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phosphopkc substrates  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphopkc substrates
    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
    Phosphopkc Substrates, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 624 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Genkwanin glycosides are major active compounds in Phaleria nisidai extract mediating improved glucose homeostasis by stimulating glucose uptake into adipose tissues"

    Article Title: Genkwanin glycosides are major active compounds in Phaleria nisidai extract mediating improved glucose homeostasis by stimulating glucose uptake into adipose tissues

    Journal: Nature Communications

    doi: 10.1038/s41467-025-62689-8

    a PhosphoPKC substrates western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
    Figure Legend Snippet: a PhosphoPKC substrates western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .

    Techniques Used: Western Blot, Positive Control, Phospho-proteomics, Immunofluorescence, Staining

    Related Articles

    Control:

    Article Title: Trichuris suis induces human non-classical patrolling monocytes via the mannose receptor and PKC: implications for multiple sclerosis.
    Article Snippet: .. The following primary antibodies (in TSM/0,05 % Tween/5 % BSA) were used: PhosphoPKC (Cell signaling, Beverly, MA, USA, #9371S) and GAPDH (Santa Cruz Biotechnology, Heidelberg, Germany, #sc-32233) as a loading control. .. Followed by incubation with polyclonal goat anti-rabbit HRP (Dako, Heverlee, Belgium, #p0448) and polyclonal rabbit anti-mouse HRP (Dako, Heverlee, Belgium, #p0161).

    Article Title: Trichuris suis induces human non-classical patrolling monocytes via the mannose receptor and PKC: implications for multiple sclerosis
    Article Snippet: .. The following primary antibodies (in TSM/0,05 % Tween/5 % BSA) were used: PhosphoPKC (Cell signaling, Beverly, MA, USA, #9371S) and GAPDH (Santa Cruz Biotechnology, Heidelberg, Germany, #sc-32233) as a loading control. .. Followed by incubation with polyclonal goat anti-rabbit HRP (Dako, Heverlee, Belgium, #p0448) and polyclonal rabbit anti-mouse HRP (Dako, Heverlee, Belgium, #p0161).

    other:

    Article Title: Phosphorylation Drives an Apoptotic Protein to Activate Antiapoptotic Genes
    Article Snippet: Antibodies against cIAP1 (7065), cIAP2 (3130), survivin (2808), XIAP (2045), phosphoPKC (9375), and lamin A/C (2032) were from Cell Signaling Technology, Inc. (Danvers, MA).



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    Cell Signaling Technology Inc phosphopkc substrates
    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
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    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
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    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
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    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
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    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
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    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
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    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
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    a <t>PhosphoPKC</t> <t>substrates</t> western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .
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    Image Search Results


    a PhosphoPKC substrates western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .

    Journal: Nature Communications

    Article Title: Genkwanin glycosides are major active compounds in Phaleria nisidai extract mediating improved glucose homeostasis by stimulating glucose uptake into adipose tissues

    doi: 10.1038/s41467-025-62689-8

    Figure Lengend Snippet: a PhosphoPKC substrates western blot. PMA (250 nM) as positive control. b , c ERK1/2 phosphorylation (Thr204, Tyr202) induced by PNe in b iBAs. c Quantification of ERK pThr202/pTyr204 . PNe n = 6, Ctrl n = 6 per time point. 2 independent experiments. d Glut1 mRNA levels in iBAs stimulated for 4 h with PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 18, PNe n = 17, PNe+PD n = 16, PD n = 16. 3 independent experiments. e Representative immunofluorescence pictures stained for nuclei (blue) and ERK1/2 (green) in iBAs. Scale bar 100 µM. f Quantification of ERK1/2 localization. 180 min of PNe/PMA treatment ± PKC inhibitor Gö−6983 (1 μM). Ctrl n = 29, PNe n = 33, PMA n = 32, Gö n = 20, Gö + PNe n = 18, Gö + PMA n = 21 images/condition. 3 independent experiments. Average 328 cells/image. g Glucose uptake rates in iBAs after 16 h of PNe ± pre-treatment with ERK1/2 inhibitor PD184352 (500 nM, 30 min). Ctrl n = 12, PNe n = 11, PNe + PD n = 12, PD n = 12. 3 independent experiments. Results are reported as mean ± SD. One-way ANOVA with Tukey’s post-hoc test between all groups was applied in ( c , d , f , and g ). Only biologically relevant comparisons are displayed. All comparisons are listed in Source Data 1. Statistical test results are indicated as exact p -values with * p < 0.05 considered significant. Source data are provided in Source Data 1. PMA phorbol 12-myristate 13-acetate, PNe Phaleria nisidai extract, PD PD184352 .

    Article Snippet: ERK1/2 pThr202/Tyr204 (1:1000, Cell Signaling 4370), HSP90 (1:1000, Cell Signaling 4877), GADPH (1:1000, Cell Signaling 5174), phosphoPKC Substrates (1:1000, Cell Signaling 2261), PPARγ(1:1000, Cell Signaling 2443).

    Techniques: Western Blot, Positive Control, Phospho-proteomics, Immunofluorescence, Staining