perk Search Results


mouse perk sirna siperk  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology mouse perk sirna siperk
Fig. 5. The effects of ER stress on STING signaling. NRCMs were pre-treated with ER stress activator (Tg, 500 nM) or inhibitor (4-PBA, 5 mM) for 4 h, followed by Ang II (1 μM) incubation for another 24 h. Then, all cells were collected for western blot analysis of (A) <t>p-PERK,</t> p-IRE-1α, p-eIF2α, STING, (B) p-TBK1, p-IRF3 and p-NF- κB. (C) NRCMs were transfected with PERK <t>siRNA</t> <t>(siPERK)</t> or siNC for 24 h, and were then subjected to transfection efficiency calculation using western blotting analysis. (D) NRCMs were transfected with siNC or siPERK for 24 h, followed by Ang II (1 μM) treatment for another 24 h. Then, all cells were collected for western blot analysis of p-PERK, PERK and STING. (E) NRCMs were transfected with siIRE-1α or siNC for 24 h, and were then subjected to transfection efficiency mea- surement via western blot analysis. (F) NRCMs were transfected with siNC or siIRE-1α for 24 h, and then were incubated with Ang II (1 μM) for another 24 h. Next, all cells were harvested for western blot analysis of p-IRE-1α, IRE-1α and STING. The data represent as the mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001.
Mouse Perk Sirna Siperk, supplied by Santa Cruz Biotechnology, 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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alphalisa surefire ultra erk1 2 kit  (Revvity)
91
Revvity alphalisa surefire ultra erk1 2 kit
Fig. 5. The effects of ER stress on STING signaling. NRCMs were pre-treated with ER stress activator (Tg, 500 nM) or inhibitor (4-PBA, 5 mM) for 4 h, followed by Ang II (1 μM) incubation for another 24 h. Then, all cells were collected for western blot analysis of (A) <t>p-PERK,</t> p-IRE-1α, p-eIF2α, STING, (B) p-TBK1, p-IRF3 and p-NF- κB. (C) NRCMs were transfected with PERK <t>siRNA</t> <t>(siPERK)</t> or siNC for 24 h, and were then subjected to transfection efficiency calculation using western blotting analysis. (D) NRCMs were transfected with siNC or siPERK for 24 h, followed by Ang II (1 μM) treatment for another 24 h. Then, all cells were collected for western blot analysis of p-PERK, PERK and STING. (E) NRCMs were transfected with siIRE-1α or siNC for 24 h, and were then subjected to transfection efficiency mea- surement via western blot analysis. (F) NRCMs were transfected with siNC or siIRE-1α for 24 h, and then were incubated with Ang II (1 μM) for another 24 h. Next, all cells were harvested for western blot analysis of p-IRE-1α, IRE-1α and STING. The data represent as the mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001.
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1 ap  (Proteintech)
96
Proteintech 1 ap
Fig. 5. The effects of ER stress on STING signaling. NRCMs were pre-treated with ER stress activator (Tg, 500 nM) or inhibitor (4-PBA, 5 mM) for 4 h, followed by Ang II (1 μM) incubation for another 24 h. Then, all cells were collected for western blot analysis of (A) <t>p-PERK,</t> p-IRE-1α, p-eIF2α, STING, (B) p-TBK1, p-IRF3 and p-NF- κB. (C) NRCMs were transfected with PERK <t>siRNA</t> <t>(siPERK)</t> or siNC for 24 h, and were then subjected to transfection efficiency calculation using western blotting analysis. (D) NRCMs were transfected with siNC or siPERK for 24 h, followed by Ang II (1 μM) treatment for another 24 h. Then, all cells were collected for western blot analysis of p-PERK, PERK and STING. (E) NRCMs were transfected with siIRE-1α or siNC for 24 h, and were then subjected to transfection efficiency mea- surement via western blot analysis. (F) NRCMs were transfected with siNC or siIRE-1α for 24 h, and then were incubated with Ang II (1 μM) for another 24 h. Next, all cells were harvested for western blot analysis of p-IRE-1α, IRE-1α and STING. The data represent as the mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001.
1 Ap, supplied by Proteintech, 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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perk cdna expression plasmid  (Addgene inc)
93
Addgene inc perk cdna expression plasmid
Fig. 5. The effects of ER stress on STING signaling. NRCMs were pre-treated with ER stress activator (Tg, 500 nM) or inhibitor (4-PBA, 5 mM) for 4 h, followed by Ang II (1 μM) incubation for another 24 h. Then, all cells were collected for western blot analysis of (A) <t>p-PERK,</t> p-IRE-1α, p-eIF2α, STING, (B) p-TBK1, p-IRF3 and p-NF- κB. (C) NRCMs were transfected with PERK <t>siRNA</t> <t>(siPERK)</t> or siNC for 24 h, and were then subjected to transfection efficiency calculation using western blotting analysis. (D) NRCMs were transfected with siNC or siPERK for 24 h, followed by Ang II (1 μM) treatment for another 24 h. Then, all cells were collected for western blot analysis of p-PERK, PERK and STING. (E) NRCMs were transfected with siIRE-1α or siNC for 24 h, and were then subjected to transfection efficiency mea- surement via western blot analysis. (F) NRCMs were transfected with siNC or siIRE-1α for 24 h, and then were incubated with Ang II (1 μM) for another 24 h. Next, all cells were harvested for western blot analysis of p-IRE-1α, IRE-1α and STING. The data represent as the mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001.
Perk Cdna Expression Plasmid, supplied by Addgene 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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eif2ak3  (OriGene)
92
OriGene eif2ak3
Fig. 5. The effects of ER stress on STING signaling. NRCMs were pre-treated with ER stress activator (Tg, 500 nM) or inhibitor (4-PBA, 5 mM) for 4 h, followed by Ang II (1 μM) incubation for another 24 h. Then, all cells were collected for western blot analysis of (A) <t>p-PERK,</t> p-IRE-1α, p-eIF2α, STING, (B) p-TBK1, p-IRF3 and p-NF- κB. (C) NRCMs were transfected with PERK <t>siRNA</t> <t>(siPERK)</t> or siNC for 24 h, and were then subjected to transfection efficiency calculation using western blotting analysis. (D) NRCMs were transfected with siNC or siPERK for 24 h, followed by Ang II (1 μM) treatment for another 24 h. Then, all cells were collected for western blot analysis of p-PERK, PERK and STING. (E) NRCMs were transfected with siIRE-1α or siNC for 24 h, and were then subjected to transfection efficiency mea- surement via western blot analysis. (F) NRCMs were transfected with siNC or siIRE-1α for 24 h, and then were incubated with Ang II (1 μM) for another 24 h. Next, all cells were harvested for western blot analysis of p-IRE-1α, IRE-1α and STING. The data represent as the mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001.
Eif2ak3, supplied by OriGene, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti p erk 1 erk 2  (R&D Systems)
90
R&D Systems anti p erk 1 erk 2
Fig. 5. The effects of ER stress on STING signaling. NRCMs were pre-treated with ER stress activator (Tg, 500 nM) or inhibitor (4-PBA, 5 mM) for 4 h, followed by Ang II (1 μM) incubation for another 24 h. Then, all cells were collected for western blot analysis of (A) <t>p-PERK,</t> p-IRE-1α, p-eIF2α, STING, (B) p-TBK1, p-IRF3 and p-NF- κB. (C) NRCMs were transfected with PERK <t>siRNA</t> <t>(siPERK)</t> or siNC for 24 h, and were then subjected to transfection efficiency calculation using western blotting analysis. (D) NRCMs were transfected with siNC or siPERK for 24 h, followed by Ang II (1 μM) treatment for another 24 h. Then, all cells were collected for western blot analysis of p-PERK, PERK and STING. (E) NRCMs were transfected with siIRE-1α or siNC for 24 h, and were then subjected to transfection efficiency mea- surement via western blot analysis. (F) NRCMs were transfected with siNC or siIRE-1α for 24 h, and then were incubated with Ang II (1 μM) for another 24 h. Next, all cells were harvested for western blot analysis of p-IRE-1α, IRE-1α and STING. The data represent as the mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001.
Anti P Erk 1 Erk 2, 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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gsk perk inhibitor  (Toronto Research Chemicals)
86
Toronto Research Chemicals gsk perk inhibitor
(A) CSE (10%)-induced CCN1 secretion in the presence of the inhibitors for ER stress related signaling. Beas2B cells were treated with JNK inhibitor II (10 µM), SB203580 (10 µM) for P38 MAPK, Bay11-7082 (10 µM) for NF-κB, <t>GSK</t> <t>PERK</t> (1 µM) for PERK and γ-secretase inhibitor (10 µM). Next, cells were exposed to CSE (10%) and CCN1 secretion was determined using ELISA as the above. (B) Reduced CCN1 secretion after CSE in the p38 MAPK and JNK siRNA transfected Beas2B cells. Beas2B cells were transfected with siRNA first. After 24 h, these cells were exposed to CSE (10%). After another 24 h, CCN1 secretion was determined using ELISA. (C) CSE (10%) induced JNK and p38 MAPK phosphorylation in Beas2B cells, determined by Western Blot analysis. (D) Deletion of Ire-1α by siRNA reduced CSE triggered CCN1 secretion. Beas2B cells were transfected with Ire-1α siRNA, followed by CSE (10%) exposure. CCN1 secretion was determined using ELISA as the above. Inset: the efficiency of Ire-1α deletion using siRNA. (E) Beas2B cells were transfected with Ire-1α siRNA or control siRNA, followed by CSE (10%). After 8 h, cell lysate was subjected to Western Blot analysis. pJNK, total JNK, p-p38 MAPK and total p38 MAPK were analyzed. (F) Beas2B cells were treated with ER stress inducer, thapsigargin (1 µM). CCN1 release was analyzed using ELISA. To determine the signaling pathways involved in the ER stress inducer triggered CCN1 release, we pre-treated the cells using a variety of pathway inhibitors as shown, followed by thapsigargin (1 µM). (G) Similarly, the above samples from (B) were subjected to ELISA to determine CCN1 secretion in p38 MAPK and JNK siRNA treated Beas2B cells. (H) Blocking of Ire-1α and/or PERK suppressed CCN1 secretion induced by thapsigargin. Beas2B cells were transfected with control siRNA or Ire-1α siRNA, treated with solvent or PERK inhibitor (10 µM), followed by thapsigargin (1 µM). CCN1 secretion was measured as above mentioned. *p<.05 All figures above represented two or three independent experiments with similar results.
Gsk Perk Inhibitor, supplied by Toronto Research Chemicals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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perk  (Rockland Immunochemicals)
93
Rockland Immunochemicals perk
(A) CSE (10%)-induced CCN1 secretion in the presence of the inhibitors for ER stress related signaling. Beas2B cells were treated with JNK inhibitor II (10 µM), SB203580 (10 µM) for P38 MAPK, Bay11-7082 (10 µM) for NF-κB, <t>GSK</t> <t>PERK</t> (1 µM) for PERK and γ-secretase inhibitor (10 µM). Next, cells were exposed to CSE (10%) and CCN1 secretion was determined using ELISA as the above. (B) Reduced CCN1 secretion after CSE in the p38 MAPK and JNK siRNA transfected Beas2B cells. Beas2B cells were transfected with siRNA first. After 24 h, these cells were exposed to CSE (10%). After another 24 h, CCN1 secretion was determined using ELISA. (C) CSE (10%) induced JNK and p38 MAPK phosphorylation in Beas2B cells, determined by Western Blot analysis. (D) Deletion of Ire-1α by siRNA reduced CSE triggered CCN1 secretion. Beas2B cells were transfected with Ire-1α siRNA, followed by CSE (10%) exposure. CCN1 secretion was determined using ELISA as the above. Inset: the efficiency of Ire-1α deletion using siRNA. (E) Beas2B cells were transfected with Ire-1α siRNA or control siRNA, followed by CSE (10%). After 8 h, cell lysate was subjected to Western Blot analysis. pJNK, total JNK, p-p38 MAPK and total p38 MAPK were analyzed. (F) Beas2B cells were treated with ER stress inducer, thapsigargin (1 µM). CCN1 release was analyzed using ELISA. To determine the signaling pathways involved in the ER stress inducer triggered CCN1 release, we pre-treated the cells using a variety of pathway inhibitors as shown, followed by thapsigargin (1 µM). (G) Similarly, the above samples from (B) were subjected to ELISA to determine CCN1 secretion in p38 MAPK and JNK siRNA treated Beas2B cells. (H) Blocking of Ire-1α and/or PERK suppressed CCN1 secretion induced by thapsigargin. Beas2B cells were transfected with control siRNA or Ire-1α siRNA, treated with solvent or PERK inhibitor (10 µM), followed by thapsigargin (1 µM). CCN1 secretion was measured as above mentioned. *p<.05 All figures above represented two or three independent experiments with similar results.
Perk, supplied by Rockland Immunochemicals, 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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gsk2606414  (Toronto Research Chemicals)
88
Toronto Research Chemicals gsk2606414
The PERK inhibitors <t>GSK2606414</t> (GSK'414) and GSK2656157 (GSK'157) protect cells from TNF-mediated RIPK1 kinase-dependent cell death. (a–c) Immortalized MEFs were pretreated for 30 min with the indicated compounds (1 μM GSK'157, 10 μM NEC-1s, 250 ng/ml CHX, 1 μM TAK1-inh, 50 μM ZVAD-fmk) and TNF-mediated cell death was measured in function of time by SytoxGreen positivity.40 RIPK1-independent apoptosis was induced by CHX+mTNF (1 ng/ml), RIPK1 kinase-dependent apoptosis by TAK1-inh+hTNF (0.1 ng/ml) and RIPK1 kinase-dependent necroptosis by ZVAD+hTNF (1 ng/ml). The results are presented as mean±S.E.M. of three independent experiments. Statistical significance was determined by two-way ANOVA. Significance between samples is indicated in the figures as follows: NS= P > 0.05; *P<0.05; **P<0.01; ***P<0.001. (d–f) Immortalized MEFs (d and e) and L929 cells (f) were pretreated for 30 min with increasing concentrations of the indicated compounds in presence or absence of TAK1-inh (1 μM) or ZVAD-fmk (50 μM) and TNF-mediated cell death was measured at 24 h post-stimulation by SytoxGreen positivity.40 (g) Immortalized MEFs were pretreated for 30 min with GSK'157 (0.1 μg/ml) or NEC-1s (10 μg/ml), stimulated with hTNF (1 ng/ml) for the indicated time, and the cell lysates were then immunoblotted as indicated. (h) Immortalized MEFs were pretreated for 30 min with ZVAD-fmk (50 μM), TAK1-inh (1 μM) and the indicated compounds and then stimulated for 2 h with hTNF (1 ng/ml). Complex IIb was isolated by FADD immunoprecipitation and RIPK1 and caspase-8 binding revealed by immunoblotting
Gsk2606414, supplied by Toronto Research Chemicals, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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alphascreen surefire phospho p erk1 2 thr202 tyr204 assay kits  (Revvity)
91
Revvity alphascreen surefire phospho p erk1 2 thr202 tyr204 assay kits
The PERK inhibitors <t>GSK2606414</t> (GSK'414) and GSK2656157 (GSK'157) protect cells from TNF-mediated RIPK1 kinase-dependent cell death. (a–c) Immortalized MEFs were pretreated for 30 min with the indicated compounds (1 μM GSK'157, 10 μM NEC-1s, 250 ng/ml CHX, 1 μM TAK1-inh, 50 μM ZVAD-fmk) and TNF-mediated cell death was measured in function of time by SytoxGreen positivity.40 RIPK1-independent apoptosis was induced by CHX+mTNF (1 ng/ml), RIPK1 kinase-dependent apoptosis by TAK1-inh+hTNF (0.1 ng/ml) and RIPK1 kinase-dependent necroptosis by ZVAD+hTNF (1 ng/ml). The results are presented as mean±S.E.M. of three independent experiments. Statistical significance was determined by two-way ANOVA. Significance between samples is indicated in the figures as follows: NS= P > 0.05; *P<0.05; **P<0.01; ***P<0.001. (d–f) Immortalized MEFs (d and e) and L929 cells (f) were pretreated for 30 min with increasing concentrations of the indicated compounds in presence or absence of TAK1-inh (1 μM) or ZVAD-fmk (50 μM) and TNF-mediated cell death was measured at 24 h post-stimulation by SytoxGreen positivity.40 (g) Immortalized MEFs were pretreated for 30 min with GSK'157 (0.1 μg/ml) or NEC-1s (10 μg/ml), stimulated with hTNF (1 ng/ml) for the indicated time, and the cell lysates were then immunoblotted as indicated. (h) Immortalized MEFs were pretreated for 30 min with ZVAD-fmk (50 μM), TAK1-inh (1 μM) and the indicated compounds and then stimulated for 2 h with hTNF (1 ng/ml). Complex IIb was isolated by FADD immunoprecipitation and RIPK1 and caspase-8 binding revealed by immunoblotting
Alphascreen Surefire Phospho P Erk1 2 Thr202 Tyr204 Assay Kits, supplied by Revvity, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pgfp c shlenti  (OriGene)
94
OriGene pgfp c shlenti
The PERK inhibitors <t>GSK2606414</t> (GSK'414) and GSK2656157 (GSK'157) protect cells from TNF-mediated RIPK1 kinase-dependent cell death. (a–c) Immortalized MEFs were pretreated for 30 min with the indicated compounds (1 μM GSK'157, 10 μM NEC-1s, 250 ng/ml CHX, 1 μM TAK1-inh, 50 μM ZVAD-fmk) and TNF-mediated cell death was measured in function of time by SytoxGreen positivity.40 RIPK1-independent apoptosis was induced by CHX+mTNF (1 ng/ml), RIPK1 kinase-dependent apoptosis by TAK1-inh+hTNF (0.1 ng/ml) and RIPK1 kinase-dependent necroptosis by ZVAD+hTNF (1 ng/ml). The results are presented as mean±S.E.M. of three independent experiments. Statistical significance was determined by two-way ANOVA. Significance between samples is indicated in the figures as follows: NS= P > 0.05; *P<0.05; **P<0.01; ***P<0.001. (d–f) Immortalized MEFs (d and e) and L929 cells (f) were pretreated for 30 min with increasing concentrations of the indicated compounds in presence or absence of TAK1-inh (1 μM) or ZVAD-fmk (50 μM) and TNF-mediated cell death was measured at 24 h post-stimulation by SytoxGreen positivity.40 (g) Immortalized MEFs were pretreated for 30 min with GSK'157 (0.1 μg/ml) or NEC-1s (10 μg/ml), stimulated with hTNF (1 ng/ml) for the indicated time, and the cell lysates were then immunoblotted as indicated. (h) Immortalized MEFs were pretreated for 30 min with ZVAD-fmk (50 μM), TAK1-inh (1 μM) and the indicated compounds and then stimulated for 2 h with hTNF (1 ng/ml). Complex IIb was isolated by FADD immunoprecipitation and RIPK1 and caspase-8 binding revealed by immunoblotting
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eif2ak3 shrna  (OriGene)
94
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The PERK inhibitors <t>GSK2606414</t> (GSK'414) and GSK2656157 (GSK'157) protect cells from TNF-mediated RIPK1 kinase-dependent cell death. (a–c) Immortalized MEFs were pretreated for 30 min with the indicated compounds (1 μM GSK'157, 10 μM NEC-1s, 250 ng/ml CHX, 1 μM TAK1-inh, 50 μM ZVAD-fmk) and TNF-mediated cell death was measured in function of time by SytoxGreen positivity.40 RIPK1-independent apoptosis was induced by CHX+mTNF (1 ng/ml), RIPK1 kinase-dependent apoptosis by TAK1-inh+hTNF (0.1 ng/ml) and RIPK1 kinase-dependent necroptosis by ZVAD+hTNF (1 ng/ml). The results are presented as mean±S.E.M. of three independent experiments. Statistical significance was determined by two-way ANOVA. Significance between samples is indicated in the figures as follows: NS= P > 0.05; *P<0.05; **P<0.01; ***P<0.001. (d–f) Immortalized MEFs (d and e) and L929 cells (f) were pretreated for 30 min with increasing concentrations of the indicated compounds in presence or absence of TAK1-inh (1 μM) or ZVAD-fmk (50 μM) and TNF-mediated cell death was measured at 24 h post-stimulation by SytoxGreen positivity.40 (g) Immortalized MEFs were pretreated for 30 min with GSK'157 (0.1 μg/ml) or NEC-1s (10 μg/ml), stimulated with hTNF (1 ng/ml) for the indicated time, and the cell lysates were then immunoblotted as indicated. (h) Immortalized MEFs were pretreated for 30 min with ZVAD-fmk (50 μM), TAK1-inh (1 μM) and the indicated compounds and then stimulated for 2 h with hTNF (1 ng/ml). Complex IIb was isolated by FADD immunoprecipitation and RIPK1 and caspase-8 binding revealed by immunoblotting
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Image Search Results


Fig. 5. The effects of ER stress on STING signaling. NRCMs were pre-treated with ER stress activator (Tg, 500 nM) or inhibitor (4-PBA, 5 mM) for 4 h, followed by Ang II (1 μM) incubation for another 24 h. Then, all cells were collected for western blot analysis of (A) p-PERK, p-IRE-1α, p-eIF2α, STING, (B) p-TBK1, p-IRF3 and p-NF- κB. (C) NRCMs were transfected with PERK siRNA (siPERK) or siNC for 24 h, and were then subjected to transfection efficiency calculation using western blotting analysis. (D) NRCMs were transfected with siNC or siPERK for 24 h, followed by Ang II (1 μM) treatment for another 24 h. Then, all cells were collected for western blot analysis of p-PERK, PERK and STING. (E) NRCMs were transfected with siIRE-1α or siNC for 24 h, and were then subjected to transfection efficiency mea- surement via western blot analysis. (F) NRCMs were transfected with siNC or siIRE-1α for 24 h, and then were incubated with Ang II (1 μM) for another 24 h. Next, all cells were harvested for western blot analysis of p-IRE-1α, IRE-1α and STING. The data represent as the mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001.

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: STING is an essential regulator of heart inflammation and fibrosis in mice with pathological cardiac hypertrophy via endoplasmic reticulum (ER) stress.

doi: 10.1016/j.biopha.2020.110022

Figure Lengend Snippet: Fig. 5. The effects of ER stress on STING signaling. NRCMs were pre-treated with ER stress activator (Tg, 500 nM) or inhibitor (4-PBA, 5 mM) for 4 h, followed by Ang II (1 μM) incubation for another 24 h. Then, all cells were collected for western blot analysis of (A) p-PERK, p-IRE-1α, p-eIF2α, STING, (B) p-TBK1, p-IRF3 and p-NF- κB. (C) NRCMs were transfected with PERK siRNA (siPERK) or siNC for 24 h, and were then subjected to transfection efficiency calculation using western blotting analysis. (D) NRCMs were transfected with siNC or siPERK for 24 h, followed by Ang II (1 μM) treatment for another 24 h. Then, all cells were collected for western blot analysis of p-PERK, PERK and STING. (E) NRCMs were transfected with siIRE-1α or siNC for 24 h, and were then subjected to transfection efficiency mea- surement via western blot analysis. (F) NRCMs were transfected with siNC or siIRE-1α for 24 h, and then were incubated with Ang II (1 μM) for another 24 h. Next, all cells were harvested for western blot analysis of p-IRE-1α, IRE-1α and STING. The data represent as the mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.001.

Article Snippet: The mouse PERK siRNA (siPERK) and IRE-1α siRNA (siIRE-1α) were purchased from Santa Cruz (USA) to knock down PERK and IRE-1α, respectively.

Techniques: Incubation, Western Blot, Transfection

(A) CSE (10%)-induced CCN1 secretion in the presence of the inhibitors for ER stress related signaling. Beas2B cells were treated with JNK inhibitor II (10 µM), SB203580 (10 µM) for P38 MAPK, Bay11-7082 (10 µM) for NF-κB, GSK PERK (1 µM) for PERK and γ-secretase inhibitor (10 µM). Next, cells were exposed to CSE (10%) and CCN1 secretion was determined using ELISA as the above. (B) Reduced CCN1 secretion after CSE in the p38 MAPK and JNK siRNA transfected Beas2B cells. Beas2B cells were transfected with siRNA first. After 24 h, these cells were exposed to CSE (10%). After another 24 h, CCN1 secretion was determined using ELISA. (C) CSE (10%) induced JNK and p38 MAPK phosphorylation in Beas2B cells, determined by Western Blot analysis. (D) Deletion of Ire-1α by siRNA reduced CSE triggered CCN1 secretion. Beas2B cells were transfected with Ire-1α siRNA, followed by CSE (10%) exposure. CCN1 secretion was determined using ELISA as the above. Inset: the efficiency of Ire-1α deletion using siRNA. (E) Beas2B cells were transfected with Ire-1α siRNA or control siRNA, followed by CSE (10%). After 8 h, cell lysate was subjected to Western Blot analysis. pJNK, total JNK, p-p38 MAPK and total p38 MAPK were analyzed. (F) Beas2B cells were treated with ER stress inducer, thapsigargin (1 µM). CCN1 release was analyzed using ELISA. To determine the signaling pathways involved in the ER stress inducer triggered CCN1 release, we pre-treated the cells using a variety of pathway inhibitors as shown, followed by thapsigargin (1 µM). (G) Similarly, the above samples from (B) were subjected to ELISA to determine CCN1 secretion in p38 MAPK and JNK siRNA treated Beas2B cells. (H) Blocking of Ire-1α and/or PERK suppressed CCN1 secretion induced by thapsigargin. Beas2B cells were transfected with control siRNA or Ire-1α siRNA, treated with solvent or PERK inhibitor (10 µM), followed by thapsigargin (1 µM). CCN1 secretion was measured as above mentioned. *p<.05 All figures above represented two or three independent experiments with similar results.

Journal: PLoS ONE

Article Title: CCN1 Secretion Induced by Cigarette Smoking Extracts Augments IL-8 Release from Bronchial Epithelial Cells

doi: 10.1371/journal.pone.0068199

Figure Lengend Snippet: (A) CSE (10%)-induced CCN1 secretion in the presence of the inhibitors for ER stress related signaling. Beas2B cells were treated with JNK inhibitor II (10 µM), SB203580 (10 µM) for P38 MAPK, Bay11-7082 (10 µM) for NF-κB, GSK PERK (1 µM) for PERK and γ-secretase inhibitor (10 µM). Next, cells were exposed to CSE (10%) and CCN1 secretion was determined using ELISA as the above. (B) Reduced CCN1 secretion after CSE in the p38 MAPK and JNK siRNA transfected Beas2B cells. Beas2B cells were transfected with siRNA first. After 24 h, these cells were exposed to CSE (10%). After another 24 h, CCN1 secretion was determined using ELISA. (C) CSE (10%) induced JNK and p38 MAPK phosphorylation in Beas2B cells, determined by Western Blot analysis. (D) Deletion of Ire-1α by siRNA reduced CSE triggered CCN1 secretion. Beas2B cells were transfected with Ire-1α siRNA, followed by CSE (10%) exposure. CCN1 secretion was determined using ELISA as the above. Inset: the efficiency of Ire-1α deletion using siRNA. (E) Beas2B cells were transfected with Ire-1α siRNA or control siRNA, followed by CSE (10%). After 8 h, cell lysate was subjected to Western Blot analysis. pJNK, total JNK, p-p38 MAPK and total p38 MAPK were analyzed. (F) Beas2B cells were treated with ER stress inducer, thapsigargin (1 µM). CCN1 release was analyzed using ELISA. To determine the signaling pathways involved in the ER stress inducer triggered CCN1 release, we pre-treated the cells using a variety of pathway inhibitors as shown, followed by thapsigargin (1 µM). (G) Similarly, the above samples from (B) were subjected to ELISA to determine CCN1 secretion in p38 MAPK and JNK siRNA treated Beas2B cells. (H) Blocking of Ire-1α and/or PERK suppressed CCN1 secretion induced by thapsigargin. Beas2B cells were transfected with control siRNA or Ire-1α siRNA, treated with solvent or PERK inhibitor (10 µM), followed by thapsigargin (1 µM). CCN1 secretion was measured as above mentioned. *p<.05 All figures above represented two or three independent experiments with similar results.

Article Snippet: NAC, ascorbic acid, GSH, brefeldin A, tetraethylammonium chloride (TEA), α18-glycyrrhetinic acid (GA), daidzein, 2-bromopalmitate (2-BP), TGN-020, thapsigargin, 4-Phenylbutyric acid (4-PBA), bay 11-7082 were purchased from Sigma-aldrich (St. Louis, MO), tauroursodeoxycholic acid (TUDCA) from EMD Millipore (Merck KGaA, Darmstadt, Germany), salubrinal from Santa Cruz Biotechnology, JNK inhibitor, SB 203580, γ-secretase inhibitor from Calbiochem (Merck KGaA, Darmstadt, Germany), GSK PERK inhibitor from Toronto Research Chemicals (Toronto, Ontario, Canada).

Techniques: Enzyme-linked Immunosorbent Assay, Transfection, Phospho-proteomics, Western Blot, Control, Protein-Protein interactions, Blocking Assay, Solvent

The PERK inhibitors GSK2606414 (GSK'414) and GSK2656157 (GSK'157) protect cells from TNF-mediated RIPK1 kinase-dependent cell death. (a–c) Immortalized MEFs were pretreated for 30 min with the indicated compounds (1 μM GSK'157, 10 μM NEC-1s, 250 ng/ml CHX, 1 μM TAK1-inh, 50 μM ZVAD-fmk) and TNF-mediated cell death was measured in function of time by SytoxGreen positivity.40 RIPK1-independent apoptosis was induced by CHX+mTNF (1 ng/ml), RIPK1 kinase-dependent apoptosis by TAK1-inh+hTNF (0.1 ng/ml) and RIPK1 kinase-dependent necroptosis by ZVAD+hTNF (1 ng/ml). The results are presented as mean±S.E.M. of three independent experiments. Statistical significance was determined by two-way ANOVA. Significance between samples is indicated in the figures as follows: NS= P > 0.05; *P<0.05; **P<0.01; ***P<0.001. (d–f) Immortalized MEFs (d and e) and L929 cells (f) were pretreated for 30 min with increasing concentrations of the indicated compounds in presence or absence of TAK1-inh (1 μM) or ZVAD-fmk (50 μM) and TNF-mediated cell death was measured at 24 h post-stimulation by SytoxGreen positivity.40 (g) Immortalized MEFs were pretreated for 30 min with GSK'157 (0.1 μg/ml) or NEC-1s (10 μg/ml), stimulated with hTNF (1 ng/ml) for the indicated time, and the cell lysates were then immunoblotted as indicated. (h) Immortalized MEFs were pretreated for 30 min with ZVAD-fmk (50 μM), TAK1-inh (1 μM) and the indicated compounds and then stimulated for 2 h with hTNF (1 ng/ml). Complex IIb was isolated by FADD immunoprecipitation and RIPK1 and caspase-8 binding revealed by immunoblotting

Journal: Cell Death and Differentiation

Article Title: When PERK inhibitors turn out to be new potent RIPK1 inhibitors: critical issues on the specificity and use of GSK2606414 and GSK2656157

doi: 10.1038/cdd.2017.58

Figure Lengend Snippet: The PERK inhibitors GSK2606414 (GSK'414) and GSK2656157 (GSK'157) protect cells from TNF-mediated RIPK1 kinase-dependent cell death. (a–c) Immortalized MEFs were pretreated for 30 min with the indicated compounds (1 μM GSK'157, 10 μM NEC-1s, 250 ng/ml CHX, 1 μM TAK1-inh, 50 μM ZVAD-fmk) and TNF-mediated cell death was measured in function of time by SytoxGreen positivity.40 RIPK1-independent apoptosis was induced by CHX+mTNF (1 ng/ml), RIPK1 kinase-dependent apoptosis by TAK1-inh+hTNF (0.1 ng/ml) and RIPK1 kinase-dependent necroptosis by ZVAD+hTNF (1 ng/ml). The results are presented as mean±S.E.M. of three independent experiments. Statistical significance was determined by two-way ANOVA. Significance between samples is indicated in the figures as follows: NS= P > 0.05; *P<0.05; **P<0.01; ***P<0.001. (d–f) Immortalized MEFs (d and e) and L929 cells (f) were pretreated for 30 min with increasing concentrations of the indicated compounds in presence or absence of TAK1-inh (1 μM) or ZVAD-fmk (50 μM) and TNF-mediated cell death was measured at 24 h post-stimulation by SytoxGreen positivity.40 (g) Immortalized MEFs were pretreated for 30 min with GSK'157 (0.1 μg/ml) or NEC-1s (10 μg/ml), stimulated with hTNF (1 ng/ml) for the indicated time, and the cell lysates were then immunoblotted as indicated. (h) Immortalized MEFs were pretreated for 30 min with ZVAD-fmk (50 μM), TAK1-inh (1 μM) and the indicated compounds and then stimulated for 2 h with hTNF (1 ng/ml). Complex IIb was isolated by FADD immunoprecipitation and RIPK1 and caspase-8 binding revealed by immunoblotting

Article Snippet: Antibodies and reagents were purchased from the following companies: anti-p-I κ B α (Ser32/36; Cell Signaling Technology, Danvers, MA, USA; no. 9246), anti-p-p38 (Thr180/Tyr182; Cell Signaling Technology; no. 9211), anti-p38 (Cell Signaling Technology; no. 9212), anti-CHOP (Cell Signaling Technology; no. 2895), anti-PERK (Cell Signaling Technology; no. 3192), anti-I κ B α (Santa Cruz Biotechnology; Dallas, TX, USA; no. sc-371), anti-FADD (Santa Cruz Biotechnology; no. sc-6036), anti-RIPK1 (BD Transduction Laboratories, San Jose, CA, USA; no. 610166), anti-Caspase-8 (Abnova, Taipei city, Taiwan; no. MAB3429), anti-FADD (Enzo Life Sciences, Farmingdale, NY, USA; no. ADI-AAM-212-E), anti-HSP90 (Abcam, Cambridge, UK; no. 13480), anti-ATF4 (Proteintech group, Manchester, UK; no. 10835-1), Tunicamicyn (Tm; Sigma-Aldrich, St Louis, MO, USA; no. T7765), Cycloheximide (CHX; Sigma-Aldrich; no. C-7698), 9-Epimer-11,12-dihydro-(5Z)-7-Oxozeanol ((5Z)-7-Oxozeaenol or TAK1-inh; AnalytiCon Discovery GmbH, Potsdam, Germany; no. NP-0009245), ZVAD-fmk (Bachem, Bubendorf, Switzerland; no. N-1510), AMG'44 (Tocris Bioscience, Bristol, UK; no. 5517), GSK2606414 (Toronto Research Chemicals, Toronto, ON, Canada; no. G797800), GSK2656157 (ApexBio, Boston, MA, USA; no. B2175), NEC-1 (Calbiochem, San Diego, CA, USA; no. 480065), NEC-1s (Laboratory of Medicinal Chemistry, University of Antwerp, Belgium), GSK'963 (Aobius, Gloucester, MA, USA; no. 9775).

Techniques: Isolation, Immunoprecipitation, Binding Assay, Western Blot

GSK2606414 and GSK2656157 are potent RIPK1 inhibitors

Journal: Cell Death and Differentiation

Article Title: When PERK inhibitors turn out to be new potent RIPK1 inhibitors: critical issues on the specificity and use of GSK2606414 and GSK2656157

doi: 10.1038/cdd.2017.58

Figure Lengend Snippet: GSK2606414 and GSK2656157 are potent RIPK1 inhibitors

Article Snippet: Antibodies and reagents were purchased from the following companies: anti-p-I κ B α (Ser32/36; Cell Signaling Technology, Danvers, MA, USA; no. 9246), anti-p-p38 (Thr180/Tyr182; Cell Signaling Technology; no. 9211), anti-p38 (Cell Signaling Technology; no. 9212), anti-CHOP (Cell Signaling Technology; no. 2895), anti-PERK (Cell Signaling Technology; no. 3192), anti-I κ B α (Santa Cruz Biotechnology; Dallas, TX, USA; no. sc-371), anti-FADD (Santa Cruz Biotechnology; no. sc-6036), anti-RIPK1 (BD Transduction Laboratories, San Jose, CA, USA; no. 610166), anti-Caspase-8 (Abnova, Taipei city, Taiwan; no. MAB3429), anti-FADD (Enzo Life Sciences, Farmingdale, NY, USA; no. ADI-AAM-212-E), anti-HSP90 (Abcam, Cambridge, UK; no. 13480), anti-ATF4 (Proteintech group, Manchester, UK; no. 10835-1), Tunicamicyn (Tm; Sigma-Aldrich, St Louis, MO, USA; no. T7765), Cycloheximide (CHX; Sigma-Aldrich; no. C-7698), 9-Epimer-11,12-dihydro-(5Z)-7-Oxozeanol ((5Z)-7-Oxozeaenol or TAK1-inh; AnalytiCon Discovery GmbH, Potsdam, Germany; no. NP-0009245), ZVAD-fmk (Bachem, Bubendorf, Switzerland; no. N-1510), AMG'44 (Tocris Bioscience, Bristol, UK; no. 5517), GSK2606414 (Toronto Research Chemicals, Toronto, ON, Canada; no. G797800), GSK2656157 (ApexBio, Boston, MA, USA; no. B2175), NEC-1 (Calbiochem, San Diego, CA, USA; no. 480065), NEC-1s (Laboratory of Medicinal Chemistry, University of Antwerp, Belgium), GSK'963 (Aobius, Gloucester, MA, USA; no. 9775).

Techniques: Activity Assay, Phospho-proteomics, Electrophoretic Mobility Shift Assay

GSK2606414 and GSK2656157 are potent inhibitors of RIPK1. (a and b) Quantification of ADP-Glo kinase assays performed with recombinant hRIPK1 (a) or hPERK (b) in presence of increasing concentrations of NEC-1s, GSK'414, GSK'157 and AMG'44. (c) Chemical structures of GSK2606414, GSK2656157, the ligand in pdb-entry 4NEU (compound 8)27 and in pdb-entry 5HX6 (GSK'481).30 (d) Zoom into the ATP-site of RIPK1 crystal structure 4NEU (cartoon, from N-blue to C-red) in complex with the aminoisoquinoline-inhibitor compound 8 (sticks, cyan). The best-docked pose of GSK'157 (sticks, white) occupies the ATP-site in a similar manner as compound 8. Figure prepared with PyMOL

Journal: Cell Death and Differentiation

Article Title: When PERK inhibitors turn out to be new potent RIPK1 inhibitors: critical issues on the specificity and use of GSK2606414 and GSK2656157

doi: 10.1038/cdd.2017.58

Figure Lengend Snippet: GSK2606414 and GSK2656157 are potent inhibitors of RIPK1. (a and b) Quantification of ADP-Glo kinase assays performed with recombinant hRIPK1 (a) or hPERK (b) in presence of increasing concentrations of NEC-1s, GSK'414, GSK'157 and AMG'44. (c) Chemical structures of GSK2606414, GSK2656157, the ligand in pdb-entry 4NEU (compound 8)27 and in pdb-entry 5HX6 (GSK'481).30 (d) Zoom into the ATP-site of RIPK1 crystal structure 4NEU (cartoon, from N-blue to C-red) in complex with the aminoisoquinoline-inhibitor compound 8 (sticks, cyan). The best-docked pose of GSK'157 (sticks, white) occupies the ATP-site in a similar manner as compound 8. Figure prepared with PyMOL

Article Snippet: Antibodies and reagents were purchased from the following companies: anti-p-I κ B α (Ser32/36; Cell Signaling Technology, Danvers, MA, USA; no. 9246), anti-p-p38 (Thr180/Tyr182; Cell Signaling Technology; no. 9211), anti-p38 (Cell Signaling Technology; no. 9212), anti-CHOP (Cell Signaling Technology; no. 2895), anti-PERK (Cell Signaling Technology; no. 3192), anti-I κ B α (Santa Cruz Biotechnology; Dallas, TX, USA; no. sc-371), anti-FADD (Santa Cruz Biotechnology; no. sc-6036), anti-RIPK1 (BD Transduction Laboratories, San Jose, CA, USA; no. 610166), anti-Caspase-8 (Abnova, Taipei city, Taiwan; no. MAB3429), anti-FADD (Enzo Life Sciences, Farmingdale, NY, USA; no. ADI-AAM-212-E), anti-HSP90 (Abcam, Cambridge, UK; no. 13480), anti-ATF4 (Proteintech group, Manchester, UK; no. 10835-1), Tunicamicyn (Tm; Sigma-Aldrich, St Louis, MO, USA; no. T7765), Cycloheximide (CHX; Sigma-Aldrich; no. C-7698), 9-Epimer-11,12-dihydro-(5Z)-7-Oxozeanol ((5Z)-7-Oxozeaenol or TAK1-inh; AnalytiCon Discovery GmbH, Potsdam, Germany; no. NP-0009245), ZVAD-fmk (Bachem, Bubendorf, Switzerland; no. N-1510), AMG'44 (Tocris Bioscience, Bristol, UK; no. 5517), GSK2606414 (Toronto Research Chemicals, Toronto, ON, Canada; no. G797800), GSK2656157 (ApexBio, Boston, MA, USA; no. B2175), NEC-1 (Calbiochem, San Diego, CA, USA; no. 480065), NEC-1s (Laboratory of Medicinal Chemistry, University of Antwerp, Belgium), GSK'963 (Aobius, Gloucester, MA, USA; no. 9775).

Techniques: Recombinant