IR activates T cell immunity through the EDAR‐NFκB‐CCL5/CX3CL1 pathway. A) The mRNA expression of CCL5 and CX3CL1 in SUNE1 after 5µ m Vin/ 2Gy IR treatment ( n = 3). B) Diagram of human T cell‐related experiments. C). After 24h of 5µ m Vin / 2Gy IR treatment, 1×10^4 SUNE1 was co‐cultured with 2.5×10^4 T cells for 48h. The suspended T cells were washed away with PBS, and the viability of tumor cells was detected by CCK8 ( n = 5). D) T‐cell chemotaxis assay. The supernatant from SUNE1 cells treated with Vin/IR was collected and placed in the lower chamber of the transwell. T cells were then placed in the upper chamber of the transwell. After 48h, the liquid from the lower chamber was collected for T‐cell counting ( n = 3). E) T cells were co‐cultured with treated SUNE1 cell supernatant for 48h, and CD45 + CD3 + CD8 + GZMB + T cells were detected by flow cytometry ( n = 3). F) The ChIP assay was conducted to detect the binding of p65 to the CCL5 and CX3CL1 promoters following treatment with 5µ m Vin / 2Gy IR for 48h ( n = 3). G) Following sh‐EDAR or NFκBi pretreatment, the mRNA expression of CCL5 and CX3CL1 in Vin/IR‐treated SUNE1 was detected using qRT‐PCR ( n = 3). H–J) After sh‐EDAR or NFκBi pretreatment, the proliferation of SUNE1 cells treated with 5µ m Vin / 2Gy IR and co‐cultured with T cells, the number of chemotactic T cells in the supernatant of Vin/IR‐treated SUNE1 cells, and the proportion of CD45 + CD3 + CD8 + GZMB + T cells were measured ( n = 3). K) EDAR and CD8 multiplex immunofluorescence staining was performed on nasopharyngeal carcinoma tissue microarrays. Comparison of mean fluorescence intensity of EDAR in tissues with recurrence ( n = 39) and without recurrence ( n = 45) in NPC patients. L) Correlation between EDAR and CD8 expression in human NPC tissues ( n = 84). M) The patients were divided into EDAR low‐expression ( n = 21) and EDAR high‐expression ( n = 21) groups based on the quartile method. Survival analysis evaluated the association between EDAR expression levels and patient survival. Multiple samples were presented using mean ± standard deviation (SD). A, D–F) Statistical analysis with One‐way ANOVA was used to analyze the statistical differences among multiple groups. C, G–J) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. K) The Mann‐Whitney test was used to analyze the expression of EDAR in patients with recurrence and those without recurrence. L) The correlation between EDAR and CD8 expression in tissue microarrays was analyzed using Pearson's and simple linear regression. M) Survival analysis (Kaplan‐Meier) was utilized to examine the correlation between EDAR expression and the prognosis of patients diagnosed with nasopharyngeal carcinoma. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Techniques Used: Expressing, Cell Culture, Chemotaxis Assay, Cell Counting, Flow Cytometry, Binding Assay, Quantitative RT-PCR, Multiplex Assay, Immunofluorescence, Staining, Comparison, Fluorescence, Standard Deviation, MANN-WHITNEY

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Article Title: Vinburnine Sensitizes Radiotherapy Efficacy in Nasopharyngeal Carcinoma by Triggering Pyroptosis and Immune Responses via Activation of EDAR‐NFκB Pathway
Article Snippet: .. EDAR knockdown lentiviral plasmids (GeneChem, China) were packaged with PSPAX2 and PMD2G in 293T cells. ..

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Journal: Advanced Science

Article Title: Vinburnine Sensitizes Radiotherapy Efficacy in Nasopharyngeal Carcinoma by Triggering Pyroptosis and Immune Responses via Activation of EDAR‐NFκB Pathway

doi: 10.1002/advs.202506139

Figure Lengend Snippet: Vinburnine promotes IR‐EDAR‐NFκB‐induced apoptosis and pyroptosis. A) Reactome analysis of upregulated differential genes after 5µ m Vin / 2Gy IR treatment for 48h. B) Heatmap of differential gene expression in transcriptomics. C) qPCR of EDAR mRNA in NPC cells treated with 5µ m Vin / 2Gy IR for 48h ( n = 3). D) Protein expression of EDAR in the cell membrane/cytoplasm after being treated with 5µ m Vin / 2Gy IR for 48h. E) Western blotting detected the protein expression levels of the NFκB pathway (p65/p50) and pyroptosis index (GSDME/N‐GSDME/ Cleaved‐Caspase3) after 5µ m Vin / 2Gy IR treatment for 48h. Upon activation of the NFκB signaling pathway, its downstream signal, Caspase3, undergoes cleavage. This cleavage then cuts GSDME to form N‐GSDME, ultimately resulting in the pyroptosis of the cells. F) The binding of p65 to the EDAR promoter in the treated SUNE1 cells was detected by ChIP assay. G) The CB‐Dock2 website predicts the structural complex of vinburnine bound with the EDAR protein. Vinburnine is colored green; EDAR is colored grey and yellow. H) SPR technology proved that EDAR is the target of vinburnine. I) The Co‐IP experiment confirmed that after treatment with 5µ m Vin+2Gy IR, EDAR formed more protein complexes with EDARADD/TRAF6. Multiple samples were presented using mean ± standard deviation (SD). C) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. F) Statistical analysis with One‐way ANOVA was used to analyze the statistical differences among multiple groups. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Article Snippet: EDAR knockdown lentiviral plasmids (GeneChem, China) were packaged with PSPAX2 and PMD2G in 293T cells.

Techniques: Gene Expression, Expressing, Membrane, Western Blot, Activation Assay, Binding Assay, Co-Immunoprecipitation Assay, Standard Deviation

Journal: Advanced Science

Article Title: Vinburnine Sensitizes Radiotherapy Efficacy in Nasopharyngeal Carcinoma by Triggering Pyroptosis and Immune Responses via Activation of EDAR‐NFκB Pathway

doi: 10.1002/advs.202506139

Figure Lengend Snippet: Knocking down EDAR suppresses the radiosensitization effect of vinburnine. A) The cytotoxic effect of 5uM Vin/2Gy IR on EDAR‐knockdown cells was assessed using the CCK‐8 assay ( n = 5). B) Following EDAR knockdown, cells were treated with 5uM Vin/2Gy IR. Colony formation was evaluated by crystal violet staining (left) and the number of colonies was quantified (right) ( n = 3). C–E) Flow cytometry detected the apoptosis/ROS levels/mitochondrial membrane potential of the Vin±IR‐treated cells after EDAR knockdown ( n = 3). F) After EDAR knockdown, western blotting detected the protein expression (p65/p50/GSDME/N‐GSDME/Cleaved‐Caspase3) in the treated group. Multiple samples were presented using mean ± standard deviation (SD). A–E) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Article Snippet: EDAR knockdown lentiviral plasmids (GeneChem, China) were packaged with PSPAX2 and PMD2G in 293T cells.

Techniques: Knockdown, CCK-8 Assay, Staining, Flow Cytometry, Membrane, Western Blot, Expressing, Standard Deviation

Journal: Advanced Science

Article Title: Vinburnine Sensitizes Radiotherapy Efficacy in Nasopharyngeal Carcinoma by Triggering Pyroptosis and Immune Responses via Activation of EDAR‐NFκB Pathway

doi: 10.1002/advs.202506139

Figure Lengend Snippet: Vin+IR activates T cell immunity through the EDAR‐NFκB‐CCL5/CX3CL1 pathway. A) The mRNA expression of CCL5 and CX3CL1 in SUNE1 after 5µ m Vin/ 2Gy IR treatment ( n = 3). B) Diagram of human T cell‐related experiments. C). After 24h of 5µ m Vin / 2Gy IR treatment, 1×10^4 SUNE1 was co‐cultured with 2.5×10^4 T cells for 48h. The suspended T cells were washed away with PBS, and the viability of tumor cells was detected by CCK8 ( n = 5). D) T‐cell chemotaxis assay. The supernatant from SUNE1 cells treated with Vin/IR was collected and placed in the lower chamber of the transwell. T cells were then placed in the upper chamber of the transwell. After 48h, the liquid from the lower chamber was collected for T‐cell counting ( n = 3). E) T cells were co‐cultured with treated SUNE1 cell supernatant for 48h, and CD45 + CD3 + CD8 + GZMB + T cells were detected by flow cytometry ( n = 3). F) The ChIP assay was conducted to detect the binding of p65 to the CCL5 and CX3CL1 promoters following treatment with 5µ m Vin / 2Gy IR for 48h ( n = 3). G) Following sh‐EDAR or NFκBi pretreatment, the mRNA expression of CCL5 and CX3CL1 in Vin/IR‐treated SUNE1 was detected using qRT‐PCR ( n = 3). H–J) After sh‐EDAR or NFκBi pretreatment, the proliferation of SUNE1 cells treated with 5µ m Vin / 2Gy IR and co‐cultured with T cells, the number of chemotactic T cells in the supernatant of Vin/IR‐treated SUNE1 cells, and the proportion of CD45 + CD3 + CD8 + GZMB + T cells were measured ( n = 3). K) EDAR and CD8 multiplex immunofluorescence staining was performed on nasopharyngeal carcinoma tissue microarrays. Comparison of mean fluorescence intensity of EDAR in tissues with recurrence ( n = 39) and without recurrence ( n = 45) in NPC patients. L) Correlation between EDAR and CD8 expression in human NPC tissues ( n = 84). M) The patients were divided into EDAR low‐expression ( n = 21) and EDAR high‐expression ( n = 21) groups based on the quartile method. Survival analysis evaluated the association between EDAR expression levels and patient survival. Multiple samples were presented using mean ± standard deviation (SD). A, D–F) Statistical analysis with One‐way ANOVA was used to analyze the statistical differences among multiple groups. C, G–J) Statistical analysis with Two‐way ANOVA was used to analyze the statistical differences among multiple groups. K) The Mann‐Whitney test was used to analyze the expression of EDAR in patients with recurrence and those without recurrence. L) The correlation between EDAR and CD8 expression in tissue microarrays was analyzed using Pearson's and simple linear regression. M) Survival analysis (Kaplan‐Meier) was utilized to examine the correlation between EDAR expression and the prognosis of patients diagnosed with nasopharyngeal carcinoma. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns for non‐significant.

Article Snippet: EDAR knockdown lentiviral plasmids (GeneChem, China) were packaged with PSPAX2 and PMD2G in 293T cells.

Techniques: Expressing, Cell Culture, Chemotaxis Assay, Cell Counting, Flow Cytometry, Binding Assay, Quantitative RT-PCR, Multiplex Assay, Immunofluorescence, Staining, Comparison, Fluorescence, Standard Deviation, MANN-WHITNEY

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edar knockdown lentiviral plasmids (Genechem)

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