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  • 99
    Millipore sp600125
    AdoR promotes transcription of TNF Egr in polarity-deficient epithelial cells. a sal > ent2 , AdoR expression enhances TNF egr transcript levels in the wing disc independently of <t>JNK</t> signalling. TNFR grnd expression, measured by RT-qPCR, is shown as a control. Fold changes are relative to rp49 , n = 6. b – d sal > ent2, AdoR expression upregulates expression of Egr-GFP from a genomic fosmid ( b , c ). This effect is not rescued by co-expression of JNK bskDN ( d ). The arrowhead in b indicates a suspected position effect of the attP site (VK00033) where the fosmid was integrated. e CADO treatment increases expression of TNF egr in explanted wild-type discs, but not in AdoR mutant discs. This effect is further enhanced by Ador overexpression. TNFR grnd expression, measured by RT-qPCR, is shown as a control. Fold changes are relative to rp49 , n ≥ 5. f en > scrib Ri discs upregulate TNF egr mRNA in an AdoR/Ent2-dependent and JNK-independent fashion. Fold changes are relative to rp49 , n ≥ 4. g Human HaCaT cells treated with adenosine upregulates TNF-α transcript levels (as assayed by qRT-PCR). Fold changes are relative to GAPDH , n = 5. Expression of PKG1 , a housekeeping gene and survivin , a JNK target gene, are also shown. h The effect shown in g was suppressed by three different adenosine receptor antagonists (CGS15943, SCH58261 or Caffeine) and by a PKA inhibitor cocktail (Merck # 20-114), but not by JNK inhibitor <t>SP600125.</t> Fold changes are relative to GAPDH , n ≥ 3 and expression of PKG1 is shown. i , j AdoR mutants live longer than wild-type flies when continuously fed with a low dose of Bleomycin ( i ) but live shorter than wild-type flies during acute desiccation (dry starvation, j ). **** P
    Sp600125, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sp600125/product/Millipore
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sp600125 - by Bioz Stars, 2021-05
    99/100 stars
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    99
    Selleck Chemicals sp600125
    BMP14 induces tenogenic signaling in BMSCs via the JNK and Smad1 pathway in a Sirt1-dependent manner. (A) BMSC cells were infected with Sirt1 overexpressing or shSirt1 lentivirus. Following treatment with 50 ng/ml BMP14, the cell extracts were blotted with anti-P-p38, p38, P-JNK, JNK, P-smad2/3, smad2/3, P-smad1 and smad1 antibodies. Quantitative analysis of the blots was performed using ImageJ software and the relative ratios are indicated above the blots. (B) mRNA levels of Scx were detected using RT-qPCR. (C) BMSC cells were treated with 50 ng/ml BMP14 plus 1 µM LDN-193189 and <t>SP600125.</t> Following 48 h the cells were harvested and cell extracts were immunoprecipitated with PPARγ antibodies; the blots were immunoblotted with acetyl-lys and PPARγ antibodies. The total cell lysate was immunoblotted with anti-β-actin antibody. β-actin was used as the control. BMSC cells were treated with 50 ng/ml BMP14 with or without 1 µM LDN-193189 or SP600125. (D) The protein expression of Scx, collagen I, collagen III and Sirt1 in BMSC cells were detected by western blot analysis. β-actin was used as the loading control. The data are presented as the mean ± standard error of the mean. *P
    Sp600125, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sp600125/product/Selleck Chemicals
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sp600125 - by Bioz Stars, 2021-05
    99/100 stars
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    99
    Tocris sp600125
    FAF1-mediated JNK1 activation triggers mitochondrial dysfunction upon ischemic stress. a Faf1 +/+ MEFs were treated with oxygen glucose deprivation for the indicated times and then fractionated into cytoplasmic and mitochondrial fractions. The fractions were analyzed by immunoblotting with anti-P-JNK, JNK1, anti-COX IV (mitochondrial marker) and anti-β-actin (cytoplasmic marker) antibodies. b Faf1 +/+ and Faf1 gt/gt MEFs were treated with oxygen glucose deprivation for 2 h and then fractionated into cytoplasmic and mitochondrial fractions. The fractions were analyzed by immunoblotting with anti-P-JNK, JNK1, anti-COX IV and anti-β-actin antibodies. c Upper panel: Faf1 +/+ and Faf1 gt/gt MEFs were transfected with DsRed-Mito plasmid for 48 h. Subsequently, the cells were treated with oxygen glucose deprivation in the presence or absence of 20 μM <t>SP600125</t> for 2 h. Fluorescence images show the alterations in mitochondrial morphology . Scale bar = 20 μm. Bottom panel: the graph shows the quantification of mitochondrial fragmentation ( n = 3). d Faf1 +/+ and Faf1 gt/gt MEFs were untreated or treated with oxygen glucose deprivation in the presence or absence of 20 μM SP600125 for 5 h. Mitochondrial superoxide was stained using 10 μM MitoSOX reagent. The population of MitoSOX-positive cells was detected by flow cytometry. The graph shows the results of the quantitative analysis of MitoSOX-positive cells ( n = 3). e Faf1 +/+ and Faf1 gt/gt MEFs were untreated or treated with oxygen glucose deprivation in the presence or absence of 20 μM SP600125 for 5 h, and the mitochondrial potential was measured using a Muse analyzer. The graph was obtained from a quantitative analysis of depolarized cells ( n = 3). The data ( c - e ) are expressed as the mean ± S.E.M. of three independent experiments. Statistical comparisons were evaluated using ANOVA followed by Tukey’s HSD ( c - e ) post hoc analysis. *** P
    Sp600125, supplied by Tocris, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sp600125/product/Tocris
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sp600125 - by Bioz Stars, 2021-05
    99/100 stars
      Buy from Supplier

    N/A
    A 10 mM 5 mg in 2270 µl of the JNK inhibitor SP600125 Cat No 1669 in anhydrous DMSO
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    N/A
    SP 600125 is an anthrone derivative that potently and reversibly inhibits c Jun N terminal kinases JNKs effecting JNK 1 3 It is reported to prevent apoptosis in many cell
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    N/A
    The three isoforms of c Jun N terminal kinase JNK are members of the MAP kinase superfamily that induce the expression of immediate early genes in response to specific stress
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    N/A
    SP 600125 Item No 10010466 is a selective cell permeable reversible inhibitor of JNK isoforms 1 3 with K values of 0 19 μM SP 600125 negative control is a
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    Image Search Results


    AdoR promotes transcription of TNF Egr in polarity-deficient epithelial cells. a sal > ent2 , AdoR expression enhances TNF egr transcript levels in the wing disc independently of JNK signalling. TNFR grnd expression, measured by RT-qPCR, is shown as a control. Fold changes are relative to rp49 , n = 6. b – d sal > ent2, AdoR expression upregulates expression of Egr-GFP from a genomic fosmid ( b , c ). This effect is not rescued by co-expression of JNK bskDN ( d ). The arrowhead in b indicates a suspected position effect of the attP site (VK00033) where the fosmid was integrated. e CADO treatment increases expression of TNF egr in explanted wild-type discs, but not in AdoR mutant discs. This effect is further enhanced by Ador overexpression. TNFR grnd expression, measured by RT-qPCR, is shown as a control. Fold changes are relative to rp49 , n ≥ 5. f en > scrib Ri discs upregulate TNF egr mRNA in an AdoR/Ent2-dependent and JNK-independent fashion. Fold changes are relative to rp49 , n ≥ 4. g Human HaCaT cells treated with adenosine upregulates TNF-α transcript levels (as assayed by qRT-PCR). Fold changes are relative to GAPDH , n = 5. Expression of PKG1 , a housekeeping gene and survivin , a JNK target gene, are also shown. h The effect shown in g was suppressed by three different adenosine receptor antagonists (CGS15943, SCH58261 or Caffeine) and by a PKA inhibitor cocktail (Merck # 20-114), but not by JNK inhibitor SP600125. Fold changes are relative to GAPDH , n ≥ 3 and expression of PKG1 is shown. i , j AdoR mutants live longer than wild-type flies when continuously fed with a low dose of Bleomycin ( i ) but live shorter than wild-type flies during acute desiccation (dry starvation, j ). **** P

    Journal: Nature Communications

    Article Title: Epithelial cells release adenosine to promote local TNF production in response to polarity disruption

    doi: 10.1038/s41467-018-07114-z

    Figure Lengend Snippet: AdoR promotes transcription of TNF Egr in polarity-deficient epithelial cells. a sal > ent2 , AdoR expression enhances TNF egr transcript levels in the wing disc independently of JNK signalling. TNFR grnd expression, measured by RT-qPCR, is shown as a control. Fold changes are relative to rp49 , n = 6. b – d sal > ent2, AdoR expression upregulates expression of Egr-GFP from a genomic fosmid ( b , c ). This effect is not rescued by co-expression of JNK bskDN ( d ). The arrowhead in b indicates a suspected position effect of the attP site (VK00033) where the fosmid was integrated. e CADO treatment increases expression of TNF egr in explanted wild-type discs, but not in AdoR mutant discs. This effect is further enhanced by Ador overexpression. TNFR grnd expression, measured by RT-qPCR, is shown as a control. Fold changes are relative to rp49 , n ≥ 5. f en > scrib Ri discs upregulate TNF egr mRNA in an AdoR/Ent2-dependent and JNK-independent fashion. Fold changes are relative to rp49 , n ≥ 4. g Human HaCaT cells treated with adenosine upregulates TNF-α transcript levels (as assayed by qRT-PCR). Fold changes are relative to GAPDH , n = 5. Expression of PKG1 , a housekeeping gene and survivin , a JNK target gene, are also shown. h The effect shown in g was suppressed by three different adenosine receptor antagonists (CGS15943, SCH58261 or Caffeine) and by a PKA inhibitor cocktail (Merck # 20-114), but not by JNK inhibitor SP600125. Fold changes are relative to GAPDH , n ≥ 3 and expression of PKG1 is shown. i , j AdoR mutants live longer than wild-type flies when continuously fed with a low dose of Bleomycin ( i ) but live shorter than wild-type flies during acute desiccation (dry starvation, j ). **** P

    Article Snippet: Adenosine, SCH58261, Caffeine and the JNK inhibitor SP600125 were obtained from Sigma.

    Techniques: Expressing, Quantitative RT-PCR, Mutagenesis, Over Expression

    BMP14 induces tenogenic signaling in BMSCs via the JNK and Smad1 pathway in a Sirt1-dependent manner. (A) BMSC cells were infected with Sirt1 overexpressing or shSirt1 lentivirus. Following treatment with 50 ng/ml BMP14, the cell extracts were blotted with anti-P-p38, p38, P-JNK, JNK, P-smad2/3, smad2/3, P-smad1 and smad1 antibodies. Quantitative analysis of the blots was performed using ImageJ software and the relative ratios are indicated above the blots. (B) mRNA levels of Scx were detected using RT-qPCR. (C) BMSC cells were treated with 50 ng/ml BMP14 plus 1 µM LDN-193189 and SP600125. Following 48 h the cells were harvested and cell extracts were immunoprecipitated with PPARγ antibodies; the blots were immunoblotted with acetyl-lys and PPARγ antibodies. The total cell lysate was immunoblotted with anti-β-actin antibody. β-actin was used as the control. BMSC cells were treated with 50 ng/ml BMP14 with or without 1 µM LDN-193189 or SP600125. (D) The protein expression of Scx, collagen I, collagen III and Sirt1 in BMSC cells were detected by western blot analysis. β-actin was used as the loading control. The data are presented as the mean ± standard error of the mean. *P

    Journal: Experimental and Therapeutic Medicine

    Article Title: BMP14 induces tenogenic differentiation of bone marrow mesenchymal stem cells in vitro

    doi: 10.3892/etm.2018.6293

    Figure Lengend Snippet: BMP14 induces tenogenic signaling in BMSCs via the JNK and Smad1 pathway in a Sirt1-dependent manner. (A) BMSC cells were infected with Sirt1 overexpressing or shSirt1 lentivirus. Following treatment with 50 ng/ml BMP14, the cell extracts were blotted with anti-P-p38, p38, P-JNK, JNK, P-smad2/3, smad2/3, P-smad1 and smad1 antibodies. Quantitative analysis of the blots was performed using ImageJ software and the relative ratios are indicated above the blots. (B) mRNA levels of Scx were detected using RT-qPCR. (C) BMSC cells were treated with 50 ng/ml BMP14 plus 1 µM LDN-193189 and SP600125. Following 48 h the cells were harvested and cell extracts were immunoprecipitated with PPARγ antibodies; the blots were immunoblotted with acetyl-lys and PPARγ antibodies. The total cell lysate was immunoblotted with anti-β-actin antibody. β-actin was used as the control. BMSC cells were treated with 50 ng/ml BMP14 with or without 1 µM LDN-193189 or SP600125. (D) The protein expression of Scx, collagen I, collagen III and Sirt1 in BMSC cells were detected by western blot analysis. β-actin was used as the loading control. The data are presented as the mean ± standard error of the mean. *P

    Article Snippet: LDN-193189 (S2618) and SP600125 (S1460) were obtained from Selleck (Shanghai, China).

    Techniques: Infection, Software, Quantitative RT-PCR, Immunoprecipitation, Expressing, Western Blot

    FAF1-mediated JNK1 activation triggers mitochondrial dysfunction upon ischemic stress. a Faf1 +/+ MEFs were treated with oxygen glucose deprivation for the indicated times and then fractionated into cytoplasmic and mitochondrial fractions. The fractions were analyzed by immunoblotting with anti-P-JNK, JNK1, anti-COX IV (mitochondrial marker) and anti-β-actin (cytoplasmic marker) antibodies. b Faf1 +/+ and Faf1 gt/gt MEFs were treated with oxygen glucose deprivation for 2 h and then fractionated into cytoplasmic and mitochondrial fractions. The fractions were analyzed by immunoblotting with anti-P-JNK, JNK1, anti-COX IV and anti-β-actin antibodies. c Upper panel: Faf1 +/+ and Faf1 gt/gt MEFs were transfected with DsRed-Mito plasmid for 48 h. Subsequently, the cells were treated with oxygen glucose deprivation in the presence or absence of 20 μM SP600125 for 2 h. Fluorescence images show the alterations in mitochondrial morphology . Scale bar = 20 μm. Bottom panel: the graph shows the quantification of mitochondrial fragmentation ( n = 3). d Faf1 +/+ and Faf1 gt/gt MEFs were untreated or treated with oxygen glucose deprivation in the presence or absence of 20 μM SP600125 for 5 h. Mitochondrial superoxide was stained using 10 μM MitoSOX reagent. The population of MitoSOX-positive cells was detected by flow cytometry. The graph shows the results of the quantitative analysis of MitoSOX-positive cells ( n = 3). e Faf1 +/+ and Faf1 gt/gt MEFs were untreated or treated with oxygen glucose deprivation in the presence or absence of 20 μM SP600125 for 5 h, and the mitochondrial potential was measured using a Muse analyzer. The graph was obtained from a quantitative analysis of depolarized cells ( n = 3). The data ( c - e ) are expressed as the mean ± S.E.M. of three independent experiments. Statistical comparisons were evaluated using ANOVA followed by Tukey’s HSD ( c - e ) post hoc analysis. *** P

    Journal: Cell Communication and Signaling : CCS

    Article Title: FAF1 mediates necrosis through JNK1-mediated mitochondrial dysfunction leading to retinal degeneration in the ganglion cell layer upon ischemic insult

    doi: 10.1186/s12964-018-0265-7

    Figure Lengend Snippet: FAF1-mediated JNK1 activation triggers mitochondrial dysfunction upon ischemic stress. a Faf1 +/+ MEFs were treated with oxygen glucose deprivation for the indicated times and then fractionated into cytoplasmic and mitochondrial fractions. The fractions were analyzed by immunoblotting with anti-P-JNK, JNK1, anti-COX IV (mitochondrial marker) and anti-β-actin (cytoplasmic marker) antibodies. b Faf1 +/+ and Faf1 gt/gt MEFs were treated with oxygen glucose deprivation for 2 h and then fractionated into cytoplasmic and mitochondrial fractions. The fractions were analyzed by immunoblotting with anti-P-JNK, JNK1, anti-COX IV and anti-β-actin antibodies. c Upper panel: Faf1 +/+ and Faf1 gt/gt MEFs were transfected with DsRed-Mito plasmid for 48 h. Subsequently, the cells were treated with oxygen glucose deprivation in the presence or absence of 20 μM SP600125 for 2 h. Fluorescence images show the alterations in mitochondrial morphology . Scale bar = 20 μm. Bottom panel: the graph shows the quantification of mitochondrial fragmentation ( n = 3). d Faf1 +/+ and Faf1 gt/gt MEFs were untreated or treated with oxygen glucose deprivation in the presence or absence of 20 μM SP600125 for 5 h. Mitochondrial superoxide was stained using 10 μM MitoSOX reagent. The population of MitoSOX-positive cells was detected by flow cytometry. The graph shows the results of the quantitative analysis of MitoSOX-positive cells ( n = 3). e Faf1 +/+ and Faf1 gt/gt MEFs were untreated or treated with oxygen glucose deprivation in the presence or absence of 20 μM SP600125 for 5 h, and the mitochondrial potential was measured using a Muse analyzer. The graph was obtained from a quantitative analysis of depolarized cells ( n = 3). The data ( c - e ) are expressed as the mean ± S.E.M. of three independent experiments. Statistical comparisons were evaluated using ANOVA followed by Tukey’s HSD ( c - e ) post hoc analysis. *** P

    Article Snippet: The weakening of the protective potential provided by SP600125 in Fig. might be due to possible off-target effects of SP600125 on other survival kinases, such as AMP-activated protein k inase and phosphatidylinositol 3-kinase [ – ].

    Techniques: Activation Assay, Marker, Transfection, Plasmid Preparation, Fluorescence, Staining, Flow Cytometry, Cytometry

    JNK1 contributes to necrosis upon ischemic stress induced by oxygen-glucose deprivation in MEFs. a MEFs were treated with oxygen glucose deprivation for the indicated times and/or 1 μM staurosporine (STS) for 12 h. The type of cell death was determined by flow cytometry using double staining with annexin V and PI. b The graph shows the quantitative results of the flow cytometry analysis. c and d MEFs were treated with oxygen glucose deprivation or 1 μM STS for the indicated times ( n = 3). Caspase-3 activity was measured using fluorometric assay ( n = 3) ( c ) and western blot analysis ( d ). e MEFs were untreated or treated with oxygen glucose deprivation for 8 h in the presence or absence of zVAD-fmk (50 μM), and cell death was determined by measuring PI uptake using a flow cytometer ( n = 3). f MEFs were pretreated with Nec-1 (50 μM), DPQ (30 μM), or SP600125 (20 μM) for 30 min and then with oxygen glucose deprivation for 8 h in the presence of the individual compounds. Cell death was detected by flow cytometry ( n = 3). g Left panel: Jnk1+/+ and Jnk1−/− MEFs were untreated or treated with oxygen glucose deprivation for 8 h. Cell death was detected using flow cytometry ( n = 3). Right panel: representative immunoblots show the JNK1, FAF1 and β-actin expression levels. The data ( b , c , e - g ) are expressed as the mean ± S.E.M. of three independent experiments. Statistical comparisons were evaluated using ANOVA followed by Dunnett’s T3 ( b, c, and e ) and Tukey’s HSD ( f and g ) post hoc analysis. *** p

    Journal: Cell Communication and Signaling : CCS

    Article Title: FAF1 mediates necrosis through JNK1-mediated mitochondrial dysfunction leading to retinal degeneration in the ganglion cell layer upon ischemic insult

    doi: 10.1186/s12964-018-0265-7

    Figure Lengend Snippet: JNK1 contributes to necrosis upon ischemic stress induced by oxygen-glucose deprivation in MEFs. a MEFs were treated with oxygen glucose deprivation for the indicated times and/or 1 μM staurosporine (STS) for 12 h. The type of cell death was determined by flow cytometry using double staining with annexin V and PI. b The graph shows the quantitative results of the flow cytometry analysis. c and d MEFs were treated with oxygen glucose deprivation or 1 μM STS for the indicated times ( n = 3). Caspase-3 activity was measured using fluorometric assay ( n = 3) ( c ) and western blot analysis ( d ). e MEFs were untreated or treated with oxygen glucose deprivation for 8 h in the presence or absence of zVAD-fmk (50 μM), and cell death was determined by measuring PI uptake using a flow cytometer ( n = 3). f MEFs were pretreated with Nec-1 (50 μM), DPQ (30 μM), or SP600125 (20 μM) for 30 min and then with oxygen glucose deprivation for 8 h in the presence of the individual compounds. Cell death was detected by flow cytometry ( n = 3). g Left panel: Jnk1+/+ and Jnk1−/− MEFs were untreated or treated with oxygen glucose deprivation for 8 h. Cell death was detected using flow cytometry ( n = 3). Right panel: representative immunoblots show the JNK1, FAF1 and β-actin expression levels. The data ( b , c , e - g ) are expressed as the mean ± S.E.M. of three independent experiments. Statistical comparisons were evaluated using ANOVA followed by Dunnett’s T3 ( b, c, and e ) and Tukey’s HSD ( f and g ) post hoc analysis. *** p

    Article Snippet: The weakening of the protective potential provided by SP600125 in Fig. might be due to possible off-target effects of SP600125 on other survival kinases, such as AMP-activated protein k inase and phosphatidylinositol 3-kinase [ – ].

    Techniques: Flow Cytometry, Cytometry, Double Staining, Activity Assay, Western Blot, Expressing