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ABclonal Biotechnology rabbit anti-birc3 antibody

<t>BIRC3</t> was the key regulator of 6-TG against EV71 infection. ( A ) HeLa cells were infected with EV71 at an MOI of 1 in the presence of NSC23766 at different concentrations (0, 5, 10, 30, 50, 100 µM). After 24 h, the intracellular EV71 VP1 (green) was examined via ICW assay and normalized by DRAQ5 (red). The percent of EV71 inhibition was analyzed by Odyssey software, and the intracellular EV71 VP1 of EV71-infected cells without NSC23766 treatment were considered as a negative control. ( B ) Identification of 14 common differential expressed genes (DEG) from untreated or 6-TG-treated HUVEC database (Control vs. 6-TG) and uninfected or EV71-infected mice database (GSE123550) (Mock vs. EV71) through SangerBox 3.0 online tools. Advanced Pie plot was performed using the OmicStudio tools at https://www.omicstudio.cn/tool . ( C ) The heatmap of the 14 common DEGs from Control vs. 6-TG group and Mock vs. EV71 group. Advanced Heatmap Plots was performed using the OmicStudio tools at https://www.omicstudio.cn . ( D and E ) HeLa cells were incubated with 1 or 3 µM 6-TG for 2 h. Then the BIRC3 mRNA was quantified by quantitative real-time PCR, normalized to GAPDH ( D ). The BIRC3 protein levels were quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( E ). ( F , G and H ) HeLa cells were infected with EV71 at an MOI of 0.5 for 24 h, and the EV71 mRNA and BIRC3 mRNA was quantified via quantitative real-time PCR, normalized against GAPDH ( F and G ). The BIRC3 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( H ). ( I , J and K ) HeLa cells were infected with EV71 at an MOI of 0.5 in the presence of 6-TG at 1 µM. The BIRC3 and EV71 VP1 expression was quantified via western blot analysis, normalized against β-actin. The intensity of BIRC3 was quantified by ImageJ software ( I ). The EV71 mRNA and BIRC3 mRNA was quantified via quantitative real-time PCR, normalized against GAPDH ( J and K ). Data were pooled from three ( D - K ) independent experiments, and were shown as the mean ± SEM (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Rabbit Anti Birc3 Antibody, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit anti-birc3 antibody - by Bioz Stars, 2026-09

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1) Product Images from "6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy"

Article Title: 6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy

Journal: BMC Microbiology

doi: 10.1186/s12866-025-03752-8

BIRC3 was the key regulator of 6-TG against EV71 infection. ( A ) HeLa cells were infected with EV71 at an MOI of 1 in the presence of NSC23766 at different concentrations (0, 5, 10, 30, 50, 100 µM). After 24 h, the intracellular EV71 VP1 (green) was examined via ICW assay and normalized by DRAQ5 (red). The percent of EV71 inhibition was analyzed by Odyssey software, and the intracellular EV71 VP1 of EV71-infected cells without NSC23766 treatment were considered as a negative control. ( B ) Identification of 14 common differential expressed genes (DEG) from untreated or 6-TG-treated HUVEC database (Control vs. 6-TG) and uninfected or EV71-infected mice database (GSE123550) (Mock vs. EV71) through SangerBox 3.0 online tools. Advanced Pie plot was performed using the OmicStudio tools at https://www.omicstudio.cn/tool . ( C ) The heatmap of the 14 common DEGs from Control vs. 6-TG group and Mock vs. EV71 group. Advanced Heatmap Plots was performed using the OmicStudio tools at https://www.omicstudio.cn . ( D and E ) HeLa cells were incubated with 1 or 3 µM 6-TG for 2 h. Then the BIRC3 mRNA was quantified by quantitative real-time PCR, normalized to GAPDH ( D ). The BIRC3 protein levels were quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( E ). ( F , G and H ) HeLa cells were infected with EV71 at an MOI of 0.5 for 24 h, and the EV71 mRNA and BIRC3 mRNA was quantified via quantitative real-time PCR, normalized against GAPDH ( F and G ). The BIRC3 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( H ). ( I , J and K ) HeLa cells were infected with EV71 at an MOI of 0.5 in the presence of 6-TG at 1 µM. The BIRC3 and EV71 VP1 expression was quantified via western blot analysis, normalized against β-actin. The intensity of BIRC3 was quantified by ImageJ software ( I ). The EV71 mRNA and BIRC3 mRNA was quantified via quantitative real-time PCR, normalized against GAPDH ( J and K ). Data were pooled from three ( D - K ) independent experiments, and were shown as the mean ± SEM (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Figure Legend Snippet: BIRC3 was the key regulator of 6-TG against EV71 infection. ( A ) HeLa cells were infected with EV71 at an MOI of 1 in the presence of NSC23766 at different concentrations (0, 5, 10, 30, 50, 100 µM). After 24 h, the intracellular EV71 VP1 (green) was examined via ICW assay and normalized by DRAQ5 (red). The percent of EV71 inhibition was analyzed by Odyssey software, and the intracellular EV71 VP1 of EV71-infected cells without NSC23766 treatment were considered as a negative control. ( B ) Identification of 14 common differential expressed genes (DEG) from untreated or 6-TG-treated HUVEC database (Control vs. 6-TG) and uninfected or EV71-infected mice database (GSE123550) (Mock vs. EV71) through SangerBox 3.0 online tools. Advanced Pie plot was performed using the OmicStudio tools at https://www.omicstudio.cn/tool . ( C ) The heatmap of the 14 common DEGs from Control vs. 6-TG group and Mock vs. EV71 group. Advanced Heatmap Plots was performed using the OmicStudio tools at https://www.omicstudio.cn . ( D and E ) HeLa cells were incubated with 1 or 3 µM 6-TG for 2 h. Then the BIRC3 mRNA was quantified by quantitative real-time PCR, normalized to GAPDH ( D ). The BIRC3 protein levels were quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( E ). ( F , G and H ) HeLa cells were infected with EV71 at an MOI of 0.5 for 24 h, and the EV71 mRNA and BIRC3 mRNA was quantified via quantitative real-time PCR, normalized against GAPDH ( F and G ). The BIRC3 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( H ). ( I , J and K ) HeLa cells were infected with EV71 at an MOI of 0.5 in the presence of 6-TG at 1 µM. The BIRC3 and EV71 VP1 expression was quantified via western blot analysis, normalized against β-actin. The intensity of BIRC3 was quantified by ImageJ software ( I ). The EV71 mRNA and BIRC3 mRNA was quantified via quantitative real-time PCR, normalized against GAPDH ( J and K ). Data were pooled from three ( D - K ) independent experiments, and were shown as the mean ± SEM (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Techniques Used: Infection, Inhibition, Software, Negative Control, Control, Incubation, Real-time Polymerase Chain Reaction, Western Blot, Expressing

BIRC3 promoted EV71 replication and reversed the anti-EV71 effect of 6-TG. ( A and B ) HeLa cells were transfected with three specific siRNAs targeting BIRC3 (siBIRC3 #1, siBIRC3 #2, siBIRC3 #3) or control siRNA (siNC) for 30 h. The cells were harvested and the BIRC3 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( A ), the BIRC3 protein levels were evaluated by western blot assay, normalized to β-actin ( B ). ( C and D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, and then infected with EV71 at an MOI of 0.5 for 24 h. The cells were harvested and the EV71 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( C ). The EV71 VP1 protein expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( D ). ( E and F ) HeLa cells were transfected with 1 µg plasmid encoding BIRC3 (pBIRC3) or control plasmid (pVector). After 30 h, the cells were collected, and the BIRC3 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( E ), the flag-BIRC3 protein expression was evaluated by western blot assay, normalized to β-actin ( F ). ( G and H ) HeLa cells were transfected with 1 µg pBIRC3 or pVector for 30 h, and then infected with EV71 at an MOI of 0.5 for 24 h. The cells were harvested and EV71 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( G ). The EV71 VP1 protein expression in harvested cells was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( H ). ( I ) HeLa cells were transfected with 1 µg pBIRC3 or pVector for 30 h, and next infected with EV71 at an MOI of 0.5 for 2 h, then the cells were washed with PBS and incubated with clear culture medium. After 24 h, the culture supernatant was collected and added to Vero cells, the viral titers were calculated as the TCID 50 after 72 h incubation. ( J and K ) HeLa cells were transfected with 1 µg pBIRC3 or an empty Vector for 30 h, then the cells were infected with EV71 at an MOI of 0.5 in the presence of 1 µM 6-TG for 24 h. The EV71 RNA levels and the BIRC3 RNA levels in harvested cells were quantified via quantitative real-time PCR, normalized against GAPDH. ( L ) HeLa cells were transfected with 1 µg pBIRC3 or an empty Vector for 30 h, then the cells were infected with EV71 at an MOI of 0.5 for 2 h. After washing with PBS, the cells were incubated with 1 µM 6-TG for 24 h. The culture supernatant was collected and added to Vero cells, the viral titers were calculated as the TCID 50 after 72 h incubation. Data were pooled from three ( A , C-E and G-L ) or two ( B and F ) independent experiments, and were shown as the mean ± SEM (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Figure Legend Snippet: BIRC3 promoted EV71 replication and reversed the anti-EV71 effect of 6-TG. ( A and B ) HeLa cells were transfected with three specific siRNAs targeting BIRC3 (siBIRC3 #1, siBIRC3 #2, siBIRC3 #3) or control siRNA (siNC) for 30 h. The cells were harvested and the BIRC3 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( A ), the BIRC3 protein levels were evaluated by western blot assay, normalized to β-actin ( B ). ( C and D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, and then infected with EV71 at an MOI of 0.5 for 24 h. The cells were harvested and the EV71 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( C ). The EV71 VP1 protein expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( D ). ( E and F ) HeLa cells were transfected with 1 µg plasmid encoding BIRC3 (pBIRC3) or control plasmid (pVector). After 30 h, the cells were collected, and the BIRC3 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( E ), the flag-BIRC3 protein expression was evaluated by western blot assay, normalized to β-actin ( F ). ( G and H ) HeLa cells were transfected with 1 µg pBIRC3 or pVector for 30 h, and then infected with EV71 at an MOI of 0.5 for 24 h. The cells were harvested and EV71 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( G ). The EV71 VP1 protein expression in harvested cells was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( H ). ( I ) HeLa cells were transfected with 1 µg pBIRC3 or pVector for 30 h, and next infected with EV71 at an MOI of 0.5 for 2 h, then the cells were washed with PBS and incubated with clear culture medium. After 24 h, the culture supernatant was collected and added to Vero cells, the viral titers were calculated as the TCID 50 after 72 h incubation. ( J and K ) HeLa cells were transfected with 1 µg pBIRC3 or an empty Vector for 30 h, then the cells were infected with EV71 at an MOI of 0.5 in the presence of 1 µM 6-TG for 24 h. The EV71 RNA levels and the BIRC3 RNA levels in harvested cells were quantified via quantitative real-time PCR, normalized against GAPDH. ( L ) HeLa cells were transfected with 1 µg pBIRC3 or an empty Vector for 30 h, then the cells were infected with EV71 at an MOI of 0.5 for 2 h. After washing with PBS, the cells were incubated with 1 µM 6-TG for 24 h. The culture supernatant was collected and added to Vero cells, the viral titers were calculated as the TCID 50 after 72 h incubation. Data were pooled from three ( A , C-E and G-L ) or two ( B and F ) independent experiments, and were shown as the mean ± SEM (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Techniques Used: Transfection, Control, Real-time Polymerase Chain Reaction, Western Blot, Infection, Expressing, Software, Plasmid Preparation, Incubation

BIRC3 knockdown affected the cleavage function of EV71 2A pro and the expression of EV71 3AB. HeLa cells were transfected with plasmid GFP-2A pro , GFP-2B, GFP-3AB, GFP-3C, GFP-3D and HA-2C for 24 h, then were transfected with siBIRC3 or siNC for 30 h. The cells were harvested and the expression of eIF4G, GFP-tag, HA-tag was evaluated by western blot assay, normalized to β-actin or GAPDH. The intensity of western blot bands signals of cleaved eIF4G, GFP-2B/3AB/3 C/3D, HA-2 C, β-actin and GAPDH were quantified by ImageJ software. Data were pooled from three independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01)

Figure Legend Snippet: BIRC3 knockdown affected the cleavage function of EV71 2A pro and the expression of EV71 3AB. HeLa cells were transfected with plasmid GFP-2A pro , GFP-2B, GFP-3AB, GFP-3C, GFP-3D and HA-2C for 24 h, then were transfected with siBIRC3 or siNC for 30 h. The cells were harvested and the expression of eIF4G, GFP-tag, HA-tag was evaluated by western blot assay, normalized to β-actin or GAPDH. The intensity of western blot bands signals of cleaved eIF4G, GFP-2B/3AB/3 C/3D, HA-2 C, β-actin and GAPDH were quantified by ImageJ software. Data were pooled from three independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01)

Techniques Used: Knockdown, Expressing, Transfection, Plasmid Preparation, Western Blot, Software

6-TG suppressed EV71 replication by diminishing BIRC3-mediated autophagy. ( A ) HeLa cells were Mock-infected or EV71 (MOI = 0.5) infected for 12 h, then cells were fixed for immunostaining using EV71 2C antibody (red). Nuclei were labeled with DAPI (blue). Scale bars, 10 μm. The white arrows showed the formed GFP-LC3 puncta. ( B ) HeLa cells were infected with EV71 at an MOI of 0.5, and the cells were harvested at 12, 24 hpi (hours post infection). The EV71 VP1, LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( C ) HeLa cells were infected with EV71 at an MOI of 0.5 in the presence of 1 µM 6-TG. After 24 h, the EV71 VP1, LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, then the cells were infected with EV71 at an MOI of 0.5 for 24 h. The BIRC3, LC3 I, LC3 II, P62 and EV71 VP1 expression in harvested cells was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. Data were pooled from three ( B-D ) or two ( A ) independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Figure Legend Snippet: 6-TG suppressed EV71 replication by diminishing BIRC3-mediated autophagy. ( A ) HeLa cells were Mock-infected or EV71 (MOI = 0.5) infected for 12 h, then cells were fixed for immunostaining using EV71 2C antibody (red). Nuclei were labeled with DAPI (blue). Scale bars, 10 μm. The white arrows showed the formed GFP-LC3 puncta. ( B ) HeLa cells were infected with EV71 at an MOI of 0.5, and the cells were harvested at 12, 24 hpi (hours post infection). The EV71 VP1, LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( C ) HeLa cells were infected with EV71 at an MOI of 0.5 in the presence of 1 µM 6-TG. After 24 h, the EV71 VP1, LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, then the cells were infected with EV71 at an MOI of 0.5 for 24 h. The BIRC3, LC3 I, LC3 II, P62 and EV71 VP1 expression in harvested cells was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. Data were pooled from three ( B-D ) or two ( A ) independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Techniques Used: Infection, Immunostaining, Labeling, Expressing, Western Blot, Software, Transfection

6-TG addition diminished BIRC3-mediated autophagy. ( A ) HeLa cells were incubated with 1 or 3 µM 6-TG for 24 h, the LC3 I, LC3 II, P62 and BIRC3 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( B ) HeLa cells were stimulated with 100 nM rapamycin for 12 h, then they were incubated with 1 µM 6-TG for 24 h. The LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( C ) HeLa cells were transfected with 0.5–1 µg pBIRC3 or pVector for 30 h. The cells were harvested and Fag-BIRC3, LC3 I, LC3 II and P62 expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, respectively. The cells were harvested and BIRC3, LC3 I, LC3 II and P62 expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. Data were pooled from three ( A-D ) independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01, *** P < 0.001)

Figure Legend Snippet: 6-TG addition diminished BIRC3-mediated autophagy. ( A ) HeLa cells were incubated with 1 or 3 µM 6-TG for 24 h, the LC3 I, LC3 II, P62 and BIRC3 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( B ) HeLa cells were stimulated with 100 nM rapamycin for 12 h, then they were incubated with 1 µM 6-TG for 24 h. The LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( C ) HeLa cells were transfected with 0.5–1 µg pBIRC3 or pVector for 30 h. The cells were harvested and Fag-BIRC3, LC3 I, LC3 II and P62 expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, respectively. The cells were harvested and BIRC3, LC3 I, LC3 II and P62 expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. Data were pooled from three ( A-D ) independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01, *** P < 0.001)

Techniques Used: Incubation, Expressing, Western Blot, Software, Transfection

Figure Legend Snippet:

Techniques Used:

Image Search Results

Journal: BMC Microbiology

Article Title: 6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy

doi: 10.1186/s12866-025-03752-8

Figure Lengend Snippet: BIRC3 was the key regulator of 6-TG against EV71 infection. ( A ) HeLa cells were infected with EV71 at an MOI of 1 in the presence of NSC23766 at different concentrations (0, 5, 10, 30, 50, 100 µM). After 24 h, the intracellular EV71 VP1 (green) was examined via ICW assay and normalized by DRAQ5 (red). The percent of EV71 inhibition was analyzed by Odyssey software, and the intracellular EV71 VP1 of EV71-infected cells without NSC23766 treatment were considered as a negative control. ( B ) Identification of 14 common differential expressed genes (DEG) from untreated or 6-TG-treated HUVEC database (Control vs. 6-TG) and uninfected or EV71-infected mice database (GSE123550) (Mock vs. EV71) through SangerBox 3.0 online tools. Advanced Pie plot was performed using the OmicStudio tools at https://www.omicstudio.cn/tool . ( C ) The heatmap of the 14 common DEGs from Control vs. 6-TG group and Mock vs. EV71 group. Advanced Heatmap Plots was performed using the OmicStudio tools at https://www.omicstudio.cn . ( D and E ) HeLa cells were incubated with 1 or 3 µM 6-TG for 2 h. Then the BIRC3 mRNA was quantified by quantitative real-time PCR, normalized to GAPDH ( D ). The BIRC3 protein levels were quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( E ). ( F , G and H ) HeLa cells were infected with EV71 at an MOI of 0.5 for 24 h, and the EV71 mRNA and BIRC3 mRNA was quantified via quantitative real-time PCR, normalized against GAPDH ( F and G ). The BIRC3 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( H ). ( I , J and K ) HeLa cells were infected with EV71 at an MOI of 0.5 in the presence of 6-TG at 1 µM. The BIRC3 and EV71 VP1 expression was quantified via western blot analysis, normalized against β-actin. The intensity of BIRC3 was quantified by ImageJ software ( I ). The EV71 mRNA and BIRC3 mRNA was quantified via quantitative real-time PCR, normalized against GAPDH ( J and K ). Data were pooled from three ( D - K ) independent experiments, and were shown as the mean ± SEM (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Article Snippet: Rabbit anti-BIRC3 antibody Mouse anti-Flag tag antibody , ABclonal (Wuhan, China) Servicebio (Wuhan, China) , A0833 GB15938-100.

Techniques: Infection, Inhibition, Software, Negative Control, Control, Incubation, Real-time Polymerase Chain Reaction, Western Blot, Expressing

Journal: BMC Microbiology

Article Title: 6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy

doi: 10.1186/s12866-025-03752-8

Figure Lengend Snippet: BIRC3 promoted EV71 replication and reversed the anti-EV71 effect of 6-TG. ( A and B ) HeLa cells were transfected with three specific siRNAs targeting BIRC3 (siBIRC3 #1, siBIRC3 #2, siBIRC3 #3) or control siRNA (siNC) for 30 h. The cells were harvested and the BIRC3 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( A ), the BIRC3 protein levels were evaluated by western blot assay, normalized to β-actin ( B ). ( C and D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, and then infected with EV71 at an MOI of 0.5 for 24 h. The cells were harvested and the EV71 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( C ). The EV71 VP1 protein expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( D ). ( E and F ) HeLa cells were transfected with 1 µg plasmid encoding BIRC3 (pBIRC3) or control plasmid (pVector). After 30 h, the cells were collected, and the BIRC3 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( E ), the flag-BIRC3 protein expression was evaluated by western blot assay, normalized to β-actin ( F ). ( G and H ) HeLa cells were transfected with 1 µg pBIRC3 or pVector for 30 h, and then infected with EV71 at an MOI of 0.5 for 24 h. The cells were harvested and EV71 RNA levels were quantified via quantitative real-time PCR, normalized against GAPDH ( G ). The EV71 VP1 protein expression in harvested cells was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals was quantified by ImageJ software ( H ). ( I ) HeLa cells were transfected with 1 µg pBIRC3 or pVector for 30 h, and next infected with EV71 at an MOI of 0.5 for 2 h, then the cells were washed with PBS and incubated with clear culture medium. After 24 h, the culture supernatant was collected and added to Vero cells, the viral titers were calculated as the TCID 50 after 72 h incubation. ( J and K ) HeLa cells were transfected with 1 µg pBIRC3 or an empty Vector for 30 h, then the cells were infected with EV71 at an MOI of 0.5 in the presence of 1 µM 6-TG for 24 h. The EV71 RNA levels and the BIRC3 RNA levels in harvested cells were quantified via quantitative real-time PCR, normalized against GAPDH. ( L ) HeLa cells were transfected with 1 µg pBIRC3 or an empty Vector for 30 h, then the cells were infected with EV71 at an MOI of 0.5 for 2 h. After washing with PBS, the cells were incubated with 1 µM 6-TG for 24 h. The culture supernatant was collected and added to Vero cells, the viral titers were calculated as the TCID 50 after 72 h incubation. Data were pooled from three ( A , C-E and G-L ) or two ( B and F ) independent experiments, and were shown as the mean ± SEM (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Article Snippet: Rabbit anti-BIRC3 antibody Mouse anti-Flag tag antibody , ABclonal (Wuhan, China) Servicebio (Wuhan, China) , A0833 GB15938-100.

Techniques: Transfection, Control, Real-time Polymerase Chain Reaction, Western Blot, Infection, Expressing, Software, Plasmid Preparation, Incubation

Journal: BMC Microbiology

Article Title: 6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy

doi: 10.1186/s12866-025-03752-8

Figure Lengend Snippet: BIRC3 knockdown affected the cleavage function of EV71 2A pro and the expression of EV71 3AB. HeLa cells were transfected with plasmid GFP-2A pro , GFP-2B, GFP-3AB, GFP-3C, GFP-3D and HA-2C for 24 h, then were transfected with siBIRC3 or siNC for 30 h. The cells were harvested and the expression of eIF4G, GFP-tag, HA-tag was evaluated by western blot assay, normalized to β-actin or GAPDH. The intensity of western blot bands signals of cleaved eIF4G, GFP-2B/3AB/3 C/3D, HA-2 C, β-actin and GAPDH were quantified by ImageJ software. Data were pooled from three independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01)

Article Snippet: Rabbit anti-BIRC3 antibody Mouse anti-Flag tag antibody , ABclonal (Wuhan, China) Servicebio (Wuhan, China) , A0833 GB15938-100.

Techniques: Knockdown, Expressing, Transfection, Plasmid Preparation, Western Blot, Software

Journal: BMC Microbiology

Article Title: 6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy

doi: 10.1186/s12866-025-03752-8

Figure Lengend Snippet: 6-TG suppressed EV71 replication by diminishing BIRC3-mediated autophagy. ( A ) HeLa cells were Mock-infected or EV71 (MOI = 0.5) infected for 12 h, then cells were fixed for immunostaining using EV71 2C antibody (red). Nuclei were labeled with DAPI (blue). Scale bars, 10 μm. The white arrows showed the formed GFP-LC3 puncta. ( B ) HeLa cells were infected with EV71 at an MOI of 0.5, and the cells were harvested at 12, 24 hpi (hours post infection). The EV71 VP1, LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( C ) HeLa cells were infected with EV71 at an MOI of 0.5 in the presence of 1 µM 6-TG. After 24 h, the EV71 VP1, LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, then the cells were infected with EV71 at an MOI of 0.5 for 24 h. The BIRC3, LC3 I, LC3 II, P62 and EV71 VP1 expression in harvested cells was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. Data were pooled from three ( B-D ) or two ( A ) independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001)

Article Snippet: Rabbit anti-BIRC3 antibody Mouse anti-Flag tag antibody , ABclonal (Wuhan, China) Servicebio (Wuhan, China) , A0833 GB15938-100.

Techniques: Infection, Immunostaining, Labeling, Expressing, Western Blot, Software, Transfection

Journal: BMC Microbiology

Article Title: 6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy

doi: 10.1186/s12866-025-03752-8

Figure Lengend Snippet: 6-TG addition diminished BIRC3-mediated autophagy. ( A ) HeLa cells were incubated with 1 or 3 µM 6-TG for 24 h, the LC3 I, LC3 II, P62 and BIRC3 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( B ) HeLa cells were stimulated with 100 nM rapamycin for 12 h, then they were incubated with 1 µM 6-TG for 24 h. The LC3 I, LC3 II and P62 expression was quantified via western blot analysis, normalized against β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( C ) HeLa cells were transfected with 0.5–1 µg pBIRC3 or pVector for 30 h. The cells were harvested and Fag-BIRC3, LC3 I, LC3 II and P62 expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. ( D ) HeLa cells were transfected with siBIRC3 or siNC for 30 h, respectively. The cells were harvested and BIRC3, LC3 I, LC3 II and P62 expression was evaluated by western blot assay, normalized to β-actin. The intensity of western blot bands signals of LC3 II/LC3 I and P62/β-actin was quantified by ImageJ software. Data were pooled from three ( A-D ) independent experiments, and were shown as the mean ± SEM (ns, no significant, * P < 0.05, ** P < 0.01, *** P < 0.001)

Article Snippet: Rabbit anti-BIRC3 antibody Mouse anti-Flag tag antibody , ABclonal (Wuhan, China) Servicebio (Wuhan, China) , A0833 GB15938-100.

Techniques: Incubation, Expressing, Western Blot, Software, Transfection

Journal: BMC Microbiology

Article Title: 6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy

doi: 10.1186/s12866-025-03752-8

Figure Lengend Snippet:

Article Snippet: Rabbit anti-BIRC3 antibody Mouse anti-Flag tag antibody , ABclonal (Wuhan, China) Servicebio (Wuhan, China) , A0833 GB15938-100.

Techniques:

(A) Differences in the number of clinicopathological variables between high and low NI groups; (B–F) differential expression of BIRC3 in clinicopathological variables (such as Grade, Stage, TMN); (G–M) differential expression of BIRC3 in clinicopathological variables in GEO test datasets; (N) line chart for the relative expression of BIRC3 in ccRCC tissues ( n = 15) and normal tissues ( n = 15); (O) bar plot for the relative expression of BIRC3 in ccRCC cell lines and normal HK2 cell line. Biological replicates. Error bars represent one SD from the mean.

Journal: PeerJ

Article Title: Identification and validation of prognostic and tumor microenvironment characteristics of necroptosis index and BIRC3 in clear cell renal cell carcinoma

doi: 10.7717/peerj.16643

Figure Lengend Snippet: (A) Differences in the number of clinicopathological variables between high and low NI groups; (B–F) differential expression of BIRC3 in clinicopathological variables (such as Grade, Stage, TMN); (G–M) differential expression of BIRC3 in clinicopathological variables in GEO test datasets; (N) line chart for the relative expression of BIRC3 in ccRCC tissues ( n = 15) and normal tissues ( n = 15); (O) bar plot for the relative expression of BIRC3 in ccRCC cell lines and normal HK2 cell line. Biological replicates. Error bars represent one SD from the mean.

Article Snippet: The primary antibodies used in this study were as follows: rabbit polyclonal BIRC3 (24304-1-AP; Proteintech, Wuhan, China) and mouse monoclonal GAPDH (60004-1-Ig; Proteintech, Wuhan, China).

Techniques: Quantitative Proteomics, Expressing

(A) Differences in MDSC, Macrophage and Regulatory.T.cell between high and low BIRC3 groups, error bars represent the mean; (B) scatter plot revealing the correlation of BIRC3 and immune cells (Regulatory.T.cell Macrophage and MDSC); (C) differences in PDCD1, CTLA4 and CD274 between high and low BIRC3 groups, error bars represent the mean; (D) scatter plot revealing the correlation of BIRC3 and immune checkpoints (CD274, CTLA4 and PDCD1); (E) differences in TME scores between high and low BIRC3 groups, error bars represent one SD from the mean; (F) gene set enrichment analysis of BIRC3; (G) the volcano map showed the drugs associated with BIRC3. Red represented positive correlation; blue represented negative correlation.

Journal: PeerJ

Article Title: Identification and validation of prognostic and tumor microenvironment characteristics of necroptosis index and BIRC3 in clear cell renal cell carcinoma

doi: 10.7717/peerj.16643

Figure Lengend Snippet: (A) Differences in MDSC, Macrophage and Regulatory.T.cell between high and low BIRC3 groups, error bars represent the mean; (B) scatter plot revealing the correlation of BIRC3 and immune cells (Regulatory.T.cell Macrophage and MDSC); (C) differences in PDCD1, CTLA4 and CD274 between high and low BIRC3 groups, error bars represent the mean; (D) scatter plot revealing the correlation of BIRC3 and immune checkpoints (CD274, CTLA4 and PDCD1); (E) differences in TME scores between high and low BIRC3 groups, error bars represent one SD from the mean; (F) gene set enrichment analysis of BIRC3; (G) the volcano map showed the drugs associated with BIRC3. Red represented positive correlation; blue represented negative correlation.

Techniques:

(A–F) The expression of BIRC3 was downregulated in A498 and 786-O cells, as determined by RT-qPCR and Western blot; (G and H) BIRC3-knockdown suppressed ccRCC cell proliferation in A498 and 786-O cells; (I and J) BIRC3-knockdown suppressed ccRCC cell metastasis in A498 and 786-O cells. * P < 0.05, ** P < 0.01, *** P < 0.001; (K and L) wound healing assay was used to detect the effect of BIRC3-knockdown on ccRCC cell migration. Cell migration ability was represented by the wound gap distance in microscopic field at the time points of 0 and 24 h. (Biological replicates).

Journal: PeerJ

Article Title: Identification and validation of prognostic and tumor microenvironment characteristics of necroptosis index and BIRC3 in clear cell renal cell carcinoma

doi: 10.7717/peerj.16643

Figure Lengend Snippet: (A–F) The expression of BIRC3 was downregulated in A498 and 786-O cells, as determined by RT-qPCR and Western blot; (G and H) BIRC3-knockdown suppressed ccRCC cell proliferation in A498 and 786-O cells; (I and J) BIRC3-knockdown suppressed ccRCC cell metastasis in A498 and 786-O cells. * P < 0.05, ** P < 0.01, *** P < 0.001; (K and L) wound healing assay was used to detect the effect of BIRC3-knockdown on ccRCC cell migration. Cell migration ability was represented by the wound gap distance in microscopic field at the time points of 0 and 24 h. (Biological replicates).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Knockdown, Wound Healing Assay, Migration

(A) “Harmony” and UMAP algorithm to remove batch effects and gathered a total of 26 clusters; (B) single-cell RNA-seq illustrated the distribution of necroptosis index by “AddModuleScore” algorithm in ccRCC; (C and D) necroptosis index wa s significantly up-regulated in ccRCC tumors tissues compared with normal samples both in all cells and tumor cells; (E and F) Single-cell RNA-seq illustrated the distribution of BIRC3 by “AddModuleScore” algorithm in ccRCC and normal tissues; (G and H) BIRC3 was significantly up-regulated in ccRCC tumors tissues compared with normal samples both in all cells and tumor cells; (I) the cell proportion among different patients and correlations of BIRC3 expression level.

Journal: PeerJ

Article Title: Identification and validation of prognostic and tumor microenvironment characteristics of necroptosis index and BIRC3 in clear cell renal cell carcinoma

doi: 10.7717/peerj.16643

Figure Lengend Snippet: (A) “Harmony” and UMAP algorithm to remove batch effects and gathered a total of 26 clusters; (B) single-cell RNA-seq illustrated the distribution of necroptosis index by “AddModuleScore” algorithm in ccRCC; (C and D) necroptosis index wa s significantly up-regulated in ccRCC tumors tissues compared with normal samples both in all cells and tumor cells; (E and F) Single-cell RNA-seq illustrated the distribution of BIRC3 by “AddModuleScore” algorithm in ccRCC and normal tissues; (G and H) BIRC3 was significantly up-regulated in ccRCC tumors tissues compared with normal samples both in all cells and tumor cells; (I) the cell proportion among different patients and correlations of BIRC3 expression level.

Techniques: RNA Sequencing, Expressing

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