c jun Search Results


c jun  (R&D Systems)
90
R&D Systems c jun
C Jun, supplied by R&D Systems, 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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Average 90 stars, based on 1 article reviews
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jun shrna  (OriGene)
90
OriGene jun shrna
Jun Shrna, supplied by OriGene, 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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Average 90 stars, based on 1 article reviews
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si c jun  (Cell Signaling Technology Inc)
93
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
Si C Jun, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
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phospho c jun ser63 rabbit mab  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc phospho c jun ser63 rabbit mab
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
Phospho C Jun Ser63 Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 1 article reviews
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phospho c jun ser 73  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc phospho c jun ser 73
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
Phospho C Jun Ser 73, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c+jun/Phospho-c-Jun+(Ser73)+Antibody/10__1074_slash_jbc__m308617200-76-35-37
Average 96 stars, based on 1 article reviews
phospho c jun ser 73 - by Bioz Stars, 2026-09
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3270 phospho p70 s6k  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc 3270 phospho p70 s6k
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
3270 Phospho P70 S6k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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3270 phospho p70 s6k - by Bioz Stars, 2026-09
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rabbit anti c jun  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc rabbit anti 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
Rabbit Anti C Jun, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c+jun/c-Jun+Rabbit+mAb/pmc07499972-63-28-30
Average 96 stars, based on 1 article reviews
rabbit anti c jun - by Bioz Stars, 2026-09
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phospho c jun thr91  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc phospho c jun thr91
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
Phospho C Jun Thr91, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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duet 8222  (Cell Signaling Technology Inc)
88
Cell Signaling Technology Inc duet 8222
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
Duet 8222, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c+jun/PhosphoPlus+c-Jun+(Ser73)+Antibody+Duet/10__1074_slash_jbc__m115__666347-48-32-34
Average 88 stars, based on 1 article reviews
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phospho c jun ser243  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc phospho c jun ser243
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
Phospho C Jun Ser243, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phospho c jun n terminal kinase jnk mouse mab  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc phospho c jun n terminal kinase jnk mouse mab
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
Phospho C Jun N Terminal Kinase Jnk Mouse Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
phospho c jun n terminal kinase jnk mouse mab - by Bioz Stars, 2026-09
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phospho c jun  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc phospho 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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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