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epithelial mesenchymal transition emt antibody sampler kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc epithelial mesenchymal transition emt antibody sampler kit
    Epithelial Mesenchymal Transition Emt Antibody Sampler Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 450 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/epithelial mesenchymal transition emt antibody sampler kit/product/Cell Signaling Technology Inc
    Average 96 stars, based on 450 article reviews
    epithelial mesenchymal transition emt antibody sampler kit - by Bioz Stars, 2026-02
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    epithelial mesenchymal transition emt antibody sampler kit  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc epithelial mesenchymal transition emt antibody sampler kit
    Epithelial Mesenchymal Transition Emt Antibody Sampler Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc epithelialmesenchymal transition emt antibody sampler kit
    Epithelialmesenchymal Transition Emt Antibody Sampler Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/epithelialmesenchymal transition emt antibody sampler kit/product/Cell Signaling Technology Inc
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    emt antibody sampler kit  (Cell Signaling Technology Inc)
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    Figure 5. MEF2B knockdown inhibits cell invasion and metastasis, which can be reversed <t>by</t> <t>Cx58</t> overexpression (A–D) Wound healing assays (A,B) and transwell assays (C,D) were performed in A549 control cells and MEF2B-silenced cells to examine their migration and invasion capabilities (scale bar: 100 μm). Data are presented as the mean ± SD (n = 3), **P < 0.01, ***P < 0.001. (E) The cytoskeleton was detected by an immunofluorescence assay of F-actin in A549 control cells and MEF2B-silenced cells (scale bar: 25 μm). (F) <t>EMT-related</t> proteins, including E- cadherin, N-cadherin, vimentin and ZO-1, were detected by western blotting in A549 cells lacking MEF2B and control cells. GAPDH was used as a loading control. (G) Kaplan-Meier survival analysis of the TCGA array data of MEF2B in NSCLC patients via kmplotter online. Red line, high MEF2B expression (n = 1445); black line, low MEF2B expression (n = 481). (H) Kaplan-Meier survival analysis of TCGA array data related to the coexpression of Cx58 and MEF2B in NSCLC patients. Red line, high coexpression (n = 1443); black line, low coexpression (n = 483).
    Emt Antibody Sampler Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    epithelial mesenchymal transition emt antibody  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc epithelial mesenchymal transition emt antibody
    ( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
    Epithelial Mesenchymal Transition Emt Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/epithelial mesenchymal transition emt antibody/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    epithelial mesenchymal transition emt antibody - by Bioz Stars, 2026-02
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    anti epithelial mesenchymal transition emt antibody kit  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc anti epithelial mesenchymal transition emt antibody kit
    ( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal <t>transition</t> <t>(EMT)</t> related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .
    Anti Epithelial Mesenchymal Transition Emt Antibody Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti epithelial mesenchymal transition emt antibody kit/product/Cell Signaling Technology Inc
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    Figure 5. MEF2B knockdown inhibits cell invasion and metastasis, which can be reversed by Cx58 overexpression (A–D) Wound healing assays (A,B) and transwell assays (C,D) were performed in A549 control cells and MEF2B-silenced cells to examine their migration and invasion capabilities (scale bar: 100 μm). Data are presented as the mean ± SD (n = 3), **P < 0.01, ***P < 0.001. (E) The cytoskeleton was detected by an immunofluorescence assay of F-actin in A549 control cells and MEF2B-silenced cells (scale bar: 25 μm). (F) EMT-related proteins, including E- cadherin, N-cadherin, vimentin and ZO-1, were detected by western blotting in A549 cells lacking MEF2B and control cells. GAPDH was used as a loading control. (G) Kaplan-Meier survival analysis of the TCGA array data of MEF2B in NSCLC patients via kmplotter online. Red line, high MEF2B expression (n = 1445); black line, low MEF2B expression (n = 481). (H) Kaplan-Meier survival analysis of TCGA array data related to the coexpression of Cx58 and MEF2B in NSCLC patients. Red line, high coexpression (n = 1443); black line, low coexpression (n = 483).

    Journal: Acta biochimica et biophysica Sinica

    Article Title: Cx58 is associated with the metastasis of non-small cell lung cancer via MEF2B/Cx58 axis.

    doi: 10.3724/abbs.2025049

    Figure Lengend Snippet: Figure 5. MEF2B knockdown inhibits cell invasion and metastasis, which can be reversed by Cx58 overexpression (A–D) Wound healing assays (A,B) and transwell assays (C,D) were performed in A549 control cells and MEF2B-silenced cells to examine their migration and invasion capabilities (scale bar: 100 μm). Data are presented as the mean ± SD (n = 3), **P < 0.01, ***P < 0.001. (E) The cytoskeleton was detected by an immunofluorescence assay of F-actin in A549 control cells and MEF2B-silenced cells (scale bar: 25 μm). (F) EMT-related proteins, including E- cadherin, N-cadherin, vimentin and ZO-1, were detected by western blotting in A549 cells lacking MEF2B and control cells. GAPDH was used as a loading control. (G) Kaplan-Meier survival analysis of the TCGA array data of MEF2B in NSCLC patients via kmplotter online. Red line, high MEF2B expression (n = 1445); black line, low MEF2B expression (n = 481). (H) Kaplan-Meier survival analysis of TCGA array data related to the coexpression of Cx58 and MEF2B in NSCLC patients. Red line, high coexpression (n = 1443); black line, low coexpression (n = 483).

    Article Snippet: The membranes were incubated with the following primary antibodies: anti-Cx58 (SAB2100922, 1:1000; Sigma-Aldrich, St Louis, USA), anti-MEF2B (AV36916, 1:1000; Sigma-Aldrich), EMT antibody sampler kit (9782, 1:1000; Cell Signaling Technology, Danvers, USA), anti-βActin antibody (SC-47778, 1:1000; Santa Cruz Biotechnology, Santa Cruz, USA) and an anti-GAPDH antibody (SC47724, 1:1000; Santa Cruz Biotechnology).

    Techniques: Knockdown, Over Expression, Control, Migration, Immunofluorescence, Western Blot, Expressing

    ( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal transition (EMT) related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .

    Journal: eLife

    Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

    doi: 10.7554/eLife.97373

    Figure Lengend Snippet: ( A–B ) Knockdown of TAK1 by Map3k7 shRNA. ECA-109 cells were transduced with lentivirus bearing Map3k7 shRNA (LV- Map3k7 shRNA) or NC shRNA (LV-NC). 48 hr post-transduction, cells were harvested for analyzing TAK1 expression by quantitative real time-PCR (qRT-PCR) ( A ) and western blot ( B ). n = 3 biologically independent replicates. ( C–E ) Decreased expression of TAK1 facilitates cell migration and invasion. ECA-109 cells were transduced with LV- Map3k7 shRNA or LV-NC. 48 hr post-transduction, cells were subjected to transwell ( C, D ) or wound healing ( E ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( C ); scale bar = 100 µm ( E ). ( F – G ) Reduced expression of TAK1 increases mesenchymal marker expression and decreases epithelial marker expression. n=3 biologically independent replicates. ( H ) Reduced expression of TAK1 in ECA-109 cells affects epithelial-mesenchymal transition (EMT) related gene expression. Protein levels were analyzed by western blot, and Actin was used as a loading control. Gene expression was detected by qRT-PCR, and Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 3—source data 1. TAK1 knockdown facilitates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 3—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 3—source data 3. Original files for western blot analysis displayed in .

    Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

    Techniques: Knockdown, shRNA, Transduction, Expressing, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Western Blot, Migration, Marker, Gene Expression, Control

    ( A–B ) TAK1 expression was decreased by Map3k7 gRNA in ECA-109 cells. TAK1 knockout was achieved by CRISPR-Cas9. (B–D) Knockout of TAK1 expression in ECA-109 cells accelerates cell migration and invasion as analyzed by transwell ( B, C ) and wound healing ( D ) assays. Scale bar = 500 µm ( B ); scale bar = 100 µm ( D ). ( E – F ) Loss of TAK1 increases mesenchymal protein marker expression and reduces epithelial protein marker expression. ECA-109 cells were treated with Map3k7 gRNA, and then cells were harvested for western blot analysis. n=3 biologically independent replicates. ( G ) Knockout of TAK1 expression in ECA-109 cells alters epithelial-mesenchymal transition (EMT) related gene expression as analyzed by quantitative real time-PCR (qRT-PCR). Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Protein levels were analyzed by western blot, and Actin was used as a loading control. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 4—source data 1. TAK1 knockout accelerates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 4—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 4—source data 3. Original files for western blot analysis displayed in .

    Journal: eLife

    Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

    doi: 10.7554/eLife.97373

    Figure Lengend Snippet: ( A–B ) TAK1 expression was decreased by Map3k7 gRNA in ECA-109 cells. TAK1 knockout was achieved by CRISPR-Cas9. (B–D) Knockout of TAK1 expression in ECA-109 cells accelerates cell migration and invasion as analyzed by transwell ( B, C ) and wound healing ( D ) assays. Scale bar = 500 µm ( B ); scale bar = 100 µm ( D ). ( E – F ) Loss of TAK1 increases mesenchymal protein marker expression and reduces epithelial protein marker expression. ECA-109 cells were treated with Map3k7 gRNA, and then cells were harvested for western blot analysis. n=3 biologically independent replicates. ( G ) Knockout of TAK1 expression in ECA-109 cells alters epithelial-mesenchymal transition (EMT) related gene expression as analyzed by quantitative real time-PCR (qRT-PCR). Gapdh was used as a house-keeping gene. n=4 biologically independent replicates. Protein levels were analyzed by western blot, and Actin was used as a loading control. Data are presented as mean ± SD. Statistical significance was tested by unpaired Student’s t-test. *p<0.05, **p<0.01, and ***p<0.001. Figure 1—figure supplement 4—source data 1. TAK1 knockout accelerates esophageal squamous cell carcinoma (ESCC) migration and invasion. Figure 1—figure supplement 4—source data 2. PDF file containing original western blots for , indicating the relevant bands. Figure 1—figure supplement 4—source data 3. Original files for western blot analysis displayed in .

    Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

    Techniques: Expressing, Knock-Out, CRISPR, Migration, Marker, Western Blot, Gene Expression, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Control

    ( A–D ) IP3R blocking inhibits PLCE1 promoted cell migration and invasion. ECA-109 cells were transfected with the plasmid expressing Plce1 for 6 hr and then cells were treated with 2-APB (10 µM) for additional 18 hr. Cell migration and invasion were analyzed by transwell ( A, B ) or wound healing ( C, D ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( A ) and 100 µm ( C ). (E) IP3R blocking counteracts PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression. The levels of mRNA were analyzed by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. * p<0.05, **p<0.01 , and *** p < 0.001. Figure 5—figure supplement 2—source data 1. 2-APB treatment counteracts PLCE1-induced cell migration.

    Journal: eLife

    Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

    doi: 10.7554/eLife.97373

    Figure Lengend Snippet: ( A–D ) IP3R blocking inhibits PLCE1 promoted cell migration and invasion. ECA-109 cells were transfected with the plasmid expressing Plce1 for 6 hr and then cells were treated with 2-APB (10 µM) for additional 18 hr. Cell migration and invasion were analyzed by transwell ( A, B ) or wound healing ( C, D ) assay. n=5 biologically independent replicates. Scale bar = 500 µm ( A ) and 100 µm ( C ). (E) IP3R blocking counteracts PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression. The levels of mRNA were analyzed by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. * p<0.05, **p<0.01 , and *** p < 0.001. Figure 5—figure supplement 2—source data 1. 2-APB treatment counteracts PLCE1-induced cell migration.

    Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

    Techniques: Blocking Assay, Migration, Transfection, Plasmid Preparation, Expressing, Gene Expression, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Two Tailed Test

    Cells were transfected with plasmid expressing Plce1 for 6 hr and then treated with 2-APB (10 µM) for additional 18 hr. ( A–B ) Transwell assay showing the application of 2-APB attenuates cell migration and invasion induced by PLCE1. Scale bar = 500 µm. n=5 biologically independent replicates. ( C–D ) Wound healing assay showing the treatment of 2-APB represses cell migration induced by PLCE1. Scale bar = 100 µm. n=5 biologically independent replicates. ( E ) 2-APB counteracts PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression. The mRNA levels were detected by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. * p < 0.05, ** p<0.01, and *** p<0.001. Figure 5—figure supplement 3—source data 1. IP3R inhibition represses PLCE1-stimulated cell migration and invasion in KYSE-150 cells.

    Journal: eLife

    Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

    doi: 10.7554/eLife.97373

    Figure Lengend Snippet: Cells were transfected with plasmid expressing Plce1 for 6 hr and then treated with 2-APB (10 µM) for additional 18 hr. ( A–B ) Transwell assay showing the application of 2-APB attenuates cell migration and invasion induced by PLCE1. Scale bar = 500 µm. n=5 biologically independent replicates. ( C–D ) Wound healing assay showing the treatment of 2-APB represses cell migration induced by PLCE1. Scale bar = 100 µm. n=5 biologically independent replicates. ( E ) 2-APB counteracts PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression. The mRNA levels were detected by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. * p < 0.05, ** p<0.01, and *** p<0.001. Figure 5—figure supplement 3—source data 1. IP3R inhibition represses PLCE1-stimulated cell migration and invasion in KYSE-150 cells.

    Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

    Techniques: Transfection, Plasmid Preparation, Expressing, Transwell Assay, Migration, Wound Healing Assay, Gene Expression, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Two Tailed Test, Inhibition

    Cells were transfected with plasmid expressing Plce1 for 6 hr and then treated with 2-APB (10 µM) for additional 18 hr. ( A–D ) Cell migration and invasion induced by PLCE1 were repressed by the application of 2-APB in TE-1 cells. Cell migration and invasion were analyzed by transwell assay (A–B, scale bar = 500 µm) and wound healing assay (C–D, scale bar = 100 µm). n=5 biologically independent replicates. ( E ) 2-APB abolishes PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression in TE-1 cells. Gene expression was analyzed by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. ** p<0.01 and *** p<0.001 . Figure 5—figure supplement 4—source data 1. IP3R inhibition reduces PLCE1-stimulated cell migration and invasion in TE-1 cells.

    Journal: eLife

    Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

    doi: 10.7554/eLife.97373

    Figure Lengend Snippet: Cells were transfected with plasmid expressing Plce1 for 6 hr and then treated with 2-APB (10 µM) for additional 18 hr. ( A–D ) Cell migration and invasion induced by PLCE1 were repressed by the application of 2-APB in TE-1 cells. Cell migration and invasion were analyzed by transwell assay (A–B, scale bar = 500 µm) and wound healing assay (C–D, scale bar = 100 µm). n=5 biologically independent replicates. ( E ) 2-APB abolishes PLCE1-induced changes in epithelial-mesenchymal transition (EMT) gene expression in TE-1 cells. Gene expression was analyzed by quantitative real time-PCR (qRT-PCR), and Gapdh was used as a house-keeping gene. n=3 biologically independent replicates. Data are presented as mean ± SD. Statistical significance was tested by two-tailed one-way ANOVA test. ** p<0.01 and *** p<0.001 . Figure 5—figure supplement 4—source data 1. IP3R inhibition reduces PLCE1-stimulated cell migration and invasion in TE-1 cells.

    Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

    Techniques: Transfection, Plasmid Preparation, Expressing, Migration, Transwell Assay, Wound Healing Assay, Gene Expression, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Two Tailed Test, Inhibition

    Journal: eLife

    Article Title: TAK1-mediated phosphorylation of PLCE1 represses PIP2 hydrolysis to impede esophageal squamous cancer metastasis

    doi: 10.7554/eLife.97373

    Figure Lengend Snippet:

    Article Snippet: Rabbit monoclonal antibodies against TAK1 (#5206), phospho-TAK1 (Ser412, #9339), PKCα (#2056), phospho-PKC (pan) (gamma Thr514) (#38938), GSK-3β (#9315), phospho-GSK-3β (Ser9) (#5558), β-Catenin (#8480), phospho-β-Catenin (Ser33/37/Thr41) (#9561), MMP-2 (#87809), mouse monoclonal antibodies against Actin (#3700), Myc-Tag (Sepharose Bead Conjugate) (#55464), Epithelial-Mesenchymal Transition (EMT) antibody sample kit (#9782), phosphor-IKK (#2078), IKK (#61294), phosphor-JNK (#4668), JNK (#9252), phospho-ERK (#4370), ERK (#9102), phospho-P38 MAPK (#9211), P38 MPAK (#9212), and normal rabbit IgG (#2729) were from Cell Signaling Technology (Beverley, MA, USA).

    Techniques: Transfection, Construct, shRNA, Recombinant, Plasmid Preparation, Sequencing, Activity Assay, Enzyme-linked Immunosorbent Assay, Software