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  • 90
    ATCC echinocandin
    Echinocandin, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Santa Cruz Biotechnology control shrna
    Absence of chloride channel <t>protein-2</t> <t>(ClC-2)</t> resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA <t>(shRNA)</t> cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.
    Control Shrna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/control shrna/product/Santa Cruz Biotechnology
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    90
    Santa Cruz Biotechnology short hairpin rna shrna
    Absence of chloride channel <t>protein-2</t> <t>(ClC-2)</t> resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA <t>(shRNA)</t> cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.
    Short Hairpin Rna Shrna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/short hairpin rna shrna/product/Santa Cruz Biotechnology
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    90
    Santa Cruz Biotechnology hairpin
    Absence of chloride channel <t>protein-2</t> <t>(ClC-2)</t> resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA <t>(shRNA)</t> cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.
    Hairpin, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hairpin/product/Santa Cruz Biotechnology
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    86
    NCIMB Ltd deposit number ncimb 42379
    Absence of chloride channel <t>protein-2</t> <t>(ClC-2)</t> resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA <t>(shRNA)</t> cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.
    Deposit Number Ncimb 42379, supplied by NCIMB Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
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    Image Search Results


    Absence of chloride channel protein-2 (ClC-2) resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA (shRNA) cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.

    Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

    Article Title: Knockout of ClC-2 reveals critical functions of adherens junctions in colonic homeostasis and tumorigenicity

    doi: 10.1152/ajpgi.00087.2018

    Figure Lengend Snippet: Absence of chloride channel protein-2 (ClC-2) resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA (shRNA) cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.

    Article Snippet: Persistent knockdown of clcn-2 gene expression using short-hairpin RNA (shRNA) was achieved by transfecting HT-29 cells with lentiviral particles encoding ClC-2 shRNA or control shRNA (catalog nos. sc-42379-V and sc-108080; Santa Cruz Biotechnology).

    Techniques: In Vitro, shRNA, Cell Counting, CCK-8 Assay, Colony Assay, Proximity Ligation Assay