additional gsk inhibitors 4 benzyl 2 methyl 1  (Millipore)


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    Structured Review

    Millipore additional gsk inhibitors 4 benzyl 2 methyl 1
    cAMP-GEF activation and <t>GSK</t> inhibition increase β-catenin levels in hepatocytes. Rat hepatocyte cultures were treated for 2 h with CPT-2-Me-cAMP (20 μM), SB415286 (25 μM), SB216763 (10 μM), bromoindirubin-3′-oxime (BIO; 10 μM), <t>4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione</t> (TDZD; 40 μM), or insulin (50 nM). Whole cell lysates and cytosol extracts were prepared. Aliquots of each preparation were immunoblotted with antibodies to β-catenin, and equal protein loading was verified with immunoblotting for GADPH. Representative blots are shown in A and B along with graphical depiction of the results of 3 separate experiments. *Significantly different from control cells treated with only vehicle.
    Additional Gsk Inhibitors 4 Benzyl 2 Methyl 1, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 204 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/additional gsk inhibitors 4 benzyl 2 methyl 1/product/Millipore
    Average 85 stars, based on 204 article reviews
    Price from $9.99 to $1999.99
    additional gsk inhibitors 4 benzyl 2 methyl 1 - by Bioz Stars, 2020-10
    85/100 stars

    Images

    1) Product Images from "cAMP-guanine exchange factor protection from bile acid-induced hepatocyte apoptosis involves glycogen synthase kinase regulation of c-Jun NH2-terminal kinase"

    Article Title: cAMP-guanine exchange factor protection from bile acid-induced hepatocyte apoptosis involves glycogen synthase kinase regulation of c-Jun NH2-terminal kinase

    Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

    doi: 10.1152/ajpgi.00430.2010

    cAMP-GEF activation and GSK inhibition increase β-catenin levels in hepatocytes. Rat hepatocyte cultures were treated for 2 h with CPT-2-Me-cAMP (20 μM), SB415286 (25 μM), SB216763 (10 μM), bromoindirubin-3′-oxime (BIO; 10 μM), 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD; 40 μM), or insulin (50 nM). Whole cell lysates and cytosol extracts were prepared. Aliquots of each preparation were immunoblotted with antibodies to β-catenin, and equal protein loading was verified with immunoblotting for GADPH. Representative blots are shown in A and B along with graphical depiction of the results of 3 separate experiments. *Significantly different from control cells treated with only vehicle.
    Figure Legend Snippet: cAMP-GEF activation and GSK inhibition increase β-catenin levels in hepatocytes. Rat hepatocyte cultures were treated for 2 h with CPT-2-Me-cAMP (20 μM), SB415286 (25 μM), SB216763 (10 μM), bromoindirubin-3′-oxime (BIO; 10 μM), 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD; 40 μM), or insulin (50 nM). Whole cell lysates and cytosol extracts were prepared. Aliquots of each preparation were immunoblotted with antibodies to β-catenin, and equal protein loading was verified with immunoblotting for GADPH. Representative blots are shown in A and B along with graphical depiction of the results of 3 separate experiments. *Significantly different from control cells treated with only vehicle.

    Techniques Used: Activation Assay, Inhibition, Cycling Probe Technology

    2) 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

    Related Articles

    Transfection:

    Article Title: Transfer-RNA-mediated enhancement of ribosomal proteins S6 kinases signaling for cell proliferation
    Article Snippet: .. HEK 293T cells were transfected with tRNA-expressing pGEM-T Easy vector using Fugene reagent (Promega, USA) for 24 h. HEK 293T cells were pre-incubated in the amino acid-deprivation medium for 3 h and then treated with rapamycin (100 nM), U0126 (ERK inhibitor) (20 mM), SP600125 (JNK inhibitor) (20 mM), and SB203580 (p38 MAPK) (20 mM) for an additional 1.5 h. All the inhibitors were purchased from Calbiochem (USA). ..

    Histone Deacetylase Assay:

    Article Title: Transitory FGF treatment results in the long-lasting suppression of the proliferative response to repeated FGF stimulation
    Article Snippet: .. Among these compounds were histone deacetylase inhibitor trichostatin A (TSA) (Sigma), DNA replication inhibitors thymidine in high concentration and aphidicolin (Sigma), DNA methylation inhibitor azacytidine (Sigma), G9a histone methylase inhibitor BIX01294 (Sigma), JNK inhibitor II (Calbiochem, San Diego, CA), p38 MAPK inhibitor SB202190 (Selleckchem, Boston. .. MA), MEK inhibitor U0126 (Selleckchem), NFκB inhibitors celastrol (Cayman Chemical, Ann Arbor, MI) and BMS-345541 (Sigma), and FGFR inhibitor, PD1666866 (a generous gift from RL Panek, Pfizer).

    DNA Methylation Assay:

    Article Title: Transitory FGF treatment results in the long-lasting suppression of the proliferative response to repeated FGF stimulation
    Article Snippet: .. Among these compounds were histone deacetylase inhibitor trichostatin A (TSA) (Sigma), DNA replication inhibitors thymidine in high concentration and aphidicolin (Sigma), DNA methylation inhibitor azacytidine (Sigma), G9a histone methylase inhibitor BIX01294 (Sigma), JNK inhibitor II (Calbiochem, San Diego, CA), p38 MAPK inhibitor SB202190 (Selleckchem, Boston. .. MA), MEK inhibitor U0126 (Selleckchem), NFκB inhibitors celastrol (Cayman Chemical, Ann Arbor, MI) and BMS-345541 (Sigma), and FGFR inhibitor, PD1666866 (a generous gift from RL Panek, Pfizer).

    Concentration Assay:

    Article Title: Transitory FGF treatment results in the long-lasting suppression of the proliferative response to repeated FGF stimulation
    Article Snippet: .. Among these compounds were histone deacetylase inhibitor trichostatin A (TSA) (Sigma), DNA replication inhibitors thymidine in high concentration and aphidicolin (Sigma), DNA methylation inhibitor azacytidine (Sigma), G9a histone methylase inhibitor BIX01294 (Sigma), JNK inhibitor II (Calbiochem, San Diego, CA), p38 MAPK inhibitor SB202190 (Selleckchem, Boston. .. MA), MEK inhibitor U0126 (Selleckchem), NFκB inhibitors celastrol (Cayman Chemical, Ann Arbor, MI) and BMS-345541 (Sigma), and FGFR inhibitor, PD1666866 (a generous gift from RL Panek, Pfizer).

    Article Title: Basal epithelial tissue folding is mediated by differential regulation of microtubules
    Article Snippet: .. Concentrations of reagents are as follows: JNK inhibitor SP600125 (420119, Calbiochem) was solubilized in DMSO and used at a final concentration of 5 μM; colchicine (C9754, Sigma-Aldrich) was solubilized in water and used at a final concentration of 100 μM; paclitaxel (T7191, Sigma-Aldrich) was solubilized in DMSO and used at a final concentration of 100 μM. ..

    other:

    Article Title: TNFα Mediated IL-6 Secretion Is Regulated by JAK/STAT Pathway but Not by MEK Phosphorylation and AKT Phosphorylation in U266 Multiple Myeloma Cells
    Article Snippet: Bay 11-7082((E)3-[(4-merhylphenyl)sulfonyl]-2-propenenitrile), TPCK (Nα -Tosyl-Phe Chloromethyl Ketone), PDTC (10 Pyrrolidinecarbodithioic Acid, Ammonium Salt), used as NF-κ B inhibitors, PI3K inhibitor (LY294002), JNK inhibitor II, MEK1/2 inhibitor (PD98059), p38 MAPK inhibitor (SB203580), JAK inhibitor I/II, and JAK/STAT inhibitor (AG490) were purchased from Calbiochem corp. (San Diego, CA, USA).

    Article Title: Amyloid precursor protein modulates Nav1.6 sodium channel currents through a Go-coupled JNK pathway
    Article Snippet: NF203 (Sigma), JNK inhibitor III (Calbiochem) and roscovitine (Calbiochem) were purchased.

    Article Title: Hepatitis C Virus Infection Increases c-Jun N-Terminal Kinase (JNK) Phosphorylation and Accentuates Hepatocyte Lipoapoptosis
    Article Snippet: The JNK inhibitor SP600125 (420119) was purchased from Calbiochem (San Diego, CA, USA).

    Inhibition:

    Article Title: Activation of PI3K/Akt signaling has a dominant negative effect on IL-12 production by macrophages infected with Leishmania amazonensis promastigotes
    Article Snippet: .. Inhibition studies were carried out with these specific inhibitors: Akt inhibitor IV (10μM), wortmannin (100nM), pertussis toxin (1μg/ml), JNK inhibitor II (20μM), PD 98059 (MEK inhibitor) (50μM), and SB203580 (p38 MAPK inhibitor) (20μM) (EMD Biosciences, San Diego, CA). ..

    Plasmid Preparation:

    Article Title: Transfer-RNA-mediated enhancement of ribosomal proteins S6 kinases signaling for cell proliferation
    Article Snippet: .. HEK 293T cells were transfected with tRNA-expressing pGEM-T Easy vector using Fugene reagent (Promega, USA) for 24 h. HEK 293T cells were pre-incubated in the amino acid-deprivation medium for 3 h and then treated with rapamycin (100 nM), U0126 (ERK inhibitor) (20 mM), SP600125 (JNK inhibitor) (20 mM), and SB203580 (p38 MAPK) (20 mM) for an additional 1.5 h. All the inhibitors were purchased from Calbiochem (USA). ..

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    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: 97/100, based on 39 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jnk inhibitor v/product/Millipore
    Average 97 stars, based on 39 article reviews
    Price from $9.99 to $1999.99
    jnk inhibitor v - by Bioz Stars, 2020-10
    97/100 stars
      Buy from Supplier

    85
    Millipore jnk inhibitor 1 3 benzothiazol 2 yl 2 2 3 pyridinyl ethyl amino 4 pyrimidinyl acetonitrile
    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 1 3 Benzothiazol 2 Yl 2 2 3 Pyridinyl Ethyl Amino 4 Pyrimidinyl Acetonitrile, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jnk inhibitor 1 3 benzothiazol 2 yl 2 2 3 pyridinyl ethyl amino 4 pyrimidinyl acetonitrile/product/Millipore
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jnk inhibitor 1 3 benzothiazol 2 yl 2 2 3 pyridinyl ethyl amino 4 pyrimidinyl acetonitrile - by Bioz Stars, 2020-10
    85/100 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: 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).

    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: 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).

    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: 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).

    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: 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).

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