Structured Review

Santa Cruz Biotechnology phospho extracellular signal regulated kinase
The key signaling pathways regulating proliferation and metastasis are suppressed during Rhein treatment. Notes: ( A ) 30 or 60 μM Rhein inhibited the expression of p-ERK, p-Akt, MMP9 and CCND1 in A498 and 786-O cells at 48 h. ( B ) The quantitative results of the key molecules changing showed in ( A ) by ImageJ software. Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MMP9, matrix metalloproteinase 9; p-JNK, <t>phospho-c-Jun</t> N-terminal <t>kinase;</t> p-ERK, <t>phospho-extracellular</t> <t>signal-regulated</t> kinase.
Phospho Extracellular Signal Regulated Kinase, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 89/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/phospho extracellular signal regulated kinase/product/Santa Cruz Biotechnology
Average 89 stars, based on 2 article reviews
Price from $9.99 to $1999.99
phospho extracellular signal regulated kinase - by Bioz Stars, 2020-09
89/100 stars

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1) Product Images from "Rhein inhibits malignant phenotypes of human renal cell carcinoma by impacting on MAPK/NF-κB signaling pathways"

Article Title: Rhein inhibits malignant phenotypes of human renal cell carcinoma by impacting on MAPK/NF-κB signaling pathways

Journal: OncoTargets and therapy

doi: 10.2147/OTT.S153798

The key signaling pathways regulating proliferation and metastasis are suppressed during Rhein treatment. Notes: ( A ) 30 or 60 μM Rhein inhibited the expression of p-ERK, p-Akt, MMP9 and CCND1 in A498 and 786-O cells at 48 h. ( B ) The quantitative results of the key molecules changing showed in ( A ) by ImageJ software. Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MMP9, matrix metalloproteinase 9; p-JNK, phospho-c-Jun N-terminal kinase; p-ERK, phospho-extracellular signal-regulated kinase.
Figure Legend Snippet: The key signaling pathways regulating proliferation and metastasis are suppressed during Rhein treatment. Notes: ( A ) 30 or 60 μM Rhein inhibited the expression of p-ERK, p-Akt, MMP9 and CCND1 in A498 and 786-O cells at 48 h. ( B ) The quantitative results of the key molecules changing showed in ( A ) by ImageJ software. Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MMP9, matrix metalloproteinase 9; p-JNK, phospho-c-Jun N-terminal kinase; p-ERK, phospho-extracellular signal-regulated kinase.

Techniques Used: Expressing, Software

2) Product Images from "Rhein inhibits malignant phenotypes of human renal cell carcinoma by impacting on MAPK/NF-κB signaling pathways"

Article Title: Rhein inhibits malignant phenotypes of human renal cell carcinoma by impacting on MAPK/NF-κB signaling pathways

Journal: OncoTargets and therapy

doi: 10.2147/OTT.S153798

The key signaling pathways regulating proliferation and metastasis are suppressed during Rhein treatment. Notes: ( A ) 30 or 60 μM Rhein inhibited the expression of p-ERK, p-Akt, MMP9 and CCND1 in A498 and 786-O cells at 48 h. ( B ) The quantitative results of the key molecules changing showed in ( A ) by ImageJ software. Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MMP9, matrix metalloproteinase 9; p-JNK, phospho-c-Jun N-terminal kinase; p-ERK, phospho-extracellular signal-regulated kinase.
Figure Legend Snippet: The key signaling pathways regulating proliferation and metastasis are suppressed during Rhein treatment. Notes: ( A ) 30 or 60 μM Rhein inhibited the expression of p-ERK, p-Akt, MMP9 and CCND1 in A498 and 786-O cells at 48 h. ( B ) The quantitative results of the key molecules changing showed in ( A ) by ImageJ software. Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MMP9, matrix metalloproteinase 9; p-JNK, phospho-c-Jun N-terminal kinase; p-ERK, phospho-extracellular signal-regulated kinase.

Techniques Used: Expressing, Software

3) Product Images from "Astaxanthin Inhibits Proliferation of Human Gastric Cancer Cell Lines by Interrupting Cell Cycle Progression"

Article Title: Astaxanthin Inhibits Proliferation of Human Gastric Cancer Cell Lines by Interrupting Cell Cycle Progression

Journal: Gut and Liver

doi: 10.5009/gnl15208

Effects of astaxanthin on the cell proliferative and cell cycle machinery profiles. KATO-III and SNU-1 cells were treated with and without astaxanthin (0, 10, 50, 100, and 200 μM) for 24 hours. Western blots showed decreased p-ERK at 50 and 100 μM in both cell lines. Nevertheless, the lack of effect of astaxanthin on the activation of p-Akt was observed in both cell lines. Astaxanthin upregulated p27 kip-1 in dose-dependent manners in both cell lines. The cyclin D1 and p-Rb protein levels were not affected by astaxanthin (each group for n=3 experiments). p-Akt, phospho-serine/threonine-specific protein kinase; p-ERK, phospho-extracellular signal-regulated kinase; p-Rb, phospho-retinoblastoma protein; DMSO, dissolved in dimethyl sulfoxide.
Figure Legend Snippet: Effects of astaxanthin on the cell proliferative and cell cycle machinery profiles. KATO-III and SNU-1 cells were treated with and without astaxanthin (0, 10, 50, 100, and 200 μM) for 24 hours. Western blots showed decreased p-ERK at 50 and 100 μM in both cell lines. Nevertheless, the lack of effect of astaxanthin on the activation of p-Akt was observed in both cell lines. Astaxanthin upregulated p27 kip-1 in dose-dependent manners in both cell lines. The cyclin D1 and p-Rb protein levels were not affected by astaxanthin (each group for n=3 experiments). p-Akt, phospho-serine/threonine-specific protein kinase; p-ERK, phospho-extracellular signal-regulated kinase; p-Rb, phospho-retinoblastoma protein; DMSO, dissolved in dimethyl sulfoxide.

Techniques Used: Western Blot, Activation Assay

Related Articles

Mutagenesis:

Article Title: Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS
Article Snippet: .. Antibodies and reagents In our experiments, we used antibodies to SOD1 (PC077, the Binding Site; Calbiochem, 574597; SDG6 clone, Sigma), mutant-SOD1 (C4F6 and A9G3 ), KHC (H2) , phospho-p38 MAPK (Cell Signaling #9215), phospho-ERK (Santa Cruz #7383), and phospho-GSK3 (Santa Cruz #11757). .. Secondary antibodies included horseradish peroxidase (HRP)-conjugated rabbit anti-sheep IgG (Upstate, 12-342) and HRP-conjugated rabbit anti-Mouse IgG (Sigma, A9044).

other:

Article Title: Chloride intracellular channel 1 regulates colon cancer cell migration and invasion through ROS/ERK pathway
Article Snippet: Antibodies against CLIC1, MMP-2, MMP-9, total-ERK and phospho-ERK were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, United States).

Article Title: Inhibition of angiotensin type 1 receptor impairs renal ability of K conservation in response to K restriction
Article Snippet: Antibodies to phospho-p38, p38, phospho-ERK, ERK, and c-Src were purchased from Santa Cruz.

Binding Assay:

Article Title: Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS
Article Snippet: .. Antibodies and reagents In our experiments, we used antibodies to SOD1 (PC077, the Binding Site; Calbiochem, 574597; SDG6 clone, Sigma), mutant-SOD1 (C4F6 and A9G3 ), KHC (H2) , phospho-p38 MAPK (Cell Signaling #9215), phospho-ERK (Santa Cruz #7383), and phospho-GSK3 (Santa Cruz #11757). .. Secondary antibodies included horseradish peroxidase (HRP)-conjugated rabbit anti-sheep IgG (Upstate, 12-342) and HRP-conjugated rabbit anti-Mouse IgG (Sigma, A9044).

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    Santa Cruz Biotechnology anti phospho erk
    Sorafenib-resistant MV4-11 and MOLM-13 cell lines display resistance to multiple FLT3 inhibitors. ( a ) MOLM-13 and MV4-11 cell lines were treated with an increasing concentration (from 0 to 1000 n M ) of multiple tyrosine kinase inhibitors. Cells were cultured with inhibitors for 46 h followed by PrestoBlue viability analysis. ( b ) Sorafenib-sensitive and -resistant cell lines were treated with increasing concentrations of AC220 and sorafenib for 46 h before processing for PrestoBlue viability assays. ( c ) Sorafenib-sensitive and -resistant MOLM-13 and MV4-11 cells were serum-starved for 4 h in the presence or absence of 100 n M sorafenib before 100 ng/ml FL stimulation for 5 min. Cells were then lysed and immunoprecipitated with an anti-FLT3 antibody. The <t>4G10</t> (anti-phospho-tyrosine) and anti-FLT3 antibodies were used to probe the blots. ( d ) Cell lysates from the experiment described in c were resolved by SDS–PAGE and analyzed by western blotting using anti-phospho AKT, anti-phospho <t>ERK</t> and anti-Tubulin antibodies. ( e ) MOLM-13 and MV4-11 cells were seeded with or without 100 n M sorafenib in semisolid medium and cultured for 7 days.
    Anti Phospho Erk, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phospho erk/product/Santa Cruz Biotechnology
    Average 93 stars, based on 50 article reviews
    Price from $9.99 to $1999.99
    anti phospho erk - by Bioz Stars, 2020-09
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    Santa Cruz Biotechnology phospho extracellular signal regulated kinase
    The key signaling pathways regulating proliferation and metastasis are suppressed during Rhein treatment. Notes: ( A ) 30 or 60 μM Rhein inhibited the expression of p-ERK, p-Akt, MMP9 and CCND1 in A498 and 786-O cells at 48 h. ( B ) The quantitative results of the key molecules changing showed in ( A ) by ImageJ software. Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MMP9, matrix metalloproteinase 9; p-JNK, <t>phospho-c-Jun</t> N-terminal <t>kinase;</t> p-ERK, <t>phospho-extracellular</t> <t>signal-regulated</t> kinase.
    Phospho Extracellular Signal Regulated Kinase, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 89/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phospho extracellular signal regulated kinase/product/Santa Cruz Biotechnology
    Average 89 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    phospho extracellular signal regulated kinase - by Bioz Stars, 2020-09
    89/100 stars
      Buy from Supplier

    Image Search Results


    Sorafenib-resistant MV4-11 and MOLM-13 cell lines display resistance to multiple FLT3 inhibitors. ( a ) MOLM-13 and MV4-11 cell lines were treated with an increasing concentration (from 0 to 1000 n M ) of multiple tyrosine kinase inhibitors. Cells were cultured with inhibitors for 46 h followed by PrestoBlue viability analysis. ( b ) Sorafenib-sensitive and -resistant cell lines were treated with increasing concentrations of AC220 and sorafenib for 46 h before processing for PrestoBlue viability assays. ( c ) Sorafenib-sensitive and -resistant MOLM-13 and MV4-11 cells were serum-starved for 4 h in the presence or absence of 100 n M sorafenib before 100 ng/ml FL stimulation for 5 min. Cells were then lysed and immunoprecipitated with an anti-FLT3 antibody. The 4G10 (anti-phospho-tyrosine) and anti-FLT3 antibodies were used to probe the blots. ( d ) Cell lysates from the experiment described in c were resolved by SDS–PAGE and analyzed by western blotting using anti-phospho AKT, anti-phospho ERK and anti-Tubulin antibodies. ( e ) MOLM-13 and MV4-11 cells were seeded with or without 100 n M sorafenib in semisolid medium and cultured for 7 days.

    Journal: Oncogene

    Article Title: Aberrant activation of the PI3K/mTOR pathway promotes resistance to sorafenib in AML

    doi: 10.1038/onc.2016.41

    Figure Lengend Snippet: Sorafenib-resistant MV4-11 and MOLM-13 cell lines display resistance to multiple FLT3 inhibitors. ( a ) MOLM-13 and MV4-11 cell lines were treated with an increasing concentration (from 0 to 1000 n M ) of multiple tyrosine kinase inhibitors. Cells were cultured with inhibitors for 46 h followed by PrestoBlue viability analysis. ( b ) Sorafenib-sensitive and -resistant cell lines were treated with increasing concentrations of AC220 and sorafenib for 46 h before processing for PrestoBlue viability assays. ( c ) Sorafenib-sensitive and -resistant MOLM-13 and MV4-11 cells were serum-starved for 4 h in the presence or absence of 100 n M sorafenib before 100 ng/ml FL stimulation for 5 min. Cells were then lysed and immunoprecipitated with an anti-FLT3 antibody. The 4G10 (anti-phospho-tyrosine) and anti-FLT3 antibodies were used to probe the blots. ( d ) Cell lysates from the experiment described in c were resolved by SDS–PAGE and analyzed by western blotting using anti-phospho AKT, anti-phospho ERK and anti-Tubulin antibodies. ( e ) MOLM-13 and MV4-11 cells were seeded with or without 100 n M sorafenib in semisolid medium and cultured for 7 days.

    Article Snippet: Additional antibodies include: anti-phosphotyrosine 4G10 (Millipore, Darmstadt, Germany), anti-phospho AKT (Epitomics, Burlingame, CA, USA), anti-phospho ERK (Santa-Cruz Biotechnology Inc., Dallas, TX, USA), anti-phospho S6K and anti-S6K (Abcam, Cambridge, UK), anti-phospho p38 and anti-p38 (BD biosciences, Sparks, MD, USA) and anti-tubulin and anti-β-actin (Sigma-Aldrich, St Louis, MO, USA).

    Techniques: Concentration Assay, Cell Culture, Immunoprecipitation, SDS Page, Western Blot

    p38 mediates the inhibition of anterograde FAT induced by SOD1ox ( a ) Immunoblotting analysis using activation-specific phosphoantibodies reveals a marked activation of p38 (p-p38) in axoplasms perfused with recombinant oxidized SOD1 (SOD1ox), compared to those perfused with recombinant unmodified WT-SOD1 (WT). In contrast, no changes were found in the activities of ERK (pERK) and GSK3 (pGSK3) in association with a specific SOD1 species. A monoclonal antibody against SOD1 (D3H5) 22 confirmed similar levels of SOD1 perfusion, and antibodies against kinesin-1 (KHC) provided a loading control for total levels of axoplasmic protein. Results from three independent experiments are shown (Squid 1-3). ( b ) Quantitation of results in (a) reveals an approximately 4-fold increase in the phosphorylation of p38 kinase (indicative of p38 activation) in SOD1ox-perfused axoplasms, compared to unmodified WT-SOD1-perfused axoplasms ( n =6, P

    Journal: Nature neuroscience

    Article Title: Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS

    doi: 10.1038/nn.2660

    Figure Lengend Snippet: p38 mediates the inhibition of anterograde FAT induced by SOD1ox ( a ) Immunoblotting analysis using activation-specific phosphoantibodies reveals a marked activation of p38 (p-p38) in axoplasms perfused with recombinant oxidized SOD1 (SOD1ox), compared to those perfused with recombinant unmodified WT-SOD1 (WT). In contrast, no changes were found in the activities of ERK (pERK) and GSK3 (pGSK3) in association with a specific SOD1 species. A monoclonal antibody against SOD1 (D3H5) 22 confirmed similar levels of SOD1 perfusion, and antibodies against kinesin-1 (KHC) provided a loading control for total levels of axoplasmic protein. Results from three independent experiments are shown (Squid 1-3). ( b ) Quantitation of results in (a) reveals an approximately 4-fold increase in the phosphorylation of p38 kinase (indicative of p38 activation) in SOD1ox-perfused axoplasms, compared to unmodified WT-SOD1-perfused axoplasms ( n =6, P

    Article Snippet: Antibodies and reagents In our experiments, we used antibodies to SOD1 (PC077, the Binding Site; Calbiochem, 574597; SDG6 clone, Sigma), mutant-SOD1 (C4F6 and A9G3 ), KHC (H2) , phospho-p38 MAPK (Cell Signaling #9215), phospho-ERK (Santa Cruz #7383), and phospho-GSK3 (Santa Cruz #11757).

    Techniques: Inhibition, Activation Assay, Recombinant, Quantitation Assay

    Fig. 7. Fibroblast migration and calpain activity are dependent on MEK, but not JNK activity. ( A ) Wild-type fibroblasts were loaded into Transwell migration chambers (10 5 cells/well) and allowed to migrate for 5 h, using 5% serum as a chemotactic agent. Calpain inhibitor PD150606 (50 µM), MEK inhibitor UO126 (10 µM) or matrix metalloproteinase inhibitor GM6001 (2 µM) were added to both the upper and lower chambers of the designated wells. ( B ) Wild-type fibroblasts were pre-incubated for 1 h with JNK inhibitor SP600125 (10 µM) or MEK inhibitor UO126 (10 µM), and calpain activity was assessed by SLLVY-AMC cleavage, and compared with that of non-treated cells. The results of both (A) and (B) are the mean ± SEM of at least three independent experiments. ( C ) Wild-type fibroblasts were pre-incubated with 10 µM SP600125 or 10 µM UO126 for 1 h and then analyzed for migration using the in vitro wound healing assay in the continuous presence of inhibitor. ( D ) Serum-starved wild-type, MEKK1–/– or MEKK1 add-back fibroblasts were treated with EGF or FGF-2 for 10 min and then lysed. ERK1/2 activation was then assessed by phospho-ERK immunoblotting. The membrane was then stripped and the total ERK2 level determined by ERK2 immunoblotting. The data are representative of at least three independent experiments. NS, no stimulus.

    Journal: The EMBO Journal

    Article Title: MEKK1 regulates calpain-dependent proteolysis of focal adhesion proteins for rear-end detachment of migrating fibroblasts

    doi: 10.1093/emboj/cdg322

    Figure Lengend Snippet: Fig. 7. Fibroblast migration and calpain activity are dependent on MEK, but not JNK activity. ( A ) Wild-type fibroblasts were loaded into Transwell migration chambers (10 5 cells/well) and allowed to migrate for 5 h, using 5% serum as a chemotactic agent. Calpain inhibitor PD150606 (50 µM), MEK inhibitor UO126 (10 µM) or matrix metalloproteinase inhibitor GM6001 (2 µM) were added to both the upper and lower chambers of the designated wells. ( B ) Wild-type fibroblasts were pre-incubated for 1 h with JNK inhibitor SP600125 (10 µM) or MEK inhibitor UO126 (10 µM), and calpain activity was assessed by SLLVY-AMC cleavage, and compared with that of non-treated cells. The results of both (A) and (B) are the mean ± SEM of at least three independent experiments. ( C ) Wild-type fibroblasts were pre-incubated with 10 µM SP600125 or 10 µM UO126 for 1 h and then analyzed for migration using the in vitro wound healing assay in the continuous presence of inhibitor. ( D ) Serum-starved wild-type, MEKK1–/– or MEKK1 add-back fibroblasts were treated with EGF or FGF-2 for 10 min and then lysed. ERK1/2 activation was then assessed by phospho-ERK immunoblotting. The membrane was then stripped and the total ERK2 level determined by ERK2 immunoblotting. The data are representative of at least three independent experiments. NS, no stimulus.

    Article Snippet: Anti-phospho ERK, ERK2 and FAK (C-terminal) antibodies used for immunoblotting were from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA).

    Techniques: Migration, Activity Assay, Incubation, In Vitro, Wound Healing Assay, Activation Assay

    The key signaling pathways regulating proliferation and metastasis are suppressed during Rhein treatment. Notes: ( A ) 30 or 60 μM Rhein inhibited the expression of p-ERK, p-Akt, MMP9 and CCND1 in A498 and 786-O cells at 48 h. ( B ) The quantitative results of the key molecules changing showed in ( A ) by ImageJ software. Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MMP9, matrix metalloproteinase 9; p-JNK, phospho-c-Jun N-terminal kinase; p-ERK, phospho-extracellular signal-regulated kinase.

    Journal: OncoTargets and therapy

    Article Title: Rhein inhibits malignant phenotypes of human renal cell carcinoma by impacting on MAPK/NF-κB signaling pathways

    doi: 10.2147/OTT.S153798

    Figure Lengend Snippet: The key signaling pathways regulating proliferation and metastasis are suppressed during Rhein treatment. Notes: ( A ) 30 or 60 μM Rhein inhibited the expression of p-ERK, p-Akt, MMP9 and CCND1 in A498 and 786-O cells at 48 h. ( B ) The quantitative results of the key molecules changing showed in ( A ) by ImageJ software. Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MMP9, matrix metalloproteinase 9; p-JNK, phospho-c-Jun N-terminal kinase; p-ERK, phospho-extracellular signal-regulated kinase.

    Article Snippet: Resultant blots were blocked with 5% skim milk and reacted with properly diluted primary antibodies against glyceraldehyde 3-phosphate dehydrogenase (Santa Cruz), phospho-extracellular signal-regulated kinase (Santa Cruz), total extracellular signal-regulated kinase (Santa Cruz), p-AKT (Cell Signaling Technology), phospho-c-Jun N-terminal kinase (Cell Signaling Technology), matrix metalloproteinase 9 (MMP9) (Cell Signaling Technology) and CCND1 (Cell Signaling Technology) for 1 h at room temperature.

    Techniques: Expressing, Software