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si c jun  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc si c jun
    Involvement of the MAPK-p38, JNK, and CaMK-II pathways in cisplatin- and erastin-induced VDAC1 overexpression. A HeLa cells were serum-starved for 5 h, pre-incubated (2 h) with the indicated concentrations of SP203580, SP600125 or KN-62, then incubated with or without cisplatin (15 µM). After 16 h, RNA was isolated and subjected to q-RT-PCR using VDAC1 mRNA specific primers (Table S2). B , C HeLa cells were serum-starved for 5 h, pre-incubated with the indicated inhibitor (10 µM, 2 h) then incubated with or without cisplatin (10 or 15 µM, 48 h) and subjected to VDAC1 oligomerization assayed as described in the Methods section. The immunoblot with the positions of VDAC1 monomers, dimers, trimers and multimers are indicated ( B ) and the levels of VDAC1 dimers were quantified ( C ). D , E HeLa cells were serum-starved for 5 h, and pre-incubated with the JNK inhibitor, SP600125 or with the CaMK-II inhibitor, KN-62 (5 or10 µM, 2 h), then incubated with or without cisplatin (15µM, 48 h) and subjected to immunoblotting using specific antibodies against P-c-Jun, P-ATF-1 or b-actin ( D ) and their levels were quantified ( E ). F , G C6 cells were serum starved for 2 h, pre-incubated with p38-MAPK inhibitor, SB203580 (5 and 10 µM, 2 h), then incubated with or without erastin (10 µM, 24 h). Cells were subjected to immunoblotting using specific antibodies against VDAC1, P-c-Jun, P-c-Fos or P-p38. Ponceau S staining is shown as a loading control ( F ). The protein relative levels were then quantified ( G ). H-K HeLa cells were transfected with non-targeting siRNA <t>(si-NT)</t> <t>or</t> <t>si-c-Jun</t> (100 nM) using JetPrime ( H , I ), or with si-p38 (100 nM) using SilentFect transfection reagent ( J , K ), as described in the Methods section. At 24 h post-transfection, cells were treated with cisplatin (15 µM, 48 h) and subjected to immunoblotting for P-c-Jun, P-p38, P-c-Fos or b-actin expression using specific antibodies (H, J) . Protein expression levels were quantified ( I , K ). Cell death was analyzed by PI standing and FACS analysis and is presented in the bottom of the blots ( H , J ). Results are the means ± SEM (n = 3). ∗p ≤ 0.05, ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.001; NS = non-significant
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    Images

    1) Product Images from "Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis"

    Article Title: Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis

    Journal: Cell Communication and Signaling : CCS

    doi: 10.1186/s12964-025-02647-5

    Involvement of the MAPK-p38, JNK, and CaMK-II pathways in cisplatin- and erastin-induced VDAC1 overexpression. A HeLa cells were serum-starved for 5 h, pre-incubated (2 h) with the indicated concentrations of SP203580, SP600125 or KN-62, then incubated with or without cisplatin (15 µM). After 16 h, RNA was isolated and subjected to q-RT-PCR using VDAC1 mRNA specific primers (Table S2). B , C HeLa cells were serum-starved for 5 h, pre-incubated with the indicated inhibitor (10 µM, 2 h) then incubated with or without cisplatin (10 or 15 µM, 48 h) and subjected to VDAC1 oligomerization assayed as described in the Methods section. The immunoblot with the positions of VDAC1 monomers, dimers, trimers and multimers are indicated ( B ) and the levels of VDAC1 dimers were quantified ( C ). D , E HeLa cells were serum-starved for 5 h, and pre-incubated with the JNK inhibitor, SP600125 or with the CaMK-II inhibitor, KN-62 (5 or10 µM, 2 h), then incubated with or without cisplatin (15µM, 48 h) and subjected to immunoblotting using specific antibodies against P-c-Jun, P-ATF-1 or b-actin ( D ) and their levels were quantified ( E ). F , G C6 cells were serum starved for 2 h, pre-incubated with p38-MAPK inhibitor, SB203580 (5 and 10 µM, 2 h), then incubated with or without erastin (10 µM, 24 h). Cells were subjected to immunoblotting using specific antibodies against VDAC1, P-c-Jun, P-c-Fos or P-p38. Ponceau S staining is shown as a loading control ( F ). The protein relative levels were then quantified ( G ). H-K HeLa cells were transfected with non-targeting siRNA (si-NT) or si-c-Jun (100 nM) using JetPrime ( H , I ), or with si-p38 (100 nM) using SilentFect transfection reagent ( J , K ), as described in the Methods section. At 24 h post-transfection, cells were treated with cisplatin (15 µM, 48 h) and subjected to immunoblotting for P-c-Jun, P-p38, P-c-Fos or b-actin expression using specific antibodies (H, J) . Protein expression levels were quantified ( I , K ). Cell death was analyzed by PI standing and FACS analysis and is presented in the bottom of the blots ( H , J ). Results are the means ± SEM (n = 3). ∗p ≤ 0.05, ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.001; NS = non-significant
    Figure Legend Snippet: Involvement of the MAPK-p38, JNK, and CaMK-II pathways in cisplatin- and erastin-induced VDAC1 overexpression. A HeLa cells were serum-starved for 5 h, pre-incubated (2 h) with the indicated concentrations of SP203580, SP600125 or KN-62, then incubated with or without cisplatin (15 µM). After 16 h, RNA was isolated and subjected to q-RT-PCR using VDAC1 mRNA specific primers (Table S2). B , C HeLa cells were serum-starved for 5 h, pre-incubated with the indicated inhibitor (10 µM, 2 h) then incubated with or without cisplatin (10 or 15 µM, 48 h) and subjected to VDAC1 oligomerization assayed as described in the Methods section. The immunoblot with the positions of VDAC1 monomers, dimers, trimers and multimers are indicated ( B ) and the levels of VDAC1 dimers were quantified ( C ). D , E HeLa cells were serum-starved for 5 h, and pre-incubated with the JNK inhibitor, SP600125 or with the CaMK-II inhibitor, KN-62 (5 or10 µM, 2 h), then incubated with or without cisplatin (15µM, 48 h) and subjected to immunoblotting using specific antibodies against P-c-Jun, P-ATF-1 or b-actin ( D ) and their levels were quantified ( E ). F , G C6 cells were serum starved for 2 h, pre-incubated with p38-MAPK inhibitor, SB203580 (5 and 10 µM, 2 h), then incubated with or without erastin (10 µM, 24 h). Cells were subjected to immunoblotting using specific antibodies against VDAC1, P-c-Jun, P-c-Fos or P-p38. Ponceau S staining is shown as a loading control ( F ). The protein relative levels were then quantified ( G ). H-K HeLa cells were transfected with non-targeting siRNA (si-NT) or si-c-Jun (100 nM) using JetPrime ( H , I ), or with si-p38 (100 nM) using SilentFect transfection reagent ( J , K ), as described in the Methods section. At 24 h post-transfection, cells were treated with cisplatin (15 µM, 48 h) and subjected to immunoblotting for P-c-Jun, P-p38, P-c-Fos or b-actin expression using specific antibodies (H, J) . Protein expression levels were quantified ( I , K ). Cell death was analyzed by PI standing and FACS analysis and is presented in the bottom of the blots ( H , J ). Results are the means ± SEM (n = 3). ∗p ≤ 0.05, ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.001; NS = non-significant

    Techniques Used: Over Expression, Incubation, Isolation, Reverse Transcription Polymerase Chain Reaction, Western Blot, Staining, Control, Transfection, Expressing



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    Involvement of the MAPK-p38, JNK, and CaMK-II pathways in cisplatin- and erastin-induced VDAC1 overexpression. A HeLa cells were serum-starved for 5 h, pre-incubated (2 h) with the indicated concentrations of SP203580, SP600125 or KN-62, then incubated with or without cisplatin (15 µM). After 16 h, RNA was isolated and subjected to q-RT-PCR using VDAC1 mRNA specific primers (Table S2). B , C HeLa cells were serum-starved for 5 h, pre-incubated with the indicated inhibitor (10 µM, 2 h) then incubated with or without cisplatin (10 or 15 µM, 48 h) and subjected to VDAC1 oligomerization assayed as described in the Methods section. The immunoblot with the positions of VDAC1 monomers, dimers, trimers and multimers are indicated ( B ) and the levels of VDAC1 dimers were quantified ( C ). D , E HeLa cells were serum-starved for 5 h, and pre-incubated with the JNK inhibitor, SP600125 or with the CaMK-II inhibitor, KN-62 (5 or10 µM, 2 h), then incubated with or without cisplatin (15µM, 48 h) and subjected to immunoblotting using specific antibodies against P-c-Jun, P-ATF-1 or b-actin ( D ) and their levels were quantified ( E ). F , G C6 cells were serum starved for 2 h, pre-incubated with p38-MAPK inhibitor, SB203580 (5 and 10 µM, 2 h), then incubated with or without erastin (10 µM, 24 h). Cells were subjected to immunoblotting using specific antibodies against VDAC1, P-c-Jun, P-c-Fos or P-p38. Ponceau S staining is shown as a loading control ( F ). The protein relative levels were then quantified ( G ). H-K HeLa cells were transfected with non-targeting siRNA (si-NT) or si-c-Jun (100 nM) using JetPrime ( H , I ), or with si-p38 (100 nM) using SilentFect transfection reagent ( J , K ), as described in the Methods section. At 24 h post-transfection, cells were treated with cisplatin (15 µM, 48 h) and subjected to immunoblotting for P-c-Jun, P-p38, P-c-Fos or b-actin expression using specific antibodies (H, J) . Protein expression levels were quantified ( I , K ). Cell death was analyzed by PI standing and FACS analysis and is presented in the bottom of the blots ( H , J ). Results are the means ± SEM (n = 3). ∗p ≤ 0.05, ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.001; NS = non-significant

    Journal: Cell Communication and Signaling : CCS

    Article Title: Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis

    doi: 10.1186/s12964-025-02647-5

    Figure Lengend Snippet: Involvement of the MAPK-p38, JNK, and CaMK-II pathways in cisplatin- and erastin-induced VDAC1 overexpression. A HeLa cells were serum-starved for 5 h, pre-incubated (2 h) with the indicated concentrations of SP203580, SP600125 or KN-62, then incubated with or without cisplatin (15 µM). After 16 h, RNA was isolated and subjected to q-RT-PCR using VDAC1 mRNA specific primers (Table S2). B , C HeLa cells were serum-starved for 5 h, pre-incubated with the indicated inhibitor (10 µM, 2 h) then incubated with or without cisplatin (10 or 15 µM, 48 h) and subjected to VDAC1 oligomerization assayed as described in the Methods section. The immunoblot with the positions of VDAC1 monomers, dimers, trimers and multimers are indicated ( B ) and the levels of VDAC1 dimers were quantified ( C ). D , E HeLa cells were serum-starved for 5 h, and pre-incubated with the JNK inhibitor, SP600125 or with the CaMK-II inhibitor, KN-62 (5 or10 µM, 2 h), then incubated with or without cisplatin (15µM, 48 h) and subjected to immunoblotting using specific antibodies against P-c-Jun, P-ATF-1 or b-actin ( D ) and their levels were quantified ( E ). F , G C6 cells were serum starved for 2 h, pre-incubated with p38-MAPK inhibitor, SB203580 (5 and 10 µM, 2 h), then incubated with or without erastin (10 µM, 24 h). Cells were subjected to immunoblotting using specific antibodies against VDAC1, P-c-Jun, P-c-Fos or P-p38. Ponceau S staining is shown as a loading control ( F ). The protein relative levels were then quantified ( G ). H-K HeLa cells were transfected with non-targeting siRNA (si-NT) or si-c-Jun (100 nM) using JetPrime ( H , I ), or with si-p38 (100 nM) using SilentFect transfection reagent ( J , K ), as described in the Methods section. At 24 h post-transfection, cells were treated with cisplatin (15 µM, 48 h) and subjected to immunoblotting for P-c-Jun, P-p38, P-c-Fos or b-actin expression using specific antibodies (H, J) . Protein expression levels were quantified ( I , K ). Cell death was analyzed by PI standing and FACS analysis and is presented in the bottom of the blots ( H , J ). Results are the means ± SEM (n = 3). ∗p ≤ 0.05, ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.001; NS = non-significant

    Article Snippet: The nucleotides in italic were 2′-O-methyl modified. si-c-JUN (CST-6203 S) and si-p38-MAPK (CST-6564 S) were purchased from Cell Signaling Technology (Danvers, MS).

    Techniques: Over Expression, Incubation, Isolation, Reverse Transcription Polymerase Chain Reaction, Western Blot, Staining, Control, Transfection, Expressing

    Cells were transfected with either PKR siRNA or control siRNA, then PKR mRNA was quantified by real-time RT-PCR; PKR was knocked down (A). Cells were transfected with PKR-expression plasmid (pPKR) or control plasmid (pOS8), then subjected to real-time RT-PCR; PKR mRNA was upregulated by pPKR (B). Mean ± SEM of six replicates. **p<0.01. The amount of HCV core protein in JFH1 and H77s cells were measured by ELISA. HCV core protein was stably expressed in both cell types at least three days after transfection with the HCV-RNA (C). The amount of HCV mRNA in JFH1 and H77s cells was measured by real-time RT-PCR. HCV RNA was expressed in both cell types at least three days after transfection with the HCV-RNA (D). Mean ± SEM of four replicates. PKR and phosphorylated PKR protein expression evaluated by Western blotting; results confirmed PKR mRNA data (E).

    Journal: PLoS ONE

    Article Title: Protein Kinase R Modulates c-Fos and c-Jun Signaling to Promote Proliferation of Hepatocellular Carcinoma with Hepatitis C Virus Infection

    doi: 10.1371/journal.pone.0067750

    Figure Lengend Snippet: Cells were transfected with either PKR siRNA or control siRNA, then PKR mRNA was quantified by real-time RT-PCR; PKR was knocked down (A). Cells were transfected with PKR-expression plasmid (pPKR) or control plasmid (pOS8), then subjected to real-time RT-PCR; PKR mRNA was upregulated by pPKR (B). Mean ± SEM of six replicates. **p<0.01. The amount of HCV core protein in JFH1 and H77s cells were measured by ELISA. HCV core protein was stably expressed in both cell types at least three days after transfection with the HCV-RNA (C). The amount of HCV mRNA in JFH1 and H77s cells was measured by real-time RT-PCR. HCV RNA was expressed in both cell types at least three days after transfection with the HCV-RNA (D). Mean ± SEM of four replicates. PKR and phosphorylated PKR protein expression evaluated by Western blotting; results confirmed PKR mRNA data (E).

    Article Snippet: Control siRNA was obtained from Cosmo Bio (Tokyo, Japan); c-Fos siRNA and c-Jun si-RNA were obtained from Thermo Fisher Scientific.

    Techniques: Transfection, Quantitative RT-PCR, Expressing, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Stable Transfection, Western Blot

    RNA from HCC specimens of 34 patients, 17 HCC specimens with HCV infection (HCC positive HCC), and 17 HCC without HCV infection (HCC negative HCC). Each group was divided into two subsections by the median PKR mRNA values: Low PKR and High PKR. c-Jun mRNA (A) and c-Fos mRNA (B) were measured. c-Fos mRNA significantly correlated with c-Jun mRNA (r = 0.816, P<0.001) (C). The four human HCC specimens having the highest (High PKR) and the four having the lowest (Low PKR) PKR protein expression were analyzed by Western blotting. c-Jun and c-Fos in the High PKR group were activated more than in the Low PKR group (D).

    Journal: PLoS ONE

    Article Title: Protein Kinase R Modulates c-Fos and c-Jun Signaling to Promote Proliferation of Hepatocellular Carcinoma with Hepatitis C Virus Infection

    doi: 10.1371/journal.pone.0067750

    Figure Lengend Snippet: RNA from HCC specimens of 34 patients, 17 HCC specimens with HCV infection (HCC positive HCC), and 17 HCC without HCV infection (HCC negative HCC). Each group was divided into two subsections by the median PKR mRNA values: Low PKR and High PKR. c-Jun mRNA (A) and c-Fos mRNA (B) were measured. c-Fos mRNA significantly correlated with c-Jun mRNA (r = 0.816, P<0.001) (C). The four human HCC specimens having the highest (High PKR) and the four having the lowest (Low PKR) PKR protein expression were analyzed by Western blotting. c-Jun and c-Fos in the High PKR group were activated more than in the Low PKR group (D).

    Article Snippet: Control siRNA was obtained from Cosmo Bio (Tokyo, Japan); c-Fos siRNA and c-Jun si-RNA were obtained from Thermo Fisher Scientific.

    Techniques: Infection, Expressing, Western Blot