anti β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti β catenin
    Cd treatment <t>activates</t> <t>Wnt/β-catenin</t> signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.
    Anti β Catenin, supplied by Cell Signaling Technology Inc, 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/anti β catenin/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti β catenin - by Bioz Stars, 2023-02
    99/100 stars

    Images

    1) Product Images from "Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter"

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    Journal: Cancer Management and Research

    doi: 10.2147/CMAR.S171200

    Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.
    Figure Legend Snippet: Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.

    Techniques Used: Methylation, Western Blot, Immunofluorescence, Staining, Luciferase, Activity Assay, Reverse Transcription Polymerase Chain Reaction

    Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.
    Figure Legend Snippet: Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.

    Techniques Used: Methylation, Western Blot, Reverse Transcription Polymerase Chain Reaction, Expressing, Migration

    Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.
    Figure Legend Snippet: Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.

    Techniques Used: Expressing, Translocation Assay

    anti β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti β catenin
    Cd treatment <t>activates</t> <t>Wnt/β-catenin</t> signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.
    Anti β Catenin, supplied by Cell Signaling Technology Inc, 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/anti β catenin/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti β catenin - by Bioz Stars, 2023-02
    99/100 stars

    Images

    1) Product Images from "Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter"

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    Journal: Cancer Management and Research

    doi: 10.2147/CMAR.S171200

    Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.
    Figure Legend Snippet: Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.

    Techniques Used: Methylation, Western Blot, Immunofluorescence, Staining, Luciferase, Activity Assay, Reverse Transcription Polymerase Chain Reaction

    Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.
    Figure Legend Snippet: Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.

    Techniques Used: Methylation, Western Blot, Reverse Transcription Polymerase Chain Reaction, Expressing, Migration

    Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.
    Figure Legend Snippet: Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.

    Techniques Used: Expressing, Translocation Assay

    β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc β catenin
    Cd treatment <t>activates</t> <t>Wnt/β-catenin</t> signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.
    β Catenin, supplied by Cell Signaling Technology Inc, 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/β catenin/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    β catenin - by Bioz Stars, 2023-02
    99/100 stars

    Images

    1) Product Images from "Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter"

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    Journal: Cancer Management and Research

    doi: 10.2147/CMAR.S171200

    Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.
    Figure Legend Snippet: Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.

    Techniques Used: Methylation, Western Blot, Immunofluorescence, Staining, Luciferase, Activity Assay, Reverse Transcription Polymerase Chain Reaction

    Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.
    Figure Legend Snippet: Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.

    Techniques Used: Methylation, Western Blot, Reverse Transcription Polymerase Chain Reaction, Expressing, Migration

    Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.
    Figure Legend Snippet: Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.

    Techniques Used: Expressing, Translocation Assay

    antibodies against β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc antibodies against β catenin
    Effect of ASP on <t>β</t> <t>-catenin</t> expression of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) The protein expression analyses of β -catenin by Western blot. Proteins were extracted from cellular cytoplasm and nucleus, respectively; β -actin was used as the internal control. (b) The cellular localization of β -catenin by immunofluorescence, PI (red) to visualize nucleus. (c) β - catenin mRNA expression by qRT-PCR, β -actin was used as the internal control. Different letters: P < 0.05.
    Antibodies Against β Catenin, supplied by Cell Signaling Technology Inc, 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/antibodies against β catenin/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against β catenin - by Bioz Stars, 2023-02
    99/100 stars

    Images

    1) Product Images from "Angelica Sinensis Polysaccharide Prevents Hematopoietic Stem Cells Senescence in D-Galactose-Induced Aging Mouse Model"

    Article Title: Angelica Sinensis Polysaccharide Prevents Hematopoietic Stem Cells Senescence in D-Galactose-Induced Aging Mouse Model

    Journal: Stem Cells International

    doi: 10.1155/2017/3508907

    Effect of ASP on β -catenin expression of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) The protein expression analyses of β -catenin by Western blot. Proteins were extracted from cellular cytoplasm and nucleus, respectively; β -actin was used as the internal control. (b) The cellular localization of β -catenin by immunofluorescence, PI (red) to visualize nucleus. (c) β - catenin mRNA expression by qRT-PCR, β -actin was used as the internal control. Different letters: P < 0.05.
    Figure Legend Snippet: Effect of ASP on β -catenin expression of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) The protein expression analyses of β -catenin by Western blot. Proteins were extracted from cellular cytoplasm and nucleus, respectively; β -actin was used as the internal control. (b) The cellular localization of β -catenin by immunofluorescence, PI (red) to visualize nucleus. (c) β - catenin mRNA expression by qRT-PCR, β -actin was used as the internal control. Different letters: P < 0.05.

    Techniques Used: Expressing, Western Blot, Immunofluorescence, Quantitative RT-PCR

    Effect of ASP on Wnt/ β -catenin signaling mediators of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) GSK-3 β , Ser9-phosphorylated GSK-3 β and TCF-4 protein expressions by Western blot. β -actin was used as the internal control. (b) The relative protein expression of GSK-3 β . (c) The relative protein expression of Ser9-phosphorylated GSK-3 β . (d) The relative protein expression of TCF-4. Different letters: P < 0.05.
    Figure Legend Snippet: Effect of ASP on Wnt/ β -catenin signaling mediators of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) GSK-3 β , Ser9-phosphorylated GSK-3 β and TCF-4 protein expressions by Western blot. β -actin was used as the internal control. (b) The relative protein expression of GSK-3 β . (c) The relative protein expression of Ser9-phosphorylated GSK-3 β . (d) The relative protein expression of TCF-4. Different letters: P < 0.05.

    Techniques Used: Western Blot, Expressing

    anti b catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti b catenin
    Mechanisms of MUC15 on osteosarcoma proliferation, migration and invasion. Western blot detected the apoptosis-inhibiting protein Livin ( A ), the migration-related proteins MMP-9 /MMP-2 ( B ), EMT related proteins ( C ) and the <t>Wnt/b-Catenin</t> signaling pathway of OS cell ( D ).
    Anti B Catenin, supplied by Cell Signaling Technology Inc, 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/anti b catenin/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti b catenin - by Bioz Stars, 2023-02
    99/100 stars

    Images

    1) Product Images from "MUC 15 Promotes Osteosarcoma Cell Proliferation, Migration and Invasion through Livin, MMP-2/MMP-9 and Wnt/β-Catenin Signal Pathway"

    Article Title: MUC 15 Promotes Osteosarcoma Cell Proliferation, Migration and Invasion through Livin, MMP-2/MMP-9 and Wnt/β-Catenin Signal Pathway

    Journal: Journal of Cancer

    doi: 10.7150/jca.49641

    Mechanisms of MUC15 on osteosarcoma proliferation, migration and invasion. Western blot detected the apoptosis-inhibiting protein Livin ( A ), the migration-related proteins MMP-9 /MMP-2 ( B ), EMT related proteins ( C ) and the Wnt/b-Catenin signaling pathway of OS cell ( D ).
    Figure Legend Snippet: Mechanisms of MUC15 on osteosarcoma proliferation, migration and invasion. Western blot detected the apoptosis-inhibiting protein Livin ( A ), the migration-related proteins MMP-9 /MMP-2 ( B ), EMT related proteins ( C ) and the Wnt/b-Catenin signaling pathway of OS cell ( D ).

    Techniques Used: Migration, Western Blot

    anti pan β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti pan β catenin
    Anti Pan β Catenin, supplied by Cell Signaling Technology Inc, 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/anti pan β catenin/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti pan β catenin - by Bioz Stars, 2023-02
    99/100 stars

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    anti β catenin antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti β catenin antibody
    Characterization of H1650-ER1 cells . (A) mRNA expression of E-cadherin, vimentin, occludin and fibronectin in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. (B) mRNA expression of Snail, Twist and Zeb1 in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. Error bars represent s.e.m. (n = 3). (C) Immunofluorescence of H1650 and H1650-ER1 cells stained with DAPI (blue) and <t>antiβ-catenin</t> antibody (green). (D) H1650 and H1650-ER1 cells were seeded on 6 well plates. After 48 hr, a scratch was induced in the confluent cell monolayer. Images were obtained at time t = 0 and after 12 hr (t = 12) to monitor cell migration. Percent cell migration was calculated based on migration of H1650 cells. The error bars represent s.e.m. (n = 3).
    Anti β Catenin Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Properties of resistant cells generated from lung cancer cell lines treated with EGFR inhibitors"

    Article Title: Properties of resistant cells generated from lung cancer cell lines treated with EGFR inhibitors

    Journal: BMC Cancer

    doi: 10.1186/1471-2407-12-95

    Characterization of H1650-ER1 cells . (A) mRNA expression of E-cadherin, vimentin, occludin and fibronectin in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. (B) mRNA expression of Snail, Twist and Zeb1 in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. Error bars represent s.e.m. (n = 3). (C) Immunofluorescence of H1650 and H1650-ER1 cells stained with DAPI (blue) and antiβ-catenin antibody (green). (D) H1650 and H1650-ER1 cells were seeded on 6 well plates. After 48 hr, a scratch was induced in the confluent cell monolayer. Images were obtained at time t = 0 and after 12 hr (t = 12) to monitor cell migration. Percent cell migration was calculated based on migration of H1650 cells. The error bars represent s.e.m. (n = 3).
    Figure Legend Snippet: Characterization of H1650-ER1 cells . (A) mRNA expression of E-cadherin, vimentin, occludin and fibronectin in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. (B) mRNA expression of Snail, Twist and Zeb1 in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. Error bars represent s.e.m. (n = 3). (C) Immunofluorescence of H1650 and H1650-ER1 cells stained with DAPI (blue) and antiβ-catenin antibody (green). (D) H1650 and H1650-ER1 cells were seeded on 6 well plates. After 48 hr, a scratch was induced in the confluent cell monolayer. Images were obtained at time t = 0 and after 12 hr (t = 12) to monitor cell migration. Percent cell migration was calculated based on migration of H1650 cells. The error bars represent s.e.m. (n = 3).

    Techniques Used: Expressing, Quantitative RT-PCR, Immunofluorescence, Staining, Migration

    anti β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti β catenin
    ( A , B ,) GCPs were treated with WNT3 for 24 h and lysates analyzed by Western blot analysis. ( A ) Immunoblotting of GCP lysates with <t>anti-active-β-catenin</t> <t>(Ac-β-cat)</t> antibody showed that WNT3 did not induce β-catenin activation. The GSK-3 inhibitor BIO was used as positive control to increase activated β-catenin and activated β-catenin levels were compared to total β-catenin levels, using anti-β-catenin antibody (n=3). ( B ) Immunoblotting using anti-Phospho(P)-216-GSK-3β, anti-GSK-3β and anti-MYCN antibodies showed that WNT3 does not regulate β-catenin signaling. GAPDH was used as loading control. ( C ) Using a Luciferase assay, WNT3 fails to activate β-catenin signaling, which is reported by the expression of pTOPflash luciferase driven by the TCF/LEF promoter. LiCl was used as a positive control to activate β-catenin signaling. Data represent the mean ± s.e.m.: *p<0.05, **p<0.01, ***p<0.001. NS, not significant.
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    1) Product Images from "WNT3 Inhibits Cerebellar Granule Neuron Progenitor Proliferation and Medulloblastoma Formation via MAPK Activation"

    Article Title: WNT3 Inhibits Cerebellar Granule Neuron Progenitor Proliferation and Medulloblastoma Formation via MAPK Activation

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0081769

    ( A , B ,) GCPs were treated with WNT3 for 24 h and lysates analyzed by Western blot analysis. ( A ) Immunoblotting of GCP lysates with anti-active-β-catenin (Ac-β-cat) antibody showed that WNT3 did not induce β-catenin activation. The GSK-3 inhibitor BIO was used as positive control to increase activated β-catenin and activated β-catenin levels were compared to total β-catenin levels, using anti-β-catenin antibody (n=3). ( B ) Immunoblotting using anti-Phospho(P)-216-GSK-3β, anti-GSK-3β and anti-MYCN antibodies showed that WNT3 does not regulate β-catenin signaling. GAPDH was used as loading control. ( C ) Using a Luciferase assay, WNT3 fails to activate β-catenin signaling, which is reported by the expression of pTOPflash luciferase driven by the TCF/LEF promoter. LiCl was used as a positive control to activate β-catenin signaling. Data represent the mean ± s.e.m.: *p<0.05, **p<0.01, ***p<0.001. NS, not significant.
    Figure Legend Snippet: ( A , B ,) GCPs were treated with WNT3 for 24 h and lysates analyzed by Western blot analysis. ( A ) Immunoblotting of GCP lysates with anti-active-β-catenin (Ac-β-cat) antibody showed that WNT3 did not induce β-catenin activation. The GSK-3 inhibitor BIO was used as positive control to increase activated β-catenin and activated β-catenin levels were compared to total β-catenin levels, using anti-β-catenin antibody (n=3). ( B ) Immunoblotting using anti-Phospho(P)-216-GSK-3β, anti-GSK-3β and anti-MYCN antibodies showed that WNT3 does not regulate β-catenin signaling. GAPDH was used as loading control. ( C ) Using a Luciferase assay, WNT3 fails to activate β-catenin signaling, which is reported by the expression of pTOPflash luciferase driven by the TCF/LEF promoter. LiCl was used as a positive control to activate β-catenin signaling. Data represent the mean ± s.e.m.: *p<0.05, **p<0.01, ***p<0.001. NS, not significant.

    Techniques Used: Western Blot, Activation Assay, Positive Control, Luciferase, Expressing

    In Hedgehog (Hh) signaling, Sonic Hedgehog (SHH) binds Patched (PTCH) receptor, relieving its inhibition of Smoothened (SMO), and stimulating GCP proliferation. In WNT3 signaling, WNT3 binds an undefined receptor to activate MAPK signaling via a non canonical WNT pathway to promote GCP differentiation, whereas other WNTs bind Frizzled (FRZ) receptor to activate the canonical β-catenin pathway and stimulate proliferation. We propose a model whereby regulation of MAPK activity by WNT3 signaling alters the balance between proliferation and differentiation in GCPs, decreasing proliferation and increasing differentiation.
    Figure Legend Snippet: In Hedgehog (Hh) signaling, Sonic Hedgehog (SHH) binds Patched (PTCH) receptor, relieving its inhibition of Smoothened (SMO), and stimulating GCP proliferation. In WNT3 signaling, WNT3 binds an undefined receptor to activate MAPK signaling via a non canonical WNT pathway to promote GCP differentiation, whereas other WNTs bind Frizzled (FRZ) receptor to activate the canonical β-catenin pathway and stimulate proliferation. We propose a model whereby regulation of MAPK activity by WNT3 signaling alters the balance between proliferation and differentiation in GCPs, decreasing proliferation and increasing differentiation.

    Techniques Used: Inhibition, Activity Assay

    β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc β catenin
    ( A ), IF was used to detect F-actin distribution in PLC8024 cells treated with or without rhIL-17A (50 ng/mL) for 48 hr. ( B ), Western blot analysis was used to compare expression levels of epithelial markers (E-cadherin, <t>α-catenin</t> <t>and</t> <t>β-catenin)</t> and mesenchymal markers (fibronectin, Vimentin, N-cadherin and α-smooth muscle actin) in PLC8024 cells treated with or without rhIL-17A (50 ng/mL) for 48 hr. β–actin was used as a loading control.
    β Catenin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Interleukin 17A Promotes Hepatocellular Carcinoma Metastasis via NF-kB Induced Matrix Metalloproteinases 2 and 9 Expression"

    Article Title: Interleukin 17A Promotes Hepatocellular Carcinoma Metastasis via NF-kB Induced Matrix Metalloproteinases 2 and 9 Expression

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0021816

    ( A ), IF was used to detect F-actin distribution in PLC8024 cells treated with or without rhIL-17A (50 ng/mL) for 48 hr. ( B ), Western blot analysis was used to compare expression levels of epithelial markers (E-cadherin, α-catenin and β-catenin) and mesenchymal markers (fibronectin, Vimentin, N-cadherin and α-smooth muscle actin) in PLC8024 cells treated with or without rhIL-17A (50 ng/mL) for 48 hr. β–actin was used as a loading control.
    Figure Legend Snippet: ( A ), IF was used to detect F-actin distribution in PLC8024 cells treated with or without rhIL-17A (50 ng/mL) for 48 hr. ( B ), Western blot analysis was used to compare expression levels of epithelial markers (E-cadherin, α-catenin and β-catenin) and mesenchymal markers (fibronectin, Vimentin, N-cadherin and α-smooth muscle actin) in PLC8024 cells treated with or without rhIL-17A (50 ng/mL) for 48 hr. β–actin was used as a loading control.

    Techniques Used: Western Blot, Expressing

    β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc β catenin
    Primers used in real-time quantitative PCR.
    β Catenin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Ginsenoside Rg1 Improves Differentiation by Inhibiting Senescence of Human Bone Marrow Mesenchymal Stem Cell via GSK-3 β and β -Catenin"

    Article Title: Ginsenoside Rg1 Improves Differentiation by Inhibiting Senescence of Human Bone Marrow Mesenchymal Stem Cell via GSK-3 β and β -Catenin

    Journal: Stem Cells International

    doi: 10.1155/2020/2365814


    Figure Legend Snippet: Primers used in real-time quantitative PCR.

    Techniques Used:

    Effect of Rg1 on the expression of Wnt/ β -catenin signaling pathway-related proteins and mRNA in hBM-MSCs. (a–c) By immunofluorescence, PI (red) cells localize β -catenin, DAPI (blue) to visualize the nucleus. (a) the <25-year-old group, (b) the >65-year-old group, and (c) the >65-year-old+Rg1 group. This test was repeated three times. Representative images were shown. (d) Analysis of protein expression of β -catenin by Western blot. β -Actin was used as an internal control. (e, i) Analysis of mRNA of signaling pathway-related mRNA by RT-PCR; mRNA expression of GAPDH was used as an internal control. (f) Expression of GSK-3 β protein was analyzed by Western blot. (g, h) Relative protein expression of LEF/TCF and C-myc proteins in different groups, and β -Actin was used as an internal control. ∗∗ P < .05 vs. the >65-year-old group, ∗ P < .05 vs. the <25-year-old group.
    Figure Legend Snippet: Effect of Rg1 on the expression of Wnt/ β -catenin signaling pathway-related proteins and mRNA in hBM-MSCs. (a–c) By immunofluorescence, PI (red) cells localize β -catenin, DAPI (blue) to visualize the nucleus. (a) the <25-year-old group, (b) the >65-year-old group, and (c) the >65-year-old+Rg1 group. This test was repeated three times. Representative images were shown. (d) Analysis of protein expression of β -catenin by Western blot. β -Actin was used as an internal control. (e, i) Analysis of mRNA of signaling pathway-related mRNA by RT-PCR; mRNA expression of GAPDH was used as an internal control. (f) Expression of GSK-3 β protein was analyzed by Western blot. (g, h) Relative protein expression of LEF/TCF and C-myc proteins in different groups, and β -Actin was used as an internal control. ∗∗ P < .05 vs. the >65-year-old group, ∗ P < .05 vs. the <25-year-old group.

    Techniques Used: Expressing, Immunofluorescence, Western Blot, Reverse Transcription Polymerase Chain Reaction

    Rg1 regulates differentiation of senile mesenchymal stem cells (hBM-MSCs) related to GSK-3 β Protein. Cell differentiation capacity was detected by differentiation culture assay in the presence or absence of Licl (a, b). This test was repeated three times. Representative images were shown. β -catenin, GSK-3 β , C-myc, TCF, and LEF were analyzed by Western blot (c–f). ∗ P < .05.
    Figure Legend Snippet: Rg1 regulates differentiation of senile mesenchymal stem cells (hBM-MSCs) related to GSK-3 β Protein. Cell differentiation capacity was detected by differentiation culture assay in the presence or absence of Licl (a, b). This test was repeated three times. Representative images were shown. β -catenin, GSK-3 β , C-myc, TCF, and LEF were analyzed by Western blot (c–f). ∗ P < .05.

    Techniques Used: Cell Differentiation, Western Blot

    β catenin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc β catenin
    Illustration of the biological effects of La-LDH scaffolds. The functional scaffolds promote osteogenic differentiation of rBMSCs-OVX by <t>activating</t> <t>Wnt/β-catenin</t> pathway, and suppress RANKL-induced osteoclastogenesis by inhibiting NF‐κB signaling pathway.
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    1) Product Images from "Bi-directional regulation functions of lanthanum-substituted layered double hydroxide nanohybrid scaffolds via activating osteogenesis and inhibiting osteoclastogenesis for osteoporotic bone regeneration"

    Article Title: Bi-directional regulation functions of lanthanum-substituted layered double hydroxide nanohybrid scaffolds via activating osteogenesis and inhibiting osteoclastogenesis for osteoporotic bone regeneration

    Journal: Theranostics

    doi: 10.7150/thno.56607

    Illustration of the biological effects of La-LDH scaffolds. The functional scaffolds promote osteogenic differentiation of rBMSCs-OVX by activating Wnt/β-catenin pathway, and suppress RANKL-induced osteoclastogenesis by inhibiting NF‐κB signaling pathway.
    Figure Legend Snippet: Illustration of the biological effects of La-LDH scaffolds. The functional scaffolds promote osteogenic differentiation of rBMSCs-OVX by activating Wnt/β-catenin pathway, and suppress RANKL-induced osteoclastogenesis by inhibiting NF‐κB signaling pathway.

    Techniques Used: Functional Assay

    La-LDH nanohybrid scaffolds activated Wnt/β-catenin signaling pathway and up-regulated OPG/RANKL. (A) Western blot results for t-GSK-3β, p-GSK-3β, β-catenin, Runx-2, OPG and RANKL expression of the rBMSCs-OVX cultured with La-LDH and LDH scaffolds for 14 days. β-actin was used as the internal reference. (B) The level of p-GSK-3β was normalized to t-GSK-3β (* p < 0.05). The levels of (C) β-catenin, (D) Runx-2, (E) OPG, (F) RANKL and (G) OPG/RANKL were normalized to β-actin (* p < 0.05).
    Figure Legend Snippet: La-LDH nanohybrid scaffolds activated Wnt/β-catenin signaling pathway and up-regulated OPG/RANKL. (A) Western blot results for t-GSK-3β, p-GSK-3β, β-catenin, Runx-2, OPG and RANKL expression of the rBMSCs-OVX cultured with La-LDH and LDH scaffolds for 14 days. β-actin was used as the internal reference. (B) The level of p-GSK-3β was normalized to t-GSK-3β (* p < 0.05). The levels of (C) β-catenin, (D) Runx-2, (E) OPG, (F) RANKL and (G) OPG/RANKL were normalized to β-actin (* p < 0.05).

    Techniques Used: Western Blot, Expressing, Cell Culture

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    Cell Signaling Technology Inc anti β catenin
    Cd treatment <t>activates</t> <t>Wnt/β-catenin</t> signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.
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    Cell Signaling Technology Inc β catenin
    Cd treatment <t>activates</t> <t>Wnt/β-catenin</t> signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.
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    Cell Signaling Technology Inc antibodies against β catenin
    Effect of ASP on <t>β</t> <t>-catenin</t> expression of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) The protein expression analyses of β -catenin by Western blot. Proteins were extracted from cellular cytoplasm and nucleus, respectively; β -actin was used as the internal control. (b) The cellular localization of β -catenin by immunofluorescence, PI (red) to visualize nucleus. (c) β - catenin mRNA expression by qRT-PCR, β -actin was used as the internal control. Different letters: P < 0.05.
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    Cell Signaling Technology Inc anti b catenin
    Mechanisms of MUC15 on osteosarcoma proliferation, migration and invasion. Western blot detected the apoptosis-inhibiting protein Livin ( A ), the migration-related proteins MMP-9 /MMP-2 ( B ), EMT related proteins ( C ) and the <t>Wnt/b-Catenin</t> signaling pathway of OS cell ( D ).
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    Cell Signaling Technology Inc anti pan β catenin
    Mechanisms of MUC15 on osteosarcoma proliferation, migration and invasion. Western blot detected the apoptosis-inhibiting protein Livin ( A ), the migration-related proteins MMP-9 /MMP-2 ( B ), EMT related proteins ( C ) and the <t>Wnt/b-Catenin</t> signaling pathway of OS cell ( D ).
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    Characterization of H1650-ER1 cells . (A) mRNA expression of E-cadherin, vimentin, occludin and fibronectin in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. (B) mRNA expression of Snail, Twist and Zeb1 in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. Error bars represent s.e.m. (n = 3). (C) Immunofluorescence of H1650 and H1650-ER1 cells stained with DAPI (blue) and <t>antiβ-catenin</t> antibody (green). (D) H1650 and H1650-ER1 cells were seeded on 6 well plates. After 48 hr, a scratch was induced in the confluent cell monolayer. Images were obtained at time t = 0 and after 12 hr (t = 12) to monitor cell migration. Percent cell migration was calculated based on migration of H1650 cells. The error bars represent s.e.m. (n = 3).
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    Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.

    Journal: Cancer Management and Research

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    doi: 10.2147/CMAR.S171200

    Figure Lengend Snippet: Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.

    Article Snippet: After blocking with goat serum for 30 minutes, the fixed and blocked cells were incubated with primary anti-β-catenin (rabbit antihuman, 1:100; Cell Signaling Technology), CK1α (rabbit anti human, 1:100; (Cell Signaling Technology) and actin filament antibodies overnight at 4°C.

    Techniques: Methylation, Western Blot, Immunofluorescence, Staining, Luciferase, Activity Assay, Reverse Transcription Polymerase Chain Reaction

    Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.

    Journal: Cancer Management and Research

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    doi: 10.2147/CMAR.S171200

    Figure Lengend Snippet: Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.

    Article Snippet: After blocking with goat serum for 30 minutes, the fixed and blocked cells were incubated with primary anti-β-catenin (rabbit antihuman, 1:100; Cell Signaling Technology), CK1α (rabbit anti human, 1:100; (Cell Signaling Technology) and actin filament antibodies overnight at 4°C.

    Techniques: Methylation, Western Blot, Reverse Transcription Polymerase Chain Reaction, Expressing, Migration

    Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.

    Journal: Cancer Management and Research

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    doi: 10.2147/CMAR.S171200

    Figure Lengend Snippet: Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.

    Article Snippet: After blocking with goat serum for 30 minutes, the fixed and blocked cells were incubated with primary anti-β-catenin (rabbit antihuman, 1:100; Cell Signaling Technology), CK1α (rabbit anti human, 1:100; (Cell Signaling Technology) and actin filament antibodies overnight at 4°C.

    Techniques: Expressing, Translocation Assay

    Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.

    Journal: Cancer Management and Research

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    doi: 10.2147/CMAR.S171200

    Figure Lengend Snippet: Cd treatment activates Wnt/β-catenin signaling and aberrant methylation of the CK1α promoter in NPC cell lines. Notes: ( A ) Western blot analysis of total β-catenin and CK1α in cCd-treated NPC cells and controls; β-actin was used as a loading control. ( B ) Immunofluorescence staining patterns of β-catenin and CK1α in NPC and CCT-NPC cells. Nuclei were stained with DAPI (magnification 400×). ( C ) Luciferase reporter assays using TOPflash/FOPflash reporter plasmids to assess the activity of Wnt/β-catenin. ( D ) RT-PCR analysis of relative transcript levels of the β-catenin target genes cyclin E, cyclin D1, c-Myc and c-Jun . * P <0.05; ** P <0.01; *** P <0.001. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; RT-PCR, reverse transcription-PCR.

    Article Snippet: Western blot was performed as previously described using monoclonal antibodies against β-actin, β-catenin, (1:1,000; Cell Signaling Technology, Beverly, MA, USA), CK1α (1:1,000; Cell Signaling Technology) as well as E-cadherin, N-cadherin and Vimentin (1:1,000; Cell Signaling Technology), at 4°C overnight followed by rinsing and addition of an anti-rabbit/mouse secondary antibody (Gene Tech, Shanghai, People’s Republic of China) at 1:1,000 dilution for 1 hour.

    Techniques: Methylation, Western Blot, Immunofluorescence, Staining, Luciferase, Activity Assay, Reverse Transcription Polymerase Chain Reaction

    Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.

    Journal: Cancer Management and Research

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    doi: 10.2147/CMAR.S171200

    Figure Lengend Snippet: Hypermethylation of CK1α induces a switch in Wnt/β-catenin signaling and malignant progression in CCT-NPC cells. Notes: ( A ) Methylation status of the CK1α promoter analyzed by MS-PCR. ( B ) Western blot analyses of CK1α and β-catenin in CCT-CNE1 cells following treatment with 50 µM 5-aza-CdR for 48 hours. ( C ) RT-PCR analysis of relative transcript levels of β-catenin target genes following treatment of cells with 5-aza-CdR (50 µM). ( D ) Western blot and RT-PCR analyses of the effect of CK1α depletion and (or) 5-aza-CdR treatment on β-catenin expression and downstream gene transcription in CCT-CNE1 cells. ( E ) MTT assays for cell viability of CCT-CNE1 and CCT-CNE2 cells with increasing concentrations of 5-aza-CdR treatment. ( F ) Invasion and migration ability of 5-aza-CdR-treated CCT-CNE1 cells. * P <0.05; ** P <0.01; *** P <0.001, compared with parental cells. # P >0.05, compared with CK1α treated cells. Abbreviations: CCT-NPC, chronic cadmium-treated nasopharyngeal carcinoma; CK1α, casein kinase 1α; MS-PCR, methylation specific-PCR; RT-PCR, reverse transcription-polymerase chain reaction.

    Article Snippet: Western blot was performed as previously described using monoclonal antibodies against β-actin, β-catenin, (1:1,000; Cell Signaling Technology, Beverly, MA, USA), CK1α (1:1,000; Cell Signaling Technology) as well as E-cadherin, N-cadherin and Vimentin (1:1,000; Cell Signaling Technology), at 4°C overnight followed by rinsing and addition of an anti-rabbit/mouse secondary antibody (Gene Tech, Shanghai, People’s Republic of China) at 1:1,000 dilution for 1 hour.

    Techniques: Methylation, Western Blot, Reverse Transcription Polymerase Chain Reaction, Expressing, Migration

    Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.

    Journal: Cancer Management and Research

    Article Title: Chronic cadmium exposure aggravates malignant phenotypes of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway via hypermethylation of the casein kinase 1α promoter

    doi: 10.2147/CMAR.S171200

    Figure Lengend Snippet: Hypothesized model for the induction of Cd on Wnt/β-catenin signaling and malignant progression in NPC cells. Notes: Chronic low-dose Cd treatment of NPC cells induces CK1α promoter hypermethylation that downregulates CK1α expression, leading to accumulation and nuclear translocation of β-catenin thereby activating Wnt/β-catenin signaling to promote malignancy. Abbreviations: APC, adenomatous polyposis coli; CK1α, casein kinase α; EMT, epithelial–mesenchymal transition; GSK-3β, glycogen synthase kinase 3β; NPC, nasopharyngeal carcinoma; TCF/LEF, T-cell factor/lymphoid enhancer factor; β-Trcp, β-transducin repeats-containing proteins.

    Article Snippet: Western blot was performed as previously described using monoclonal antibodies against β-actin, β-catenin, (1:1,000; Cell Signaling Technology, Beverly, MA, USA), CK1α (1:1,000; Cell Signaling Technology) as well as E-cadherin, N-cadherin and Vimentin (1:1,000; Cell Signaling Technology), at 4°C overnight followed by rinsing and addition of an anti-rabbit/mouse secondary antibody (Gene Tech, Shanghai, People’s Republic of China) at 1:1,000 dilution for 1 hour.

    Techniques: Expressing, Translocation Assay

    Effect of ASP on β -catenin expression of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) The protein expression analyses of β -catenin by Western blot. Proteins were extracted from cellular cytoplasm and nucleus, respectively; β -actin was used as the internal control. (b) The cellular localization of β -catenin by immunofluorescence, PI (red) to visualize nucleus. (c) β - catenin mRNA expression by qRT-PCR, β -actin was used as the internal control. Different letters: P < 0.05.

    Journal: Stem Cells International

    Article Title: Angelica Sinensis Polysaccharide Prevents Hematopoietic Stem Cells Senescence in D-Galactose-Induced Aging Mouse Model

    doi: 10.1155/2017/3508907

    Figure Lengend Snippet: Effect of ASP on β -catenin expression of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) The protein expression analyses of β -catenin by Western blot. Proteins were extracted from cellular cytoplasm and nucleus, respectively; β -actin was used as the internal control. (b) The cellular localization of β -catenin by immunofluorescence, PI (red) to visualize nucleus. (c) β - catenin mRNA expression by qRT-PCR, β -actin was used as the internal control. Different letters: P < 0.05.

    Article Snippet: Slides were then incubated with antibodies against β -catenin (1 : 100) (Cell Signaling Technology, USA) overnight at 4°C.

    Techniques: Expressing, Western Blot, Immunofluorescence, Quantitative RT-PCR

    Effect of ASP on Wnt/ β -catenin signaling mediators of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) GSK-3 β , Ser9-phosphorylated GSK-3 β and TCF-4 protein expressions by Western blot. β -actin was used as the internal control. (b) The relative protein expression of GSK-3 β . (c) The relative protein expression of Ser9-phosphorylated GSK-3 β . (d) The relative protein expression of TCF-4. Different letters: P < 0.05.

    Journal: Stem Cells International

    Article Title: Angelica Sinensis Polysaccharide Prevents Hematopoietic Stem Cells Senescence in D-Galactose-Induced Aging Mouse Model

    doi: 10.1155/2017/3508907

    Figure Lengend Snippet: Effect of ASP on Wnt/ β -catenin signaling mediators of Sca-1 + HSC/HPCs in D-gal- induced aging mice. The Sca-1+ HSC/HPCs were collected after the treatment. (a) GSK-3 β , Ser9-phosphorylated GSK-3 β and TCF-4 protein expressions by Western blot. β -actin was used as the internal control. (b) The relative protein expression of GSK-3 β . (c) The relative protein expression of Ser9-phosphorylated GSK-3 β . (d) The relative protein expression of TCF-4. Different letters: P < 0.05.

    Article Snippet: Slides were then incubated with antibodies against β -catenin (1 : 100) (Cell Signaling Technology, USA) overnight at 4°C.

    Techniques: Western Blot, Expressing

    Mechanisms of MUC15 on osteosarcoma proliferation, migration and invasion. Western blot detected the apoptosis-inhibiting protein Livin ( A ), the migration-related proteins MMP-9 /MMP-2 ( B ), EMT related proteins ( C ) and the Wnt/b-Catenin signaling pathway of OS cell ( D ).

    Journal: Journal of Cancer

    Article Title: MUC 15 Promotes Osteosarcoma Cell Proliferation, Migration and Invasion through Livin, MMP-2/MMP-9 and Wnt/β-Catenin Signal Pathway

    doi: 10.7150/jca.49641

    Figure Lengend Snippet: Mechanisms of MUC15 on osteosarcoma proliferation, migration and invasion. Western blot detected the apoptosis-inhibiting protein Livin ( A ), the migration-related proteins MMP-9 /MMP-2 ( B ), EMT related proteins ( C ) and the Wnt/b-Catenin signaling pathway of OS cell ( D ).

    Article Snippet: The primary antibodies included anti-MUC15 (Abcam, ab224468), anti-Livin (Abcam, ab97350), anti-MMP2 (Invitrogen, 35-1300Z), anti-MMP9 (Invitrogen, MA5-15886), anti-E-cadherin (GeneTex, GTX124198), anti-Vimentin (Abcam, ab92547), anti-b-Catenin (CST, #9562) and anti-c-Myc (CST, #5605).

    Techniques: Migration, Western Blot

    Characterization of H1650-ER1 cells . (A) mRNA expression of E-cadherin, vimentin, occludin and fibronectin in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. (B) mRNA expression of Snail, Twist and Zeb1 in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. Error bars represent s.e.m. (n = 3). (C) Immunofluorescence of H1650 and H1650-ER1 cells stained with DAPI (blue) and antiβ-catenin antibody (green). (D) H1650 and H1650-ER1 cells were seeded on 6 well plates. After 48 hr, a scratch was induced in the confluent cell monolayer. Images were obtained at time t = 0 and after 12 hr (t = 12) to monitor cell migration. Percent cell migration was calculated based on migration of H1650 cells. The error bars represent s.e.m. (n = 3).

    Journal: BMC Cancer

    Article Title: Properties of resistant cells generated from lung cancer cell lines treated with EGFR inhibitors

    doi: 10.1186/1471-2407-12-95

    Figure Lengend Snippet: Characterization of H1650-ER1 cells . (A) mRNA expression of E-cadherin, vimentin, occludin and fibronectin in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. (B) mRNA expression of Snail, Twist and Zeb1 in H1650 and H1650-ER1 cells was measured by quantitative RT-PCR. Fold change expression was normalized with respect to H1650 cells. Error bars represent s.e.m. (n = 3). (C) Immunofluorescence of H1650 and H1650-ER1 cells stained with DAPI (blue) and antiβ-catenin antibody (green). (D) H1650 and H1650-ER1 cells were seeded on 6 well plates. After 48 hr, a scratch was induced in the confluent cell monolayer. Images were obtained at time t = 0 and after 12 hr (t = 12) to monitor cell migration. Percent cell migration was calculated based on migration of H1650 cells. The error bars represent s.e.m. (n = 3).

    Article Snippet: Then the cells were incubated overnight with anti-β-catenin antibody (Cell Signaling Technology, Danvers, MA) at 4°C.

    Techniques: Expressing, Quantitative RT-PCR, Immunofluorescence, Staining, Migration