jnk inhibitor v  (Millipore)


Bioz Verified Symbol Millipore is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 95

    Structured Review

    Millipore jnk inhibitor v
    POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM <t>JNK</t> <t>inhibitor</t> V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Jnk Inhibitor V, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jnk inhibitor v/product/Millipore
    Average 95 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    jnk inhibitor v - by Bioz Stars, 2020-02
    95/100 stars

    Images

    1) Product Images from "Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol"

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol

    Journal: Molecular Cancer

    doi: 10.1186/s12943-015-0374-5

    POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Figure Legend Snippet: POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Techniques Used:

    The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p
    Figure Legend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Techniques Used: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Figure Legend Snippet: POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Techniques Used:

    The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p
    Figure Legend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Techniques Used: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    2) Product Images from "Protective Role of Complement C3 Against Cytokine-Mediated β-Cell Apoptosis"

    Article Title: Protective Role of Complement C3 Against Cytokine-Mediated β-Cell Apoptosis

    Journal: Endocrinology

    doi: 10.1210/en.2017-00104

    C3 inhibition activates the JNK pathway. (a–e) INS-1E cells were transfected with siCtrl (C) or siRNA targeting rat C3 (siC3 no. 1, C3). Cells were then left untreated or treated with IL-1 β plus IFN- γ (10 and 100 U/mL, respectively) as indicated under the figure. (a–d) P-JNK, JNK, P–c-Jun, c-Jun, and α -tubulin were measured by western blot. (a) Images are representative of four independent experiments. (b–d) Densitometry analysis of the western blots for (b) P-JNK, (c) P–c-Jun, and (d) c-Jun. Quantification of the area under curve (AUC) of P-JNK and P–c-Jun are shown in the inset graphs in (b) and (c), respectively. (e) c-Jun mRNA expression was analyzed by real-time polymerase chain reaction (RT-PCR) and normalized by the housekeeping gene GAPDH. (f and g) INS-1E cells transfec ted with siCtrl (C) or siRNAs targeting rat C3 (siC3 no. 1, C3), JNK (J), or both (C3 + J). Cells were then left untreated (NT) or treated with IL-1 β plus IFN- γ (10 and 100 U/mL, respectively) for 16 hours. (f) P-JNK, JNK, cleaved caspase-3, and α -tubulin were measured by western blot. Images are representative of four independent experiments. (g) Apoptosis was evaluated using HO and PI staining in INS-1E cells. (h and i) INS-1E cells were transfected with siCtrl (C) or siRNA targeting rat C3 (siC3 no. 1, C3). Cells were then left untreated (NT) or treated with IL-1 β plus IFN- γ in the absence or presence of JNK inhibitor V (JNKi). (h) Cleaved caspase-3 and α -tubulin were measured by western blot. Images are representative of four independent experiments. (i) Apoptosis was evaluated using HO and PI staining in INS-1E. (j) Apoptosis was evaluated using HO and PI staining in dispersed human islets transfected with siCtrl, siC3 no. 2 h , siJNK h , or siC3 no. 2 h + siJNK h and exposed for 48 hours to cytokines. Results are means ± SEM of three to five independent experiments. * P ≤ 0.05, ** P ≤ 0.01, and *** P
    Figure Legend Snippet: C3 inhibition activates the JNK pathway. (a–e) INS-1E cells were transfected with siCtrl (C) or siRNA targeting rat C3 (siC3 no. 1, C3). Cells were then left untreated or treated with IL-1 β plus IFN- γ (10 and 100 U/mL, respectively) as indicated under the figure. (a–d) P-JNK, JNK, P–c-Jun, c-Jun, and α -tubulin were measured by western blot. (a) Images are representative of four independent experiments. (b–d) Densitometry analysis of the western blots for (b) P-JNK, (c) P–c-Jun, and (d) c-Jun. Quantification of the area under curve (AUC) of P-JNK and P–c-Jun are shown in the inset graphs in (b) and (c), respectively. (e) c-Jun mRNA expression was analyzed by real-time polymerase chain reaction (RT-PCR) and normalized by the housekeeping gene GAPDH. (f and g) INS-1E cells transfec ted with siCtrl (C) or siRNAs targeting rat C3 (siC3 no. 1, C3), JNK (J), or both (C3 + J). Cells were then left untreated (NT) or treated with IL-1 β plus IFN- γ (10 and 100 U/mL, respectively) for 16 hours. (f) P-JNK, JNK, cleaved caspase-3, and α -tubulin were measured by western blot. Images are representative of four independent experiments. (g) Apoptosis was evaluated using HO and PI staining in INS-1E cells. (h and i) INS-1E cells were transfected with siCtrl (C) or siRNA targeting rat C3 (siC3 no. 1, C3). Cells were then left untreated (NT) or treated with IL-1 β plus IFN- γ in the absence or presence of JNK inhibitor V (JNKi). (h) Cleaved caspase-3 and α -tubulin were measured by western blot. Images are representative of four independent experiments. (i) Apoptosis was evaluated using HO and PI staining in INS-1E. (j) Apoptosis was evaluated using HO and PI staining in dispersed human islets transfected with siCtrl, siC3 no. 2 h , siJNK h , or siC3 no. 2 h + siJNK h and exposed for 48 hours to cytokines. Results are means ± SEM of three to five independent experiments. * P ≤ 0.05, ** P ≤ 0.01, and *** P

    Techniques Used: Inhibition, Transfection, Western Blot, Expressing, Real-time Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Staining

    3) Product Images from "Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol"

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol

    Journal: Molecular Cancer

    doi: 10.1186/s12943-015-0374-5

    POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Figure Legend Snippet: POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Techniques Used:

    The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p
    Figure Legend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Techniques Used: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Figure Legend Snippet: POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Techniques Used:

    The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p
    Figure Legend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Techniques Used: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    4) Product Images from "Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol"

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol

    Journal: Molecular Cancer

    doi: 10.1186/s12943-015-0374-5

    POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Figure Legend Snippet: POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Techniques Used:

    The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p
    Figure Legend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Techniques Used: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Figure Legend Snippet: POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Techniques Used:

    The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p
    Figure Legend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Techniques Used: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    5) Product Images from "Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells"

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells

    Journal: Journal of Innate Immunity

    doi: 10.1159/000496034

    JNK activation is required for CVB replication and cell death following infection of pancreatic human islets. a–d Dispersed pancreatic human islets were infected with CVB5 or CVB4 at MOI 5 for 24 h, in the presence or not of JNK inhibitor V (JNK inh V; 5 μM). a Cell viability was quantified using nuclear dyes ( n = 5). b Viral titers were determined in the presence or absence of JNK inhibitor V ( n = 4). c , d VP1 expression was evaluated by Western blot ( n = 3–4). * p
    Figure Legend Snippet: JNK activation is required for CVB replication and cell death following infection of pancreatic human islets. a–d Dispersed pancreatic human islets were infected with CVB5 or CVB4 at MOI 5 for 24 h, in the presence or not of JNK inhibitor V (JNK inh V; 5 μM). a Cell viability was quantified using nuclear dyes ( n = 5). b Viral titers were determined in the presence or absence of JNK inhibitor V ( n = 4). c , d VP1 expression was evaluated by Western blot ( n = 3–4). * p

    Techniques Used: Activation Assay, Infection, Expressing, Western Blot

    JNK inhibition reduces CVB5-induced β cell apoptosis and viral replication in INS-1E cells. a–e INS-1E cells were infected with CVB5 at MOI 1 for 24 h in the presence or absence of the chemical JNK inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM). a Phosphorylation of JNK was determined by Western blot and quantified by densitometry ( n = 3–4). b , c Apoptosis was evaluated using nuclear dyes and cleavage of caspase 3 (Casp 3), was evaluated by Western blot ( n = 3–4). d Viral replication was quantified by viral titration (described in Methods) ( n = 2–4). e VP1 expression was determined by Western blot and quantified by densitometry ( n = 3). * p
    Figure Legend Snippet: JNK inhibition reduces CVB5-induced β cell apoptosis and viral replication in INS-1E cells. a–e INS-1E cells were infected with CVB5 at MOI 1 for 24 h in the presence or absence of the chemical JNK inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM). a Phosphorylation of JNK was determined by Western blot and quantified by densitometry ( n = 3–4). b , c Apoptosis was evaluated using nuclear dyes and cleavage of caspase 3 (Casp 3), was evaluated by Western blot ( n = 3–4). d Viral replication was quantified by viral titration (described in Methods) ( n = 2–4). e VP1 expression was determined by Western blot and quantified by densitometry ( n = 3). * p

    Techniques Used: Inhibition, Infection, Western Blot, Titration, Expressing

    Prevention of JNK phosphorylation regulates virus-induced cell death and viral protein expression in the human β cell line, EndoC-βH1. a–f EndoC-βH1 cells were infected or not with CVB5 at MOI 5, alone or in combination with the JNK chemical inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM), for 24 h. a , d JNK activation was determined by Western blot ( n = 3). b , e Cell viability was quantified using nuclear dyes ( n = 4). c , f VP1 expression was evaluated by Western blot ( n = 3–4). * p
    Figure Legend Snippet: Prevention of JNK phosphorylation regulates virus-induced cell death and viral protein expression in the human β cell line, EndoC-βH1. a–f EndoC-βH1 cells were infected or not with CVB5 at MOI 5, alone or in combination with the JNK chemical inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM), for 24 h. a , d JNK activation was determined by Western blot ( n = 3). b , e Cell viability was quantified using nuclear dyes ( n = 4). c , f VP1 expression was evaluated by Western blot ( n = 3–4). * p

    Techniques Used: Expressing, Infection, Activation Assay, Western Blot

    6) Product Images from "Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells"

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells

    Journal: Journal of Innate Immunity

    doi: 10.1159/000496034

    JNK activation is required for CVB replication and cell death following infection of pancreatic human islets. a–d Dispersed pancreatic human islets were infected with CVB5 or CVB4 at MOI 5 for 24 h, in the presence or not of JNK inhibitor V (JNK inh V; 5 μM). a Cell viability was quantified using nuclear dyes ( n = 5). b Viral titers were determined in the presence or absence of JNK inhibitor V ( n = 4). c , d VP1 expression was evaluated by Western blot ( n = 3–4). * p
    Figure Legend Snippet: JNK activation is required for CVB replication and cell death following infection of pancreatic human islets. a–d Dispersed pancreatic human islets were infected with CVB5 or CVB4 at MOI 5 for 24 h, in the presence or not of JNK inhibitor V (JNK inh V; 5 μM). a Cell viability was quantified using nuclear dyes ( n = 5). b Viral titers were determined in the presence or absence of JNK inhibitor V ( n = 4). c , d VP1 expression was evaluated by Western blot ( n = 3–4). * p

    Techniques Used: Activation Assay, Infection, Expressing, Western Blot

    JNK inhibition reduces CVB5-induced β cell apoptosis and viral replication in INS-1E cells. a–e INS-1E cells were infected with CVB5 at MOI 1 for 24 h in the presence or absence of the chemical JNK inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM). a Phosphorylation of JNK was determined by Western blot and quantified by densitometry ( n = 3–4). b , c Apoptosis was evaluated using nuclear dyes and cleavage of caspase 3 (Casp 3), was evaluated by Western blot ( n = 3–4). d Viral replication was quantified by viral titration (described in Methods) ( n = 2–4). e VP1 expression was determined by Western blot and quantified by densitometry ( n = 3). * p
    Figure Legend Snippet: JNK inhibition reduces CVB5-induced β cell apoptosis and viral replication in INS-1E cells. a–e INS-1E cells were infected with CVB5 at MOI 1 for 24 h in the presence or absence of the chemical JNK inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM). a Phosphorylation of JNK was determined by Western blot and quantified by densitometry ( n = 3–4). b , c Apoptosis was evaluated using nuclear dyes and cleavage of caspase 3 (Casp 3), was evaluated by Western blot ( n = 3–4). d Viral replication was quantified by viral titration (described in Methods) ( n = 2–4). e VP1 expression was determined by Western blot and quantified by densitometry ( n = 3). * p

    Techniques Used: Inhibition, Infection, Western Blot, Titration, Expressing

    Prevention of JNK phosphorylation regulates virus-induced cell death and viral protein expression in the human β cell line, EndoC-βH1. a–f EndoC-βH1 cells were infected or not with CVB5 at MOI 5, alone or in combination with the JNK chemical inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM), for 24 h. a , d JNK activation was determined by Western blot ( n = 3). b , e Cell viability was quantified using nuclear dyes ( n = 4). c , f VP1 expression was evaluated by Western blot ( n = 3–4). * p
    Figure Legend Snippet: Prevention of JNK phosphorylation regulates virus-induced cell death and viral protein expression in the human β cell line, EndoC-βH1. a–f EndoC-βH1 cells were infected or not with CVB5 at MOI 5, alone or in combination with the JNK chemical inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM), for 24 h. a , d JNK activation was determined by Western blot ( n = 3). b , e Cell viability was quantified using nuclear dyes ( n = 4). c , f VP1 expression was evaluated by Western blot ( n = 3–4). * p

    Techniques Used: Expressing, Infection, Activation Assay, Western Blot

    7) Product Images from "Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol"

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol

    Journal: Molecular Cancer

    doi: 10.1186/s12943-015-0374-5

    POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Figure Legend Snippet: POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Techniques Used:

    The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p
    Figure Legend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Techniques Used: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Figure Legend Snippet: POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Techniques Used:

    The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p
    Figure Legend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Techniques Used: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    8) Product Images from "TRAIL enhances paracetamol-induced liver sinusoidal endothelial cell death in a Bim- and Bid-dependent manner"

    Article Title: TRAIL enhances paracetamol-induced liver sinusoidal endothelial cell death in a Bim- and Bid-dependent manner

    Journal: Cell Death & Disease

    doi: 10.1038/cddis.2012.185

    Paracetamol induced Bim expression is JNK-dependent. skHep-1 or EA.hy926 cells were pretreated (60 min) with increasing concentrations of the JNK inhibitor V (1, 3 and 10 μ M) and stimulated with 10 mM paracetamol for 6 h. bim -mRNA expression was measured by quantitative RT-PCR. GAPDH was used to normalize bim -expression levels ( a ). skHep-1 and EA.hy926 cells were treated as described above and Bim protein expression was analyzed by western blot. Tubulin was used to normalize protein loadings ( b ). After pretreatment with 3 μ M JNK inhibitor V, cells were stimulated with 10 mM paracetamol and 30 ng/ml, respectively 3 ng/ml TRAIL, or the combination thereof for 6 h and DEVD cleavage was measured ( c ). Mean values±S.D. triplicates are shown for quantitative RT-PCR and DEVDase assay. A typical experiment out of three is shown for western blot analysis. ** P
    Figure Legend Snippet: Paracetamol induced Bim expression is JNK-dependent. skHep-1 or EA.hy926 cells were pretreated (60 min) with increasing concentrations of the JNK inhibitor V (1, 3 and 10 μ M) and stimulated with 10 mM paracetamol for 6 h. bim -mRNA expression was measured by quantitative RT-PCR. GAPDH was used to normalize bim -expression levels ( a ). skHep-1 and EA.hy926 cells were treated as described above and Bim protein expression was analyzed by western blot. Tubulin was used to normalize protein loadings ( b ). After pretreatment with 3 μ M JNK inhibitor V, cells were stimulated with 10 mM paracetamol and 30 ng/ml, respectively 3 ng/ml TRAIL, or the combination thereof for 6 h and DEVD cleavage was measured ( c ). Mean values±S.D. triplicates are shown for quantitative RT-PCR and DEVDase assay. A typical experiment out of three is shown for western blot analysis. ** P

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot

    9) Product Images from "Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells"

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells

    Journal: Journal of Innate Immunity

    doi: 10.1159/000496034

    JNK activation is required for CVB replication and cell death following infection of pancreatic human islets. a–d Dispersed pancreatic human islets were infected with CVB5 or CVB4 at MOI 5 for 24 h, in the presence or not of JNK inhibitor V (JNK inh V; 5 μM). a Cell viability was quantified using nuclear dyes ( n = 5). b Viral titers were determined in the presence or absence of JNK inhibitor V ( n = 4). c , d VP1 expression was evaluated by Western blot ( n = 3–4). * p
    Figure Legend Snippet: JNK activation is required for CVB replication and cell death following infection of pancreatic human islets. a–d Dispersed pancreatic human islets were infected with CVB5 or CVB4 at MOI 5 for 24 h, in the presence or not of JNK inhibitor V (JNK inh V; 5 μM). a Cell viability was quantified using nuclear dyes ( n = 5). b Viral titers were determined in the presence or absence of JNK inhibitor V ( n = 4). c , d VP1 expression was evaluated by Western blot ( n = 3–4). * p

    Techniques Used: Activation Assay, Infection, Expressing, Western Blot

    JNK inhibition reduces CVB5-induced β cell apoptosis and viral replication in INS-1E cells. a–e INS-1E cells were infected with CVB5 at MOI 1 for 24 h in the presence or absence of the chemical JNK inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM). a Phosphorylation of JNK was determined by Western blot and quantified by densitometry ( n = 3–4). b , c Apoptosis was evaluated using nuclear dyes and cleavage of caspase 3 (Casp 3), was evaluated by Western blot ( n = 3–4). d Viral replication was quantified by viral titration (described in Methods) ( n = 2–4). e VP1 expression was determined by Western blot and quantified by densitometry ( n = 3). * p
    Figure Legend Snippet: JNK inhibition reduces CVB5-induced β cell apoptosis and viral replication in INS-1E cells. a–e INS-1E cells were infected with CVB5 at MOI 1 for 24 h in the presence or absence of the chemical JNK inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM). a Phosphorylation of JNK was determined by Western blot and quantified by densitometry ( n = 3–4). b , c Apoptosis was evaluated using nuclear dyes and cleavage of caspase 3 (Casp 3), was evaluated by Western blot ( n = 3–4). d Viral replication was quantified by viral titration (described in Methods) ( n = 2–4). e VP1 expression was determined by Western blot and quantified by densitometry ( n = 3). * p

    Techniques Used: Inhibition, Infection, Western Blot, Titration, Expressing

    Prevention of JNK phosphorylation regulates virus-induced cell death and viral protein expression in the human β cell line, EndoC-βH1. a–f EndoC-βH1 cells were infected or not with CVB5 at MOI 5, alone or in combination with the JNK chemical inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM), for 24 h. a , d JNK activation was determined by Western blot ( n = 3). b , e Cell viability was quantified using nuclear dyes ( n = 4). c , f VP1 expression was evaluated by Western blot ( n = 3–4). * p
    Figure Legend Snippet: Prevention of JNK phosphorylation regulates virus-induced cell death and viral protein expression in the human β cell line, EndoC-βH1. a–f EndoC-βH1 cells were infected or not with CVB5 at MOI 5, alone or in combination with the JNK chemical inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM), for 24 h. a , d JNK activation was determined by Western blot ( n = 3). b , e Cell viability was quantified using nuclear dyes ( n = 4). c , f VP1 expression was evaluated by Western blot ( n = 3–4). * p

    Techniques Used: Expressing, Infection, Activation Assay, Western Blot

    10) Product Images from "Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells"

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells

    Journal: Journal of Innate Immunity

    doi: 10.1159/000496034

    JNK activation is required for CVB replication and cell death following infection of pancreatic human islets. a–d Dispersed pancreatic human islets were infected with CVB5 or CVB4 at MOI 5 for 24 h, in the presence or not of JNK inhibitor V (JNK inh V; 5 μM). a Cell viability was quantified using nuclear dyes ( n = 5). b Viral titers were determined in the presence or absence of JNK inhibitor V ( n = 4). c , d VP1 expression was evaluated by Western blot ( n = 3–4). * p
    Figure Legend Snippet: JNK activation is required for CVB replication and cell death following infection of pancreatic human islets. a–d Dispersed pancreatic human islets were infected with CVB5 or CVB4 at MOI 5 for 24 h, in the presence or not of JNK inhibitor V (JNK inh V; 5 μM). a Cell viability was quantified using nuclear dyes ( n = 5). b Viral titers were determined in the presence or absence of JNK inhibitor V ( n = 4). c , d VP1 expression was evaluated by Western blot ( n = 3–4). * p

    Techniques Used: Activation Assay, Infection, Expressing, Western Blot

    JNK inhibition reduces CVB5-induced β cell apoptosis and viral replication in INS-1E cells. a–e INS-1E cells were infected with CVB5 at MOI 1 for 24 h in the presence or absence of the chemical JNK inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM). a Phosphorylation of JNK was determined by Western blot and quantified by densitometry ( n = 3–4). b , c Apoptosis was evaluated using nuclear dyes and cleavage of caspase 3 (Casp 3), was evaluated by Western blot ( n = 3–4). d Viral replication was quantified by viral titration (described in Methods) ( n = 2–4). e VP1 expression was determined by Western blot and quantified by densitometry ( n = 3). * p
    Figure Legend Snippet: JNK inhibition reduces CVB5-induced β cell apoptosis and viral replication in INS-1E cells. a–e INS-1E cells were infected with CVB5 at MOI 1 for 24 h in the presence or absence of the chemical JNK inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM). a Phosphorylation of JNK was determined by Western blot and quantified by densitometry ( n = 3–4). b , c Apoptosis was evaluated using nuclear dyes and cleavage of caspase 3 (Casp 3), was evaluated by Western blot ( n = 3–4). d Viral replication was quantified by viral titration (described in Methods) ( n = 2–4). e VP1 expression was determined by Western blot and quantified by densitometry ( n = 3). * p

    Techniques Used: Inhibition, Infection, Western Blot, Titration, Expressing

    Prevention of JNK phosphorylation regulates virus-induced cell death and viral protein expression in the human β cell line, EndoC-βH1. a–f EndoC-βH1 cells were infected or not with CVB5 at MOI 5, alone or in combination with the JNK chemical inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM), for 24 h. a , d JNK activation was determined by Western blot ( n = 3). b , e Cell viability was quantified using nuclear dyes ( n = 4). c , f VP1 expression was evaluated by Western blot ( n = 3–4). * p
    Figure Legend Snippet: Prevention of JNK phosphorylation regulates virus-induced cell death and viral protein expression in the human β cell line, EndoC-βH1. a–f EndoC-βH1 cells were infected or not with CVB5 at MOI 5, alone or in combination with the JNK chemical inhibitors SP600125 (10 μM) or JNK inhibitor V (JNK inh V; 5 μM), for 24 h. a , d JNK activation was determined by Western blot ( n = 3). b , e Cell viability was quantified using nuclear dyes ( n = 4). c , f VP1 expression was evaluated by Western blot ( n = 3–4). * p

    Techniques Used: Expressing, Infection, Activation Assay, Western Blot

    Related Articles

    Flow Cytometry:

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol
    Article Snippet: Cell death assay U87 and U251 cells were pretreated for 30 minutes with JNK inhibitor V [1,3-Benzothiazol-2-yl-(2-((2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl)acetonitrile; Calbiochem], an inhibitor of JNK1/2 activation, before treatment with 0.5 mM POH and 0.5 mM POH plus 0.5 μM JNK inhibitor V. After 24 hours of incubation, the cells were suspended in annexin and propidium iodide binding buffer as specified in the TACS Annexin V-FITC apoptosis detection kit (R & D Systems). .. The samples were analyzed using a BD Accuri C6 flow cytometer (BD Biosciences).

    Luciferase:

    Article Title: Gremlin 2 promotes differentiation of embryonic stem cells to atrial fate by activation of the JNK signaling pathway
    Article Snippet: The effectiveness of BMP signaling inhibition was monitored using ES cells stably transfected with the luciferase gene under the control of the BMP responsive element in the Id2 promoter ( BRE2 -Luc ) [ ]. .. JNK 2inhibitor II (SP600125, Tocris Biosciences) and JNK Inhibitor V (AS601245, EMD Millipore) were used at 10 μM.

    Binding Assay:

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol
    Article Snippet: .. Cell death assay U87 and U251 cells were pretreated for 30 minutes with JNK inhibitor V [1,3-Benzothiazol-2-yl-(2-((2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl)acetonitrile; Calbiochem], an inhibitor of JNK1/2 activation, before treatment with 0.5 mM POH and 0.5 mM POH plus 0.5 μM JNK inhibitor V. After 24 hours of incubation, the cells were suspended in annexin and propidium iodide binding buffer as specified in the TACS Annexin V-FITC apoptosis detection kit (R & D Systems). .. The samples were analyzed using a BD Accuri C6 flow cytometer (BD Biosciences).

    Stable Transfection:

    Article Title: Gremlin 2 promotes differentiation of embryonic stem cells to atrial fate by activation of the JNK signaling pathway
    Article Snippet: The effectiveness of BMP signaling inhibition was monitored using ES cells stably transfected with the luciferase gene under the control of the BMP responsive element in the Id2 promoter ( BRE2 -Luc ) [ ]. .. JNK 2inhibitor II (SP600125, Tocris Biosciences) and JNK Inhibitor V (AS601245, EMD Millipore) were used at 10 μM.

    Activation Assay:

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells
    Article Snippet: .. Prevention of JNK activation by SP600125 or JNK inhibitor V decreased the viral titers of both viruses by > 60 and > 90%, respectively (Fig. ; online suppl.), which is in line with their potency as JNK inhibitors (Fig. ; online suppl.). .. JNK inhibition also reduced viral protein expression (Fig. ; online suppl.).

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol
    Article Snippet: .. Cell death assay U87 and U251 cells were pretreated for 30 minutes with JNK inhibitor V [1,3-Benzothiazol-2-yl-(2-((2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl)acetonitrile; Calbiochem], an inhibitor of JNK1/2 activation, before treatment with 0.5 mM POH and 0.5 mM POH plus 0.5 μM JNK inhibitor V. After 24 hours of incubation, the cells were suspended in annexin and propidium iodide binding buffer as specified in the TACS Annexin V-FITC apoptosis detection kit (R & D Systems). .. The samples were analyzed using a BD Accuri C6 flow cytometer (BD Biosciences).

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol
    Article Snippet: .. Caspase-3 activation U87 and U251 cells were treated for 24 hours with 0.1% DMSO or 0.5 μM JNK inhibitor V (control groups) and 0.5 mM POH or 0.5 mM POH plus 0.5 μM JNK inhibitor V. The cells that received JNK inhibitor V were pretreated with this inhibitor for 30 minutes before treatment. .. After 24 hours of incubation, the cells were fixed with 4% paraformaldehyde for 15 min. After this period, the cells were extensively washed in PBS (phosphate buffered saline) and unspecific sites were blocked with 3% bovine serum albumin (BSA), 5% normal goat serum (NGS) and 0.2% Triton X-100 (Vetec) diluted in PBS for 1 hour before immunoreactions with the following primary antibody: rabbit anti-cleaved caspase-3 (1:100, Cell Signaling).

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells
    Article Snippet: .. Since the JNK activation was not observed early during viral infection, SP600125, JNK inhibitor V, or DMSO alone (control) was added to the cell medium at the moment of the viral infection and maintained until the end of the experiment. .. The chemical chaperone TUDCA (Calbiochem) was dissolved in water and used at a final concentration of 125 μM, based on previous dose-response experiments [ ].

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells
    Article Snippet: The JNK inhibitors SP600125 (Sigma-Aldrich) and JNK inhibitor V (Calbiochem, Darmstadt, Germany) were prepared in DMSO and used at concentrations of 10 and 5 µM, respectively. .. Since the JNK activation was not observed early during viral infection, SP600125, JNK inhibitor V, or DMSO alone (control) was added to the cell medium at the moment of the viral infection and maintained until the end of the experiment.

    Transfection:

    Article Title: Protective Role of Complement C3 Against Cytokine-Mediated β-Cell Apoptosis
    Article Snippet: Where indicated, cells were transfected with 1 μg/mL of the synthetic double-stranded analog polyinosinic-polycytidylic acid (PIC; InvivoGen, San Diego, CA) ( ). .. Forskolin (FK), diazoxide, the phosphoinositide 3-kinase (PI3K) inhibitor wortmannin (Sigma-Aldrich, Bornem, Belgium) and the JNK inhibitor V (Calbiochem, San Diego, CA) were diluted in dimethyl sulfoxide and used at concentrations of 20 μM, 100 μM, 100 nM, and 5 μM, respectively.

    Article Title: Gremlin 2 promotes differentiation of embryonic stem cells to atrial fate by activation of the JNK signaling pathway
    Article Snippet: The effectiveness of BMP signaling inhibition was monitored using ES cells stably transfected with the luciferase gene under the control of the BMP responsive element in the Id2 promoter ( BRE2 -Luc ) [ ]. .. JNK 2inhibitor II (SP600125, Tocris Biosciences) and JNK Inhibitor V (AS601245, EMD Millipore) were used at 10 μM.

    Infection:

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells
    Article Snippet: .. Furthermore, the JNK inhibitor V decreased (by > 60%) the viral titers in human islets infected with CVB5 or CVB4 (Fig. ). .. This was paralleled by a significant reduction in viral protein expression in CVB5 and CVB4-infected EndoC-βH1 cells (Fig. ; online suppl. ) and human islets (Fig. ).

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells
    Article Snippet: .. Since the JNK activation was not observed early during viral infection, SP600125, JNK inhibitor V, or DMSO alone (control) was added to the cell medium at the moment of the viral infection and maintained until the end of the experiment. .. The chemical chaperone TUDCA (Calbiochem) was dissolved in water and used at a final concentration of 125 μM, based on previous dose-response experiments [ ].

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells
    Article Snippet: The JNK inhibitors SP600125 (Sigma-Aldrich) and JNK inhibitor V (Calbiochem, Darmstadt, Germany) were prepared in DMSO and used at concentrations of 10 and 5 µM, respectively. .. Since the JNK activation was not observed early during viral infection, SP600125, JNK inhibitor V, or DMSO alone (control) was added to the cell medium at the moment of the viral infection and maintained until the end of the experiment.

    Cytometry:

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol
    Article Snippet: Cell death assay U87 and U251 cells were pretreated for 30 minutes with JNK inhibitor V [1,3-Benzothiazol-2-yl-(2-((2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl)acetonitrile; Calbiochem], an inhibitor of JNK1/2 activation, before treatment with 0.5 mM POH and 0.5 mM POH plus 0.5 μM JNK inhibitor V. After 24 hours of incubation, the cells were suspended in annexin and propidium iodide binding buffer as specified in the TACS Annexin V-FITC apoptosis detection kit (R & D Systems). .. The samples were analyzed using a BD Accuri C6 flow cytometer (BD Biosciences).

    Concentration Assay:

    Article Title: Protective Role of Complement C3 Against Cytokine-Mediated β-Cell Apoptosis
    Article Snippet: Forskolin (FK), diazoxide, the phosphoinositide 3-kinase (PI3K) inhibitor wortmannin (Sigma-Aldrich, Bornem, Belgium) and the JNK inhibitor V (Calbiochem, San Diego, CA) were diluted in dimethyl sulfoxide and used at concentrations of 20 μM, 100 μM, 100 nM, and 5 μM, respectively. .. At the concentration used, diazoxide inhibited insulin secretion by > 60% (data not shown).

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells
    Article Snippet: The JNK inhibitors SP600125 (Sigma-Aldrich) and JNK inhibitor V (Calbiochem, Darmstadt, Germany) were prepared in DMSO and used at concentrations of 10 and 5 µM, respectively. .. We have previously shown that this concentration induces specific JNK inhibition [ ].

    Incubation:

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol
    Article Snippet: .. Cell death assay U87 and U251 cells were pretreated for 30 minutes with JNK inhibitor V [1,3-Benzothiazol-2-yl-(2-((2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl)acetonitrile; Calbiochem], an inhibitor of JNK1/2 activation, before treatment with 0.5 mM POH and 0.5 mM POH plus 0.5 μM JNK inhibitor V. After 24 hours of incubation, the cells were suspended in annexin and propidium iodide binding buffer as specified in the TACS Annexin V-FITC apoptosis detection kit (R & D Systems). .. The samples were analyzed using a BD Accuri C6 flow cytometer (BD Biosciences).

    Inhibition:

    Article Title: IL-4 induces proliferation in prostate cancer PC3 cells under nutrient-depletion stress through the activation of the JNK-pathway and survivin upregulation
    Article Snippet: .. Supporting the importance of JNK is the fact that a JNK-inhibitor-V, which demonstrated specific inhibition of JNK phosphorylation , also showed suppression of IL-4-induced proliferation ( ). ..

    Article Title: Gremlin 2 promotes differentiation of embryonic stem cells to atrial fate by activation of the JNK signaling pathway
    Article Snippet: The effectiveness of BMP signaling inhibition was monitored using ES cells stably transfected with the luciferase gene under the control of the BMP responsive element in the Id2 promoter ( BRE2 -Luc ) [ ]. .. JNK 2inhibitor II (SP600125, Tocris Biosciences) and JNK Inhibitor V (AS601245, EMD Millipore) were used at 10 μM.

    Article Title: Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells
    Article Snippet: Paragraph title: Cell Treatment and JNK Inhibition ... The JNK inhibitors SP600125 (Sigma-Aldrich) and JNK inhibitor V (Calbiochem, Darmstadt, Germany) were prepared in DMSO and used at concentrations of 10 and 5 µM, respectively.

    Activity Assay:

    Article Title: TRAIL enhances paracetamol-induced liver sinusoidal endothelial cell death in a Bim- and Bid-dependent manner
    Article Snippet: Paragraph title: Caspase 3/7 activity assay (DEVDase assay) ... After O/N adherence, cells were stimulated with 5, 10 or 20 mM APAP and/or 30 or 3 ng/ml TRAIL, and harvested after 6 h. In some experiments cells were pretreated with the JNK inhibitor V (Calbiochem, Merck KGaA, Darmstadt, Germany).

    Cell Culture:

    Article Title: Multiple Kinases Regulate mafA Expression in the Pancreatic Beta Cell Line MIN6 *
    Article Snippet: SP600125, JNK inhibitor V, staurosporine, and ionomycin were obtained from Calbiochem (San Diego, CA). .. Cell culture media were obtained from Atlanta Biologicals (Lawrenceville, GA).

    Article Title: Gremlin 2 promotes differentiation of embryonic stem cells to atrial fate by activation of the JNK signaling pathway
    Article Snippet: Paragraph title: ES cell culture and embryoid body (EB) formation ... JNK 2inhibitor II (SP600125, Tocris Biosciences) and JNK Inhibitor V (AS601245, EMD Millipore) were used at 10 μM.

    Expressing:

    Article Title: IL-4 induces proliferation in prostate cancer PC3 cells under nutrient-depletion stress through the activation of the JNK-pathway and survivin upregulation
    Article Snippet: Cells were detached using 0.25 mM EDTA, then plated in 6-well-culture-plates at a density of 1.5x105 cells/ml and treated with IL-4 and (or) the inhibitors U0126 (MEK1/2 inhibitor), SB 220025 (p38-inhibitor) and JNK-inhibitor-V; EMD/Calbiochem) at the indicated concentrations. .. To analyze survivin expression during cell proliferation, cells were detached and plated in RPMI (0.5–1% FBS) supplemented with IL-4 (100 ng/ml, Symansis, 4004C).

    Lysis:

    Article Title: TRAIL enhances paracetamol-induced liver sinusoidal endothelial cell death in a Bim- and Bid-dependent manner
    Article Snippet: After O/N adherence, cells were stimulated with 5, 10 or 20 mM APAP and/or 30 or 3 ng/ml TRAIL, and harvested after 6 h. In some experiments cells were pretreated with the JNK inhibitor V (Calbiochem, Merck KGaA, Darmstadt, Germany). .. After overnight lysis at −20 °C, cells were centrifuged for 10 min at 1500 × g at 4 °C, supernatant was harvested and 50 μ l were mixed with 50 μ l HEPES Buffer (100 mM HEPES, pH 7.5, 20% glycerol, 0.5 mM EDTA, 4 mMDTT) containing 100 mM Ac-DEVD-AFC (Enzo Life Sciences AG, Lausen, Switzerland).

    Western Blot:

    Article Title: IL-4 induces proliferation in prostate cancer PC3 cells under nutrient-depletion stress through the activation of the JNK-pathway and survivin upregulation
    Article Snippet: Paragraph title: Western Blot Analysis ... Cells were detached using 0.25 mM EDTA, then plated in 6-well-culture-plates at a density of 1.5x105 cells/ml and treated with IL-4 and (or) the inhibitors U0126 (MEK1/2 inhibitor), SB 220025 (p38-inhibitor) and JNK-inhibitor-V; EMD/Calbiochem) at the indicated concentrations.

    Recombinant:

    Article Title: Protective Role of Complement C3 Against Cytokine-Mediated β-Cell Apoptosis
    Article Snippet: On the basis of previous dose-response experiments done by our group in rodent and human cells, the following cytokine concentrations were used: recombinant human IL-1 β (R & D Systems, Abingdon, UK) at 10 or 50 U/mL as indicated; recombinant rat IFN- γ (R & D Systems) at 100 and 500 U/mL for INS-1E cells and primary rat α - and β -cells, respectively; and human IFN- γ (PeproTech, Rocky Hill, NJ) at 1000 U/mL for EndoC- β H1 cells and dispersed human islets ( – ). .. Forskolin (FK), diazoxide, the phosphoinositide 3-kinase (PI3K) inhibitor wortmannin (Sigma-Aldrich, Bornem, Belgium) and the JNK inhibitor V (Calbiochem, San Diego, CA) were diluted in dimethyl sulfoxide and used at concentrations of 20 μM, 100 μM, 100 nM, and 5 μM, respectively.

    Viability Assay:

    Article Title: IL-4 induces proliferation in prostate cancer PC3 cells under nutrient-depletion stress through the activation of the JNK-pathway and survivin upregulation
    Article Snippet: Paragraph title: WST-1 Cell Viability Assay ... After attachment, cells were stimulated with IL-4 (100ng/mL) and (or) treated with the inhibitors (U0126-MEK1/2 inhibitor), SB 220025 (p38-inhibitor) and JNK-inhibitor-V; EMD/Calbiochem) at the indicated concentrations.

    Software:

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol
    Article Snippet: Cell death assay U87 and U251 cells were pretreated for 30 minutes with JNK inhibitor V [1,3-Benzothiazol-2-yl-(2-((2-(3-pyridinyl)ethyl)amino)-4-pyrimidinyl)acetonitrile; Calbiochem], an inhibitor of JNK1/2 activation, before treatment with 0.5 mM POH and 0.5 mM POH plus 0.5 μM JNK inhibitor V. After 24 hours of incubation, the cells were suspended in annexin and propidium iodide binding buffer as specified in the TACS Annexin V-FITC apoptosis detection kit (R & D Systems). .. The BD Accuri software was used to determine the Annexin V-positive apoptotic cells.

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 95
    Millipore jnk inhibitor v
    POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM <t>JNK</t> <t>inhibitor</t> V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P
    Jnk Inhibitor V, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jnk inhibitor v/product/Millipore
    Average 95 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    jnk inhibitor v - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    Image Search Results


    POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Journal: Molecular Cancer

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol

    doi: 10.1186/s12943-015-0374-5

    Figure Lengend Snippet: POH-induced apoptosis in U251 cells. U251 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Article Snippet: Then, the treatment was carried out with the addition of 0.1% DMSO or 0.5 mM POH either with or without 0.5 μM JNK inhibitor V for 24 hours.

    Techniques:

    The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Journal: Molecular Cancer

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol

    doi: 10.1186/s12943-015-0374-5

    Figure Lengend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U251 cells. Before treatment, U251 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A) , 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 7E represents the percentage of dead cells as indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 7A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Article Snippet: Then, the treatment was carried out with the addition of 0.1% DMSO or 0.5 mM POH either with or without 0.5 μM JNK inhibitor V for 24 hours.

    Techniques: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Journal: Molecular Cancer

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol

    doi: 10.1186/s12943-015-0374-5

    Figure Lengend Snippet: POH-induced apoptosis in U87 cells. U87 in the control condition (Control, A) . The cells were treated with 0.5 mM POH (POH, B) and 0.5 mM POH plus 0.5 μM JNK inhibitor V (POH + IJNK, C) . After 24 hours, the cells were immunostained for cleaved caspase-3 and the number of positive cells was analyzed (D) . Whereas POH induced cell apoptosis, the addition of the JNK inhibitor completely inhibited this effect. The addition of DMSO or JNK inhibitor V alone had no effect on cell death. Scale bar: 20 μm.*P

    Article Snippet: Then, the treatment was carried out with the addition of 0.1% DMSO or 0.5 mM POH either with or without 0.5 μM JNK inhibitor V for 24 hours.

    Techniques:

    The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Journal: Molecular Cancer

    Article Title: Na/K-ATPase as a target for anticancer drugs: studies with perillyl alcohol

    doi: 10.1186/s12943-015-0374-5

    Figure Lengend Snippet: The effects of JNK inhibition on the induction of cell death by POH in U87 cells. Before treatment, U87 cells were incubated without (A and B) or with (C and D) JNK inhibitor V (0.5 μM) for 30 minutes. The cells were treated with 0.1% DMSO (A), 0.5 mM POH (B) 0.1% DMSO plus JNK inhibitor V (C) , and 0.5 mM POH plus JNK inhibitor V (D) . After 24 hours of incubation, the cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometry. Figure 6E represents the percentage of dead cells indicated by early apoptosis and late apoptosis or necrosis (right lower quadrant + right upper quadrant, respectively), which was calculated from the data shown in Figures 6A-D. The data were expressed as the means ± SD from at least three different experiments. ***p

    Article Snippet: Then, the treatment was carried out with the addition of 0.1% DMSO or 0.5 mM POH either with or without 0.5 μM JNK inhibitor V for 24 hours.

    Techniques: Inhibition, Incubation, Staining, Flow Cytometry, Cytometry

    c-Jun N-terminal kinase (JNK)-dependent unfolded protein response (UPR) during hepatic stellate cell (HSC) activation. a Freshly isolated mouse HSCs (mHSCs) were treated with the JNK V inhibitor starting at the moment of seeding. Bright-field images of control (days 1 and 7) and JNK inhibitor-treated HSCs (day 7) were taken. b At regular intervals during culture, expression of activation and endoplasmic reticulum (ER) stress markers was determined and compared with untreated cells at the mRNA level by quantitative real-time polymerase chain reaction (qPCR). c Immunofluorescent images for Bip (green, upper left panel) of JNK inhibitor-treated and control cells after 10 h in culture were taken with a confocal microscope. 4′,6-Diamidino-2-phenylindole (DAPI; blue) was used as a nuclear staining. Graph representing the quantification of % mean intensity in at least 25 cells for each time point (right panel). d Control cells (days 1 and 7) and 7-day treated HSCs with JNK inhibitor were fixed and stained for α-smooth muscle actin (α-SMA; red) and DAPI (blue). Images were taken with a confocal microscope. We had to slightly overexpose all groups to be able to observe α-SMA staining in the 10 µM JNK inhibitor-treated group and to keep the same exposure time between the different conditions. Images and graphics are representatives of at least two different HSC isolations. * P

    Journal: Cell Death & Disease

    Article Title: Unfolded protein response is an early, non-critical event during hepatic stellate cell activation

    doi: 10.1038/s41419-019-1327-5

    Figure Lengend Snippet: c-Jun N-terminal kinase (JNK)-dependent unfolded protein response (UPR) during hepatic stellate cell (HSC) activation. a Freshly isolated mouse HSCs (mHSCs) were treated with the JNK V inhibitor starting at the moment of seeding. Bright-field images of control (days 1 and 7) and JNK inhibitor-treated HSCs (day 7) were taken. b At regular intervals during culture, expression of activation and endoplasmic reticulum (ER) stress markers was determined and compared with untreated cells at the mRNA level by quantitative real-time polymerase chain reaction (qPCR). c Immunofluorescent images for Bip (green, upper left panel) of JNK inhibitor-treated and control cells after 10 h in culture were taken with a confocal microscope. 4′,6-Diamidino-2-phenylindole (DAPI; blue) was used as a nuclear staining. Graph representing the quantification of % mean intensity in at least 25 cells for each time point (right panel). d Control cells (days 1 and 7) and 7-day treated HSCs with JNK inhibitor were fixed and stained for α-smooth muscle actin (α-SMA; red) and DAPI (blue). Images were taken with a confocal microscope. We had to slightly overexpose all groups to be able to observe α-SMA staining in the 10 µM JNK inhibitor-treated group and to keep the same exposure time between the different conditions. Images and graphics are representatives of at least two different HSC isolations. * P

    Article Snippet: Treatment with 5 and 10 µM JNK V inhibitor (Calbiochem, Merck, Overijse, Belgium) was started from the moment of seeding and refreshed every day.

    Techniques: Activation Assay, Isolation, Expressing, Real-time Polymerase Chain Reaction, Microscopy, Staining

    JNK mediates Bim and Puma induction and activation. ( a ) Caco-2 cells were pretreated with buffer control or JNK V inhibitor (2.5 μ M) for 1 h before treatment with 0.1% DMSO or 20 μ M RM4819 for 2, 4 and 8 h. Mcl-1, Bcl-x L , Bim, and Puma were detected by western blot. Tubulin served as a loading control. ( b and c ) Caco-2 cells were pretreated with JNK V inhibitor for 1 h, before stimulation with RM4819 or DMSO for 8 h. Bcl-x L ( b ) and Mcl-1 ( c ) were immunoprecipitated, and Puma and Bim were detected by western blotting. IgG, isotype control; HC, immunoglobulin heavy chain; LC, immunoglobulin light chain

    Journal: Cell Death & Disease

    Article Title: Thiazolides promote apoptosis in colorectal tumor cells via MAP kinase-induced Bim and Puma activation

    doi: 10.1038/cddis.2015.137

    Figure Lengend Snippet: JNK mediates Bim and Puma induction and activation. ( a ) Caco-2 cells were pretreated with buffer control or JNK V inhibitor (2.5 μ M) for 1 h before treatment with 0.1% DMSO or 20 μ M RM4819 for 2, 4 and 8 h. Mcl-1, Bcl-x L , Bim, and Puma were detected by western blot. Tubulin served as a loading control. ( b and c ) Caco-2 cells were pretreated with JNK V inhibitor for 1 h, before stimulation with RM4819 or DMSO for 8 h. Bcl-x L ( b ) and Mcl-1 ( c ) were immunoprecipitated, and Puma and Bim were detected by western blotting. IgG, isotype control; HC, immunoglobulin heavy chain; LC, immunoglobulin light chain

    Article Snippet: JNK V inhibitor and p38 inhibitor SB202190 were purchased from Calbiochem (Darmstadt, Germany), the dye 6-carboxy-2′, 7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) from Life Technologies (Darmstadt, Germany).

    Techniques: Activation Assay, Western Blot, Immunoprecipitation

    Thiazolide-induced cell death is JNK and p38-dependent. ( a ) Caco-2 cells were treated with indicated concentrations of RM4819, compound 2, cisplatin, or DMSO as solvent control for 40 h. Cell death induction was calculated by an MTT assay. Mean values of triplicates±S.D. of a representative experiment are shown ( n > 3). ( b ) Caco-2 cells were control treated (ctrl), or with thiazolides (20 μ M), cisplatin (10 μ g/ml), or DMSO (0.1%) for indicated time intervals. Phospho-JNK (p-JNK), phospho-p38 (p-p38), and tubulin as a loading control were detected by western blotting. ( c–e) Caco-2 cells were pretreated with JNK V inhibitor (2.5 μ M) ( c ), p38 inhibitor (10 μ M), ( d ) or the combination of both ( e ) 1 h before stimulation with 20 μ M RM4819 for further 40 h. Cell death induction was assessed by an MTT assay. Mean values of triplicates±S.D. of a representative experiment are shown ( n > 3). * P

    Journal: Cell Death & Disease

    Article Title: Thiazolides promote apoptosis in colorectal tumor cells via MAP kinase-induced Bim and Puma activation

    doi: 10.1038/cddis.2015.137

    Figure Lengend Snippet: Thiazolide-induced cell death is JNK and p38-dependent. ( a ) Caco-2 cells were treated with indicated concentrations of RM4819, compound 2, cisplatin, or DMSO as solvent control for 40 h. Cell death induction was calculated by an MTT assay. Mean values of triplicates±S.D. of a representative experiment are shown ( n > 3). ( b ) Caco-2 cells were control treated (ctrl), or with thiazolides (20 μ M), cisplatin (10 μ g/ml), or DMSO (0.1%) for indicated time intervals. Phospho-JNK (p-JNK), phospho-p38 (p-p38), and tubulin as a loading control were detected by western blotting. ( c–e) Caco-2 cells were pretreated with JNK V inhibitor (2.5 μ M) ( c ), p38 inhibitor (10 μ M), ( d ) or the combination of both ( e ) 1 h before stimulation with 20 μ M RM4819 for further 40 h. Cell death induction was assessed by an MTT assay. Mean values of triplicates±S.D. of a representative experiment are shown ( n > 3). * P

    Article Snippet: JNK V inhibitor and p38 inhibitor SB202190 were purchased from Calbiochem (Darmstadt, Germany), the dye 6-carboxy-2′, 7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) from Life Technologies (Darmstadt, Germany).

    Techniques: MTT Assay, Western Blot