erk inhibitor u0126 Millipore Search Results


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  • 99
    Millipore u0126
    BaP-induced vimentin protein expression is modulated by ERK activation. Cells were seeded in 60-mm plates and treated with 4 µM BaP or 20 µM <t>U0126</t> for 48 h. Western blot analysis was performed to analyze the level of protein expression. BaP, benzo(a)pyrene; ERK, extracellular signal-regulated kinase; p, phosphorylated; Akt, protein kinase B.
    U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 7643 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore sb203580
    MAPK but not PI3 K signaling is targeted by (+)-JQ1. BV2 cells were pretreated with either (+)-JQ1 (400 nM) or DMSO for 30 min and subjected to LPS stimulation. The phosphorylation of ERK, p38, JNK ( a ) and Akt ( b ) as well as the total protein content, was analyzed by immunoblot. The relative intensity of a given band was normalized. Representative results from three independent experiments are depicted here. The relative intensity of a given band was normalized (n = 6). c BV2 cells were treated with LPS (100 ng/ml) or JQ1 (400 nM), together with or without U0126 (ERK inhibitor) or <t>SB203580</t> (p38 inhibitor). 24 h later, cell culture medium were collected and IL-1β, IL-6 and TNFα were tested by ELISA (n = 3). The data are presented as the mean ± SEM (* p ≤ 0.05, ** p ≤ 0.01)
    Sb203580, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 8881 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore sp600125
    The <t>JNK</t> signaling pathway is crucial for HBx-induced autophagosome formation. (A) HepG2 cells were transfected with increasing doses of pHBx. At 24 h posttransfection, Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 4). (B) HepG2 cells were pretreated with the ERK inhibitor U0126 (10 μM), the p38 inhibitor SB202190 (10 μM), or the JNK inhibitor <t>SP600125</t> (10 μM) for 30 min and then transfected with pHBx for 48 h. Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 5). *, P
    Sp600125, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 7172 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore pd98059
    The <t>JNK</t> signaling pathway is crucial for HBx-induced autophagosome formation. (A) HepG2 cells were transfected with increasing doses of pHBx. At 24 h posttransfection, Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 4). (B) HepG2 cells were pretreated with the ERK inhibitor U0126 (10 μM), the p38 inhibitor SB202190 (10 μM), or the JNK inhibitor <t>SP600125</t> (10 μM) for 30 min and then transfected with pHBx for 48 h. Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 5). *, P
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    99
    Millipore ly294002
    ERK or PI3K rather than TGFβ signaling is involved in dPPA induced furin expression ( A and B ) SH-SY5Y (A) and HEK293 cells (B) were treated with 25 μM RepSox (Rep, TGFβ receptor inhibitor) in absence or presence of dPA or dPPA for 72 h, and the Western blotting results show that dPA or dPPA increases the expression in the presence of RepSox. ( C and D ) SH-SY5Y cells were treated with 0.2 μM dPPA or dPA for 72 h, and mRNA levels of Smad2 and Smad7 were determined by real-time PCR. ( E ) SH-SY5Y cells were treated with 20 μM U0126 (ERK inhibitor) or 10 μM <t>LY294002</t> (PI3K inhibitor) in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK or PI3K pathway prevents dPPA induced furin expression. ( F ) SH-SY5Y cells were transfected with pcDNA3-CEBPβ or pcDNA3 (vector) for 24 h and then treated with 20 μM U0126 or 10 μM LY294002 for 24 h, and the Western blotting results show that in cells overexpressing CEBPβ, U0126 or LY294002 had no effect on furin expression ( G ) SH-SY5Y cells were treated jointly with 20 μM U0126 and 10 μM LY294002 in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK and PI3K completely blocks dPPA induced furin expression. * P
    Ly294002, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 9720 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore mek erk inhibitor u0126
    ERK or PI3K rather than TGFβ signaling is involved in dPPA induced furin expression ( A and B ) SH-SY5Y (A) and HEK293 cells (B) were treated with 25 μM RepSox (Rep, TGFβ receptor inhibitor) in absence or presence of dPA or dPPA for 72 h, and the Western blotting results show that dPA or dPPA increases the expression in the presence of RepSox. ( C and D ) SH-SY5Y cells were treated with 0.2 μM dPPA or dPA for 72 h, and mRNA levels of Smad2 and Smad7 were determined by real-time PCR. ( E ) SH-SY5Y cells were treated with 20 μM U0126 (ERK inhibitor) or 10 μM <t>LY294002</t> (PI3K inhibitor) in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK or PI3K pathway prevents dPPA induced furin expression. ( F ) SH-SY5Y cells were transfected with pcDNA3-CEBPβ or pcDNA3 (vector) for 24 h and then treated with 20 μM U0126 or 10 μM LY294002 for 24 h, and the Western blotting results show that in cells overexpressing CEBPβ, U0126 or LY294002 had no effect on furin expression ( G ) SH-SY5Y cells were treated jointly with 20 μM U0126 and 10 μM LY294002 in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK and PI3K completely blocks dPPA induced furin expression. * P
    Mek Erk Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 132 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore pi3k inhibitor
    ERK or PI3K rather than TGFβ signaling is involved in dPPA induced furin expression ( A and B ) SH-SY5Y (A) and HEK293 cells (B) were treated with 25 μM RepSox (Rep, TGFβ receptor inhibitor) in absence or presence of dPA or dPPA for 72 h, and the Western blotting results show that dPA or dPPA increases the expression in the presence of RepSox. ( C and D ) SH-SY5Y cells were treated with 0.2 μM dPPA or dPA for 72 h, and mRNA levels of Smad2 and Smad7 were determined by real-time PCR. ( E ) SH-SY5Y cells were treated with 20 μM U0126 (ERK inhibitor) or 10 μM <t>LY294002</t> (PI3K inhibitor) in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK or PI3K pathway prevents dPPA induced furin expression. ( F ) SH-SY5Y cells were transfected with pcDNA3-CEBPβ or pcDNA3 (vector) for 24 h and then treated with 20 μM U0126 or 10 μM LY294002 for 24 h, and the Western blotting results show that in cells overexpressing CEBPβ, U0126 or LY294002 had no effect on furin expression ( G ) SH-SY5Y cells were treated jointly with 20 μM U0126 and 10 μM LY294002 in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK and PI3K completely blocks dPPA induced furin expression. * P
    Pi3k Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1097 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore wortmannin
    ERK or PI3K rather than TGFβ signaling is involved in dPPA induced furin expression ( A and B ) SH-SY5Y (A) and HEK293 cells (B) were treated with 25 μM RepSox (Rep, TGFβ receptor inhibitor) in absence or presence of dPA or dPPA for 72 h, and the Western blotting results show that dPA or dPPA increases the expression in the presence of RepSox. ( C and D ) SH-SY5Y cells were treated with 0.2 μM dPPA or dPA for 72 h, and mRNA levels of Smad2 and Smad7 were determined by real-time PCR. ( E ) SH-SY5Y cells were treated with 20 μM U0126 (ERK inhibitor) or 10 μM <t>LY294002</t> (PI3K inhibitor) in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK or PI3K pathway prevents dPPA induced furin expression. ( F ) SH-SY5Y cells were transfected with pcDNA3-CEBPβ or pcDNA3 (vector) for 24 h and then treated with 20 μM U0126 or 10 μM LY294002 for 24 h, and the Western blotting results show that in cells overexpressing CEBPβ, U0126 or LY294002 had no effect on furin expression ( G ) SH-SY5Y cells were treated jointly with 20 μM U0126 and 10 μM LY294002 in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK and PI3K completely blocks dPPA induced furin expression. * P
    Wortmannin, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 9936 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore sb202190
    Effects of pretreatment with MAPK inhibitors on MβCD-induced IL-8 production. (A) IL-8 production was decreased by pretreatment with the ERK inhibitor U0126 (50 µM) but not by JNK inhibitor II (100 µM) or the p38 MAPK inhibitor <t>SB202190</t> (50 µM). ** P
    Sb202190, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 2525 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    97
    Millipore jnk inhibitor ii
    Effects of pretreatment with MAPK inhibitors on MβCD-induced IL-8 production. (A) IL-8 production was decreased by pretreatment with the ERK inhibitor U0126 (50 µM) but not by JNK inhibitor II (100 µM) or the p38 MAPK inhibitor <t>SB202190</t> (50 µM). ** P
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    99
    Millipore actinomycin d
    The Ba 2+ current reduction induced by TNF- α is not mediated by a synthetic pathway activation in guinea pig tracheal myocytes. Ba 2+ current evoked by step depolarization from −60 to 50 mV in tracheal cells from nonsensitized guinea pigs added with fetal bovine serum (NS + FBS, n = 7) were significantly diminished when myocytes were grown with TNF- α ( n = 7). Neither <t>actinomycin</t> D (Act D, n = 6) nor cycloheximide (Cyclohex, n = 9) addition during myocyte growth altered TNF- α induced effect on the Ba 2+ current. Inset represents original recordings. ∗ p
    Actinomycin D, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 12624 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore egf
    The Ba 2+ current reduction induced by TNF- α is not mediated by a synthetic pathway activation in guinea pig tracheal myocytes. Ba 2+ current evoked by step depolarization from −60 to 50 mV in tracheal cells from nonsensitized guinea pigs added with fetal bovine serum (NS + FBS, n = 7) were significantly diminished when myocytes were grown with TNF- α ( n = 7). Neither <t>actinomycin</t> D (Act D, n = 6) nor cycloheximide (Cyclohex, n = 9) addition during myocyte growth altered TNF- α induced effect on the Ba 2+ current. Inset represents original recordings. ∗ p
    Egf, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 7521 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore p38 map kinase inhibitor
    Effect of <t>p38</t> <t>MAP</t> kinase inhibition upon expression of PARs1–4 in HUVECs assessed by quantitative PCR. HUVECs were pretreated with SB203580 at concentrations of 1, 10 and 20 μ M 30 min before 24 h TNF α treatment.
    P38 Map Kinase Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 71 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore p38 mapk
    AQP2 accumulation at the cell surface, but not the trans -Golgi region, following acute hypertonicity depends on <t>p38</t> <t>MAPK</t> activity. mCCDc l1 , LLC-AQP2, LLC-AQP2 (S256D), and LLC-AQP2 (S256A) cells were preincubated or not for 30 min with p38 MAPK inhibitors
    P38 Mapk, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 843 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore dimethyl sulfoxide
    AQP2 accumulation at the cell surface, but not the trans -Golgi region, following acute hypertonicity depends on <t>p38</t> <t>MAPK</t> activity. mCCDc l1 , LLC-AQP2, LLC-AQP2 (S256D), and LLC-AQP2 (S256A) cells were preincubated or not for 30 min with p38 MAPK inhibitors
    Dimethyl Sulfoxide, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 27840 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    Millipore mitogen activated protein kinase
    AQP2 accumulation at the cell surface, but not the trans -Golgi region, following acute hypertonicity depends on <t>p38</t> <t>MAPK</t> activity. mCCDc l1 , LLC-AQP2, LLC-AQP2 (S256D), and LLC-AQP2 (S256A) cells were preincubated or not for 30 min with p38 MAPK inhibitors
    Mitogen Activated Protein Kinase, supplied by Millipore, used in various techniques. Bioz Stars score: 96/100, based on 99 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    BaP-induced vimentin protein expression is modulated by ERK activation. Cells were seeded in 60-mm plates and treated with 4 µM BaP or 20 µM U0126 for 48 h. Western blot analysis was performed to analyze the level of protein expression. BaP, benzo(a)pyrene; ERK, extracellular signal-regulated kinase; p, phosphorylated; Akt, protein kinase B.

    Journal: Oncology Letters

    Article Title: Benzo(a)pyrene promotes Hep-G2 cell migration and invasion by upregulating phosphorylated extracellular signal-regulated kinase expression

    doi: 10.3892/ol.2018.8379

    Figure Lengend Snippet: BaP-induced vimentin protein expression is modulated by ERK activation. Cells were seeded in 60-mm plates and treated with 4 µM BaP or 20 µM U0126 for 48 h. Western blot analysis was performed to analyze the level of protein expression. BaP, benzo(a)pyrene; ERK, extracellular signal-regulated kinase; p, phosphorylated; Akt, protein kinase B.

    Article Snippet: A total of 2 ml DMEM (GE Healthcare Bio-Sciences) with 4 µM BaP or 20 µM ERK inhibitor, U0126 (U120-1MG; ≥98% HPLC; Sigma-Aldrich; Merck KGaA), was added to each well.

    Techniques: Expressing, Activation Assay, Western Blot

    ERK activation is required for BaP-induced Hep-G2 cell migration and invasion. Wound-healing assay was (A) performed and (B) quantified to evaluate the potential role of p-ERK in BaP-induced Hep-G2 cell migration. Cells were wounded by scratching and cultured in the presence of BaP (4 µM) or U0126 (20 µM) for 48 h. Images were captured at 0 and 48 h. The healing width was calculated as the wound width at 0 h minus the wound width at 48 h and was normalized to the control. Values are expressed as the mean ± standard deviation. Transwell invasion assay was (C) performed and (D) quantified to assess the potential role of p-ERK in BaP-induced Hep-G2 cell invasion. Cells were harvested and seeded into the upper chamber with Matrigel and were cultured in the presence of BaP (4 µM) or U0126 (20 µM) for 24 h. The number of migrated cells was counted and normalized to the control. Values are expressed as mean ± standard deviation. ERK, extracellular signal-regulated kinase; BaP, benzo(a)pyrene; p-ERK, phosphorylated ERK.

    Journal: Oncology Letters

    Article Title: Benzo(a)pyrene promotes Hep-G2 cell migration and invasion by upregulating phosphorylated extracellular signal-regulated kinase expression

    doi: 10.3892/ol.2018.8379

    Figure Lengend Snippet: ERK activation is required for BaP-induced Hep-G2 cell migration and invasion. Wound-healing assay was (A) performed and (B) quantified to evaluate the potential role of p-ERK in BaP-induced Hep-G2 cell migration. Cells were wounded by scratching and cultured in the presence of BaP (4 µM) or U0126 (20 µM) for 48 h. Images were captured at 0 and 48 h. The healing width was calculated as the wound width at 0 h minus the wound width at 48 h and was normalized to the control. Values are expressed as the mean ± standard deviation. Transwell invasion assay was (C) performed and (D) quantified to assess the potential role of p-ERK in BaP-induced Hep-G2 cell invasion. Cells were harvested and seeded into the upper chamber with Matrigel and were cultured in the presence of BaP (4 µM) or U0126 (20 µM) for 24 h. The number of migrated cells was counted and normalized to the control. Values are expressed as mean ± standard deviation. ERK, extracellular signal-regulated kinase; BaP, benzo(a)pyrene; p-ERK, phosphorylated ERK.

    Article Snippet: A total of 2 ml DMEM (GE Healthcare Bio-Sciences) with 4 µM BaP or 20 µM ERK inhibitor, U0126 (U120-1MG; ≥98% HPLC; Sigma-Aldrich; Merck KGaA), was added to each well.

    Techniques: Activation Assay, Migration, Wound Healing Assay, Cell Culture, Standard Deviation, Transwell Invasion Assay

    The JNK signaling pathway is crucial for HBx-induced autophagosome formation. (A) HepG2 cells were transfected with increasing doses of pHBx. At 24 h posttransfection, Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 4). (B) HepG2 cells were pretreated with the ERK inhibitor U0126 (10 μM), the p38 inhibitor SB202190 (10 μM), or the JNK inhibitor SP600125 (10 μM) for 30 min and then transfected with pHBx for 48 h. Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 5). *, P

    Journal: Journal of Virology

    Article Title: Reactive Oxygen Species-Mediated c-Jun NH2-Terminal Kinase Activation Contributes to Hepatitis B Virus X Protein-Induced Autophagy via Regulation of the Beclin-1/Bcl-2 Interaction

    doi: 10.1128/JVI.00001-17

    Figure Lengend Snippet: The JNK signaling pathway is crucial for HBx-induced autophagosome formation. (A) HepG2 cells were transfected with increasing doses of pHBx. At 24 h posttransfection, Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 4). (B) HepG2 cells were pretreated with the ERK inhibitor U0126 (10 μM), the p38 inhibitor SB202190 (10 μM), or the JNK inhibitor SP600125 (10 μM) for 30 min and then transfected with pHBx for 48 h. Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 5). *, P

    Article Snippet: Chemicals, including the ERK inhibitor U0126 (catalog no. U120), the p38 inhibitor SB202190 (catalog no. S7067), the JNK inhibitor SP600125 (catalog no. S5567), the class III PI3K inhibitor 3-MA (catalog no. M9281), and the ROS inhibitor NAC (catalog no. A7250), were obtained from Sigma-Aldrich.

    Techniques: Transfection, Western Blot, Plasmid Preparation

    Inhibition of growth factor mediated signaling reduced p-cPLA2 and lipid droplet biogenesis. ( A ) OV202 NTC, Sh1 and Sh2 cells were treated for 24 hours with 20μm of U0126, a MEK inhibitor, followed by western blot analysis to detect the protein expression of p-ERK, t-ERK, p-cPLA2, t-cPLA2 and GAPDH. Band intensity was quantified using Image J software. ( B ) Bodipy staining for lipid droplets (LD) in OV202 Sh1 and Sh2 cells after treatment with 20μM U0126. ( C ) Immunoblot analysis of p-cPLA2 and t-cPLA2 in OV202 Sh1 cells is shown after treatment with 10 and 20μM PG545. ( D ) Bodipy staining of LDs in OV202 Sh1 cells after treating them with 10 and 20μM of PG545. ( E ) Immunoblot analysis of p-cPLA2 and t-cPLA2 in lysates from untreated and PG545 treated OV202 Sh1 xenografts. Data shown in Fig. 3( A to D ) is a representative image from 3 independent experiments.

    Journal: Scientific Reports

    Article Title: Loss of HSulf-1: The Missing Link between Autophagy and Lipid Droplets in Ovarian Cancer

    doi: 10.1038/srep41977

    Figure Lengend Snippet: Inhibition of growth factor mediated signaling reduced p-cPLA2 and lipid droplet biogenesis. ( A ) OV202 NTC, Sh1 and Sh2 cells were treated for 24 hours with 20μm of U0126, a MEK inhibitor, followed by western blot analysis to detect the protein expression of p-ERK, t-ERK, p-cPLA2, t-cPLA2 and GAPDH. Band intensity was quantified using Image J software. ( B ) Bodipy staining for lipid droplets (LD) in OV202 Sh1 and Sh2 cells after treatment with 20μM U0126. ( C ) Immunoblot analysis of p-cPLA2 and t-cPLA2 in OV202 Sh1 cells is shown after treatment with 10 and 20μM PG545. ( D ) Bodipy staining of LDs in OV202 Sh1 cells after treating them with 10 and 20μM of PG545. ( E ) Immunoblot analysis of p-cPLA2 and t-cPLA2 in lysates from untreated and PG545 treated OV202 Sh1 xenografts. Data shown in Fig. 3( A to D ) is a representative image from 3 independent experiments.

    Article Snippet: MEK inhibitor U0126 (Sigma-Aldrich, cat# U120) was used to inhibit ERK activity.

    Techniques: Inhibition, Western Blot, Expressing, Software, Staining

    MAPK but not PI3 K signaling is targeted by (+)-JQ1. BV2 cells were pretreated with either (+)-JQ1 (400 nM) or DMSO for 30 min and subjected to LPS stimulation. The phosphorylation of ERK, p38, JNK ( a ) and Akt ( b ) as well as the total protein content, was analyzed by immunoblot. The relative intensity of a given band was normalized. Representative results from three independent experiments are depicted here. The relative intensity of a given band was normalized (n = 6). c BV2 cells were treated with LPS (100 ng/ml) or JQ1 (400 nM), together with or without U0126 (ERK inhibitor) or SB203580 (p38 inhibitor). 24 h later, cell culture medium were collected and IL-1β, IL-6 and TNFα were tested by ELISA (n = 3). The data are presented as the mean ± SEM (* p ≤ 0.05, ** p ≤ 0.01)

    Journal: Cell & Bioscience

    Article Title: (+)-JQ1 attenuated LPS-induced microglial inflammation via MAPK/NFκB signaling

    doi: 10.1186/s13578-018-0258-7

    Figure Lengend Snippet: MAPK but not PI3 K signaling is targeted by (+)-JQ1. BV2 cells were pretreated with either (+)-JQ1 (400 nM) or DMSO for 30 min and subjected to LPS stimulation. The phosphorylation of ERK, p38, JNK ( a ) and Akt ( b ) as well as the total protein content, was analyzed by immunoblot. The relative intensity of a given band was normalized. Representative results from three independent experiments are depicted here. The relative intensity of a given band was normalized (n = 6). c BV2 cells were treated with LPS (100 ng/ml) or JQ1 (400 nM), together with or without U0126 (ERK inhibitor) or SB203580 (p38 inhibitor). 24 h later, cell culture medium were collected and IL-1β, IL-6 and TNFα were tested by ELISA (n = 3). The data are presented as the mean ± SEM (* p ≤ 0.05, ** p ≤ 0.01)

    Article Snippet: For NFκB signaling test, PDTC (p65 inhibitor), U0126 (ERK inhibitor) or SB203580 (p38 inhibitor) (Calbiochem, Germany) were treated with LPS or (+)-JQ1 for 24 h, followed by medium collection.

    Techniques: Cell Culture, Enzyme-linked Immunosorbent Assay

    Protein levels of I κ B α , p105, p50 and p65 in H. pylori -infected AGS cells treated with MAPK inhibitors. AGS cells were seeded in 12-well culture plates at 10 5 cells per well and cultured to reach 80% confluency. The MAP kinase inhibitors, U0126 (an ERK inhibitor) and SB203580 (a p38 inhibitor) (at 20 μ M final concentration), were pretreated to the culture medium 1 h before the treatment of H. pylori . The bacterial cells were added to the cultured cells at a bacterium/cell ratio of 500:1 for 1 h (I κ B α , A) and 2 h (p105, p50 and p65, B), respectively. None, AGS cells without treatment and cultured in the absence of H. pylori ; Control, AGS cells without treatment and cultured in the presence of H. pylori ; U0126, AGS cells treated with U0126 and cultured in the presence of H. pylori ; SB203580, AGS cells treated with SB203580 and cultured in the presence of H. pylori .

    Journal: Journal of Cancer Prevention

    Article Title: Differential Role of ERK and p38 on NF-κB Activation in Helicobacter pylori-Infected Gastric Epithelial Cells

    doi: 10.15430/JCP.2013.18.4.346

    Figure Lengend Snippet: Protein levels of I κ B α , p105, p50 and p65 in H. pylori -infected AGS cells treated with MAPK inhibitors. AGS cells were seeded in 12-well culture plates at 10 5 cells per well and cultured to reach 80% confluency. The MAP kinase inhibitors, U0126 (an ERK inhibitor) and SB203580 (a p38 inhibitor) (at 20 μ M final concentration), were pretreated to the culture medium 1 h before the treatment of H. pylori . The bacterial cells were added to the cultured cells at a bacterium/cell ratio of 500:1 for 1 h (I κ B α , A) and 2 h (p105, p50 and p65, B), respectively. None, AGS cells without treatment and cultured in the absence of H. pylori ; Control, AGS cells without treatment and cultured in the presence of H. pylori ; U0126, AGS cells treated with U0126 and cultured in the presence of H. pylori ; SB203580, AGS cells treated with SB203580 and cultured in the presence of H. pylori .

    Article Snippet: A ratio of bacterium/cell was adapted from previous studies., An ERK inhibitor U0126 (Catalog # 9903, Cell Signaling Technology, Inc., Beverly, MA, USA) and a p38 inhibitor SB203580 (Catalog # 559389, Calbiochem Biochemicals, San diego, CA, USA) were dissolved in dimethylsulfoxide at 50 mM stock solution.

    Techniques: Infection, Cell Culture, Concentration Assay

    4-Methoxy-TEMPO activated the MAPK signaling pathway. a HepG2 cells were treated with the indicated concentrations of 4-methoxy-TEMPO for 4 h. Total cellular proteins were extracted and the levels of JNK, p-JNK, ERK1/2, p-ERK1/2, p38, and p-p38 were determined by Western blot. b The densitometric analysis of ( a ) was quantified from three independent experiments. Intensities of bands were normalized to the amount of GAPDH. * Indicates p

    Journal: Archives of toxicology

    Article Title: ROS generation and JNK activation contribute to 4-methoxy-TEMPO-induced cytotoxicity, autophagy, and DNA damage in HepG2 cells

    doi: 10.1007/s00204-017-2084-9

    Figure Lengend Snippet: 4-Methoxy-TEMPO activated the MAPK signaling pathway. a HepG2 cells were treated with the indicated concentrations of 4-methoxy-TEMPO for 4 h. Total cellular proteins were extracted and the levels of JNK, p-JNK, ERK1/2, p-ERK1/2, p38, and p-p38 were determined by Western blot. b The densitometric analysis of ( a ) was quantified from three independent experiments. Intensities of bands were normalized to the amount of GAPDH. * Indicates p

    Article Snippet: 2,2,6,6-Tetramethylpiperidine 1-oxyl (TEMPO), 4-methoxy-2,2,6,6-tetramethyl-1-piperidinyloxy (4-methoxy-TEMPO), Williams’ medium E, Dulbecco’s Modified Eagle’s Medium (DMEM), JNK inhibitor SP600125, ERK inhibitor U0126, p38 MAPK inhibitor SB203580, N -acetylcysteine (NAC), and dimethylsulfoxide (DMSO) were purchased from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Western Blot

    The JNK signaling pathway is crucial for HBx-induced autophagosome formation. (A) HepG2 cells were transfected with increasing doses of pHBx. At 24 h posttransfection, Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 4). (B) HepG2 cells were pretreated with the ERK inhibitor U0126 (10 μM), the p38 inhibitor SB202190 (10 μM), or the JNK inhibitor SP600125 (10 μM) for 30 min and then transfected with pHBx for 48 h. Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 5). *, P

    Journal: Journal of Virology

    Article Title: Reactive Oxygen Species-Mediated c-Jun NH2-Terminal Kinase Activation Contributes to Hepatitis B Virus X Protein-Induced Autophagy via Regulation of the Beclin-1/Bcl-2 Interaction

    doi: 10.1128/JVI.00001-17

    Figure Lengend Snippet: The JNK signaling pathway is crucial for HBx-induced autophagosome formation. (A) HepG2 cells were transfected with increasing doses of pHBx. At 24 h posttransfection, Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 4). (B) HepG2 cells were pretreated with the ERK inhibitor U0126 (10 μM), the p38 inhibitor SB202190 (10 μM), or the JNK inhibitor SP600125 (10 μM) for 30 min and then transfected with pHBx for 48 h. Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-ERK, p-p38, and p-JNK relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 5). *, P

    Article Snippet: Chemicals, including the ERK inhibitor U0126 (catalog no. U120), the p38 inhibitor SB202190 (catalog no. S7067), the JNK inhibitor SP600125 (catalog no. S5567), the class III PI3K inhibitor 3-MA (catalog no. M9281), and the ROS inhibitor NAC (catalog no. A7250), were obtained from Sigma-Aldrich.

    Techniques: Transfection, Western Blot, Plasmid Preparation

    Inhibition of ROS-JNK signaling decreases HBV-induced autophagosome formation and its following replication. (A) HepG2 cells were transfected with pHBV1.3, pHBV1.3 with HBx-minus, or the control vector. At 48 h posttransfection, cells were treated with NAC (10 mM) for 24 h or left untreated and ROS activity was determined by FACS analysis. (B) HepG2 cells were transfected with pHBV1.3, pHBV1.3 with HBx-minus, or the control vector as in panel A. Cells were then treated with NAC (10 mM) or SP600125 (10 μM) or left untreated for 24 h, and Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-JNK and p-Bcl-2 relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 4). *, P

    Journal: Journal of Virology

    Article Title: Reactive Oxygen Species-Mediated c-Jun NH2-Terminal Kinase Activation Contributes to Hepatitis B Virus X Protein-Induced Autophagy via Regulation of the Beclin-1/Bcl-2 Interaction

    doi: 10.1128/JVI.00001-17

    Figure Lengend Snippet: Inhibition of ROS-JNK signaling decreases HBV-induced autophagosome formation and its following replication. (A) HepG2 cells were transfected with pHBV1.3, pHBV1.3 with HBx-minus, or the control vector. At 48 h posttransfection, cells were treated with NAC (10 mM) for 24 h or left untreated and ROS activity was determined by FACS analysis. (B) HepG2 cells were transfected with pHBV1.3, pHBV1.3 with HBx-minus, or the control vector as in panel A. Cells were then treated with NAC (10 mM) or SP600125 (10 μM) or left untreated for 24 h, and Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-JNK and p-Bcl-2 relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 4). *, P

    Article Snippet: Chemicals, including the ERK inhibitor U0126 (catalog no. U120), the p38 inhibitor SB202190 (catalog no. S7067), the JNK inhibitor SP600125 (catalog no. S5567), the class III PI3K inhibitor 3-MA (catalog no. M9281), and the ROS inhibitor NAC (catalog no. A7250), were obtained from Sigma-Aldrich.

    Techniques: Inhibition, Transfection, Plasmid Preparation, Activity Assay, FACS, Western Blot

    JNK signaling is important for HBx-mediated Bcl-2 phosphorylation and disassociation of beclin-1 from Bcl-2. (A) HepG2 cells were pretreated with the JNK inhibitor SP600125 (10 μM) for 30 min and then transfected with pHBx. At 48 h posttransfection, Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-Bcl-2 relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 5). *, P

    Journal: Journal of Virology

    Article Title: Reactive Oxygen Species-Mediated c-Jun NH2-Terminal Kinase Activation Contributes to Hepatitis B Virus X Protein-Induced Autophagy via Regulation of the Beclin-1/Bcl-2 Interaction

    doi: 10.1128/JVI.00001-17

    Figure Lengend Snippet: JNK signaling is important for HBx-mediated Bcl-2 phosphorylation and disassociation of beclin-1 from Bcl-2. (A) HepG2 cells were pretreated with the JNK inhibitor SP600125 (10 μM) for 30 min and then transfected with pHBx. At 48 h posttransfection, Western blot analysis was performed with the antibodies indicated. (Left panel) Levels of p-Bcl-2 relative to the level of GAPDH were examined by densitometric analysis, and the value from empty-vector-transfected cells was set at 1.0 ( n = 5). *, P

    Article Snippet: Chemicals, including the ERK inhibitor U0126 (catalog no. U120), the p38 inhibitor SB202190 (catalog no. S7067), the JNK inhibitor SP600125 (catalog no. S5567), the class III PI3K inhibitor 3-MA (catalog no. M9281), and the ROS inhibitor NAC (catalog no. A7250), were obtained from Sigma-Aldrich.

    Techniques: Transfection, Western Blot, Plasmid Preparation

    Effects of inhibition JNK and ERK on RESG-mediated antiumor effect. SMMC-7721 cell was pretreated with SP600125 (10 μM) and U0126 (20 μM) for 2 h, and then it treated with 20 μM RESG for 48 h, ( A ) the inhibition rates were calculated by MTT assay. Data were expressed as means ± SD. ** p

    Journal: Molecules

    Article Title: Resveratrol-4-O-d-(2'-galloyl)-glucopyranoside Isolated from Polygonum cuspidatum Exhibits Anti-Hepatocellular Carcinoma Viability by Inducing Apoptosis via the JNK and ERK Pathway

    doi: 10.3390/molecules19021592

    Figure Lengend Snippet: Effects of inhibition JNK and ERK on RESG-mediated antiumor effect. SMMC-7721 cell was pretreated with SP600125 (10 μM) and U0126 (20 μM) for 2 h, and then it treated with 20 μM RESG for 48 h, ( A ) the inhibition rates were calculated by MTT assay. Data were expressed as means ± SD. ** p

    Article Snippet: Reagents Methylthiazdyldiphenyltetrazolium bromide (MTT), ERK inhibitor (U0126) and JNK inhibitor (SP600125) were purchased from Sigma (St. Louis, MO, USA).

    Techniques: Inhibition, MTT Assay

    ERK or PI3K rather than TGFβ signaling is involved in dPPA induced furin expression ( A and B ) SH-SY5Y (A) and HEK293 cells (B) were treated with 25 μM RepSox (Rep, TGFβ receptor inhibitor) in absence or presence of dPA or dPPA for 72 h, and the Western blotting results show that dPA or dPPA increases the expression in the presence of RepSox. ( C and D ) SH-SY5Y cells were treated with 0.2 μM dPPA or dPA for 72 h, and mRNA levels of Smad2 and Smad7 were determined by real-time PCR. ( E ) SH-SY5Y cells were treated with 20 μM U0126 (ERK inhibitor) or 10 μM LY294002 (PI3K inhibitor) in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK or PI3K pathway prevents dPPA induced furin expression. ( F ) SH-SY5Y cells were transfected with pcDNA3-CEBPβ or pcDNA3 (vector) for 24 h and then treated with 20 μM U0126 or 10 μM LY294002 for 24 h, and the Western blotting results show that in cells overexpressing CEBPβ, U0126 or LY294002 had no effect on furin expression ( G ) SH-SY5Y cells were treated jointly with 20 μM U0126 and 10 μM LY294002 in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK and PI3K completely blocks dPPA induced furin expression. * P

    Journal: Oncotarget

    Article Title: Phorbol esters dPPA/dPA promote furin expression involving transcription factor CEBPβ in neuronal cells

    doi: 10.18632/oncotarget.18569

    Figure Lengend Snippet: ERK or PI3K rather than TGFβ signaling is involved in dPPA induced furin expression ( A and B ) SH-SY5Y (A) and HEK293 cells (B) were treated with 25 μM RepSox (Rep, TGFβ receptor inhibitor) in absence or presence of dPA or dPPA for 72 h, and the Western blotting results show that dPA or dPPA increases the expression in the presence of RepSox. ( C and D ) SH-SY5Y cells were treated with 0.2 μM dPPA or dPA for 72 h, and mRNA levels of Smad2 and Smad7 were determined by real-time PCR. ( E ) SH-SY5Y cells were treated with 20 μM U0126 (ERK inhibitor) or 10 μM LY294002 (PI3K inhibitor) in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK or PI3K pathway prevents dPPA induced furin expression. ( F ) SH-SY5Y cells were transfected with pcDNA3-CEBPβ or pcDNA3 (vector) for 24 h and then treated with 20 μM U0126 or 10 μM LY294002 for 24 h, and the Western blotting results show that in cells overexpressing CEBPβ, U0126 or LY294002 had no effect on furin expression ( G ) SH-SY5Y cells were treated jointly with 20 μM U0126 and 10 μM LY294002 in absence or presence of 0.2 μM dPPA for 72 h, and the Western blotting results show that inhibition of ERK and PI3K completely blocks dPPA induced furin expression. * P

    Article Snippet: Chemicals The PMA, PDBu, dPA, dPPA, LY294002 (PI3K inhibitor) and U0126 (ERK inhibitor) were obtained from Sigma (Saint Louis, USA).

    Techniques: Expressing, Western Blot, Real-time Polymerase Chain Reaction, Inhibition, Transfection, Plasmid Preparation

    Effects of pretreatment with MAPK inhibitors on MβCD-induced IL-8 production. (A) IL-8 production was decreased by pretreatment with the ERK inhibitor U0126 (50 µM) but not by JNK inhibitor II (100 µM) or the p38 MAPK inhibitor SB202190 (50 µM). ** P

    Journal: Allergy, Asthma & Immunology Research

    Article Title: Effect of Cholesterol Depletion on Interleukin-8 Production in Human Respiratory Epithelial Cells

    doi: 10.4168/aair.2013.5.6.402

    Figure Lengend Snippet: Effects of pretreatment with MAPK inhibitors on MβCD-induced IL-8 production. (A) IL-8 production was decreased by pretreatment with the ERK inhibitor U0126 (50 µM) but not by JNK inhibitor II (100 µM) or the p38 MAPK inhibitor SB202190 (50 µM). ** P

    Article Snippet: To investigate the effect of changes in transcription factor activity on IL-8 expression in human lung epithelial cells, the selective MAP/extracellular signal-regulated kinase (ERK) [MEK] inhibitor PD98059 or U0126, c-JUN NH2-terminal kinase (JNK) inhibitor JNK II Inhibitor, or p38 MAPK inhibitor SB203580 or SB202190 (Calbiochem-Novabiochem) was added 1 h before stimulation with MβCD and was present throughout the incubation period.

    Techniques:

    Glabridin activates the phosphorylation of ERK1/2, p38 MAPK and JNK1/2 in HL-60 cells. (A–C, upper panel)) Cells were treated with different concentrations of glabridin (0–40 µM) for 24 h and then subjected to western blotting with an antibody against ERK1/2, JNK1/2, and p38 MAPK. (A–C, lower panel) Quantitative results of p-ERK1/2, p-p38, and p-JNK1/2 protein levels, which were adjusted with the total ERK1/2, p38, and JNK1/2 protein levels and expressed as multiples of induction beyond each respective control. Values represent the mean ± SE of three independent experiments. (*) p

    Journal: PLoS ONE

    Article Title: Glabridin Mediate Caspases Activation and Induces Apoptosis through JNK1/2 and p38 MAPK Pathway in Human Promyelocytic Leukemia Cells

    doi: 10.1371/journal.pone.0098943

    Figure Lengend Snippet: Glabridin activates the phosphorylation of ERK1/2, p38 MAPK and JNK1/2 in HL-60 cells. (A–C, upper panel)) Cells were treated with different concentrations of glabridin (0–40 µM) for 24 h and then subjected to western blotting with an antibody against ERK1/2, JNK1/2, and p38 MAPK. (A–C, lower panel) Quantitative results of p-ERK1/2, p-p38, and p-JNK1/2 protein levels, which were adjusted with the total ERK1/2, p38, and JNK1/2 protein levels and expressed as multiples of induction beyond each respective control. Values represent the mean ± SE of three independent experiments. (*) p

    Article Snippet: Specific inhibitors for ERK1/2 (U0126), JNK1/2 (SP600125) or p38 (SB202190) were purchased from Calbiochem (San Diego, CA).

    Techniques: Western Blot

    JNK1/2 and p38 MAPK are essential for caspase activation induced by glabridin. (A) HL-60 cells were treated for 24 hours with 40 µM glabridin with or without a 1-hour pretreatment of 20 µM U0126, SP600125, or SB202190. The expression of cleaved caspase-9, -8 and -3 were detected by western blotting. (B–D) Quantitative results of cleaved caspase-9, -8, and -3 protein levels, which were adjusted to the β-actin protein level and expressed as multiples of induction beyond each respective control. Values represent the mean ± SE of three independen experiments. Data were analyzed using a one-way ANOVA with Tukey’s posthoc tests at 95% confidence intervals; different letters represent different levels of significance.

    Journal: PLoS ONE

    Article Title: Glabridin Mediate Caspases Activation and Induces Apoptosis through JNK1/2 and p38 MAPK Pathway in Human Promyelocytic Leukemia Cells

    doi: 10.1371/journal.pone.0098943

    Figure Lengend Snippet: JNK1/2 and p38 MAPK are essential for caspase activation induced by glabridin. (A) HL-60 cells were treated for 24 hours with 40 µM glabridin with or without a 1-hour pretreatment of 20 µM U0126, SP600125, or SB202190. The expression of cleaved caspase-9, -8 and -3 were detected by western blotting. (B–D) Quantitative results of cleaved caspase-9, -8, and -3 protein levels, which were adjusted to the β-actin protein level and expressed as multiples of induction beyond each respective control. Values represent the mean ± SE of three independen experiments. Data were analyzed using a one-way ANOVA with Tukey’s posthoc tests at 95% confidence intervals; different letters represent different levels of significance.

    Article Snippet: Specific inhibitors for ERK1/2 (U0126), JNK1/2 (SP600125) or p38 (SB202190) were purchased from Calbiochem (San Diego, CA).

    Techniques: Activation Assay, Expressing, Western Blot

    The Ba 2+ current reduction induced by TNF- α is not mediated by a synthetic pathway activation in guinea pig tracheal myocytes. Ba 2+ current evoked by step depolarization from −60 to 50 mV in tracheal cells from nonsensitized guinea pigs added with fetal bovine serum (NS + FBS, n = 7) were significantly diminished when myocytes were grown with TNF- α ( n = 7). Neither actinomycin D (Act D, n = 6) nor cycloheximide (Cyclohex, n = 9) addition during myocyte growth altered TNF- α induced effect on the Ba 2+ current. Inset represents original recordings. ∗ p

    Journal: Mediators of Inflammation

    Article Title: Tumor Necrosis Factor Alpha Inhibits L-Type Ca2+ Channels in Sensitized Guinea Pig Airway Smooth Muscle through ERK 1/2 Pathway

    doi: 10.1155/2016/5972302

    Figure Lengend Snippet: The Ba 2+ current reduction induced by TNF- α is not mediated by a synthetic pathway activation in guinea pig tracheal myocytes. Ba 2+ current evoked by step depolarization from −60 to 50 mV in tracheal cells from nonsensitized guinea pigs added with fetal bovine serum (NS + FBS, n = 7) were significantly diminished when myocytes were grown with TNF- α ( n = 7). Neither actinomycin D (Act D, n = 6) nor cycloheximide (Cyclohex, n = 9) addition during myocyte growth altered TNF- α induced effect on the Ba 2+ current. Inset represents original recordings. ∗ p

    Article Snippet: Drugs and Chemicals Tumor necrosis factor alpha (TNF-α ), U0126 ethanolate, an inhibitor of ERK 1/2 kinase (1,4-diamino-2,3-dicyano-1,4-bis-(0-amino-phenylmercapto)butadiene ethanolate), cycloheximide, actinomycin D, and indomethacin were purchased from Sigma Chem.

    Techniques: Activation Assay, Activated Clotting Time Assay

    Effect of p38 MAP kinase inhibition upon expression of PARs1–4 in HUVECs assessed by quantitative PCR. HUVECs were pretreated with SB203580 at concentrations of 1, 10 and 20 μ M 30 min before 24 h TNF α treatment.

    Journal:

    Article Title: Cytokine upregulation of proteinase-activated-receptors 2 and 4 expression mediated by p38 MAP kinase and inhibitory kappa B kinase β in human endothelial cells

    doi: 10.1038/sj.bjp.0707150

    Figure Lengend Snippet: Effect of p38 MAP kinase inhibition upon expression of PARs1–4 in HUVECs assessed by quantitative PCR. HUVECs were pretreated with SB203580 at concentrations of 1, 10 and 20 μ M 30 min before 24 h TNF α treatment.

    Article Snippet: The p38 MAP kinase inhibitor, SB203580, JNK inhibitor, SP600125 and MEK inhibitors, PD98059 and U0126, were obtained from Calbiochem (San Diego, CA, USA).

    Techniques: Inhibition, Expressing, Real-time Polymerase Chain Reaction

    Activation of ERK, p38 MAP kinase and I κ B α degradation by TNF α , IL-1 β and trypsin in HUVECs. Cells were stimulated with TNF α (10 ng ml −1 ), IL-1 β (10 ng ml −1

    Journal:

    Article Title: Cytokine upregulation of proteinase-activated-receptors 2 and 4 expression mediated by p38 MAP kinase and inhibitory kappa B kinase β in human endothelial cells

    doi: 10.1038/sj.bjp.0707150

    Figure Lengend Snippet: Activation of ERK, p38 MAP kinase and I κ B α degradation by TNF α , IL-1 β and trypsin in HUVECs. Cells were stimulated with TNF α (10 ng ml −1 ), IL-1 β (10 ng ml −1

    Article Snippet: The p38 MAP kinase inhibitor, SB203580, JNK inhibitor, SP600125 and MEK inhibitors, PD98059 and U0126, were obtained from Calbiochem (San Diego, CA, USA).

    Techniques: Activation Assay

    AQP2 accumulation at the cell surface, but not the trans -Golgi region, following acute hypertonicity depends on p38 MAPK activity. mCCDc l1 , LLC-AQP2, LLC-AQP2 (S256D), and LLC-AQP2 (S256A) cells were preincubated or not for 30 min with p38 MAPK inhibitors

    Journal:

    Article Title: Acute Hypertonicity Alters Aquaporin-2 Trafficking and Induces a MAPK-dependent Accumulation at the Plasma Membrane of Renal Epithelial Cells *

    doi: 10.1074/jbc.M801071200

    Figure Lengend Snippet: AQP2 accumulation at the cell surface, but not the trans -Golgi region, following acute hypertonicity depends on p38 MAPK activity. mCCDc l1 , LLC-AQP2, LLC-AQP2 (S256D), and LLC-AQP2 (S256A) cells were preincubated or not for 30 min with p38 MAPK inhibitors

    Article Snippet: For this purpose, we used two inhibitors of p38 MAPK (SB 202190 and SB 203580; EMD Biosciences, La Jolla, CA), two inhibitors of MAPK kinase (MEK)-1 and -2 (PD 98059 and U0126; EMD Biosciences) that subsequently block ERK phosphorylation/activation, and an inhibitor of JNK1 to -3 kinases (SP600125; EMD Biosciences).

    Techniques: Activity Assay

    Effect of MAPK pharmacological inhibitors on hypertonicity-induced MAPK activity. mCCDc l1 and LLC-AQP2 cells were preincubated or not 30 min with p38 MAPK inhibitors SB 202190 ( SB202 ) or SB 203580 ( SB203 ) ( A ), with MEK-1 and -2 inhibitors PD 98059

    Journal:

    Article Title: Acute Hypertonicity Alters Aquaporin-2 Trafficking and Induces a MAPK-dependent Accumulation at the Plasma Membrane of Renal Epithelial Cells *

    doi: 10.1074/jbc.M801071200

    Figure Lengend Snippet: Effect of MAPK pharmacological inhibitors on hypertonicity-induced MAPK activity. mCCDc l1 and LLC-AQP2 cells were preincubated or not 30 min with p38 MAPK inhibitors SB 202190 ( SB202 ) or SB 203580 ( SB203 ) ( A ), with MEK-1 and -2 inhibitors PD 98059

    Article Snippet: For this purpose, we used two inhibitors of p38 MAPK (SB 202190 and SB 203580; EMD Biosciences, La Jolla, CA), two inhibitors of MAPK kinase (MEK)-1 and -2 (PD 98059 and U0126; EMD Biosciences) that subsequently block ERK phosphorylation/activation, and an inhibitor of JNK1 to -3 kinases (SP600125; EMD Biosciences).

    Techniques: Activity Assay