anti sox2  (Proteintech)

 
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    Name:
    Mouse SOX2 Monoclonal
    Description:
    The SOX2 antibody from Proteintech is a mouse monoclonal antibody to a recombinant protein of human SOX2 This antibody recognizes human pig mouse antigen The SOX2 antibody has been validated for the following applications ELISA IF IHC WB analysis
    Catalog Number:
    66411-1-Ig
    Price:
    [321.93]
    Applications:
    IHC,Western Blot,ELISA,Immunofluorescence
    Host:
    Mouse
    Conjugate:
    Unconjugated
    Immunogen:
    Recombinant Protein
    Size:
    150 ul
    Category:
    Antibody
    Antibody Type:
    Primary antibody
    Isotype:
    IgG1
    Reactivity:
    Human Mouse Pig
    Buy from Supplier


    Structured Review

    Proteintech anti sox2
    Ectopic expression of WIP1 reduces the levels of activated p38 and enhances stemness-related protein expression and CSC properties in NSCLC cells. a Western blotting was used to analyze the expression of WIP1, phospho-p38, p38, <t>SOX2,</t> OCT4, NANOG, and ALDH1A1 in H1299 (left panels) and H460 (right panels) cells transduced with a WIP1-overexpressing plasmid (WIP1) or vector control (pLV). Arrows indicate the positions of p38 isoforms. b Western blotting was used to analyze MK2, phospho-MK2 (Thr222), phospho-MK2 (Thr334), HSP27, and phospho-HSP27 (Ser82) in H460 cells transduced with the WIP1-overexpressing plasmid (WIP1) or vector control (pLV). c , d A sphere formation assay was performed with H1299 (top graphs) and H460 (bottom graphs) cells transduced with the WIP1-overexpressing (WIP1) or vector control (pLV) plasmid. Quantifications of sphere sizes ( d ) and numbers ( e ) are shown in bar graphs. The data are presented as the mean ± SD of three independent experiments. * indicates P
    The SOX2 antibody from Proteintech is a mouse monoclonal antibody to a recombinant protein of human SOX2 This antibody recognizes human pig mouse antigen The SOX2 antibody has been validated for the following applications ELISA IF IHC WB analysis
    https://www.bioz.com/result/anti sox2/product/Proteintech
    Average 94 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    anti sox2 - by Bioz Stars, 2020-09
    94/100 stars

    Images

    1) Product Images from "WIP1 promotes cancer stem cell properties by inhibiting p38 MAPK in NSCLC"

    Article Title: WIP1 promotes cancer stem cell properties by inhibiting p38 MAPK in NSCLC

    Journal: Signal Transduction and Targeted Therapy

    doi: 10.1038/s41392-020-0126-x

    Ectopic expression of WIP1 reduces the levels of activated p38 and enhances stemness-related protein expression and CSC properties in NSCLC cells. a Western blotting was used to analyze the expression of WIP1, phospho-p38, p38, SOX2, OCT4, NANOG, and ALDH1A1 in H1299 (left panels) and H460 (right panels) cells transduced with a WIP1-overexpressing plasmid (WIP1) or vector control (pLV). Arrows indicate the positions of p38 isoforms. b Western blotting was used to analyze MK2, phospho-MK2 (Thr222), phospho-MK2 (Thr334), HSP27, and phospho-HSP27 (Ser82) in H460 cells transduced with the WIP1-overexpressing plasmid (WIP1) or vector control (pLV). c , d A sphere formation assay was performed with H1299 (top graphs) and H460 (bottom graphs) cells transduced with the WIP1-overexpressing (WIP1) or vector control (pLV) plasmid. Quantifications of sphere sizes ( d ) and numbers ( e ) are shown in bar graphs. The data are presented as the mean ± SD of three independent experiments. * indicates P
    Figure Legend Snippet: Ectopic expression of WIP1 reduces the levels of activated p38 and enhances stemness-related protein expression and CSC properties in NSCLC cells. a Western blotting was used to analyze the expression of WIP1, phospho-p38, p38, SOX2, OCT4, NANOG, and ALDH1A1 in H1299 (left panels) and H460 (right panels) cells transduced with a WIP1-overexpressing plasmid (WIP1) or vector control (pLV). Arrows indicate the positions of p38 isoforms. b Western blotting was used to analyze MK2, phospho-MK2 (Thr222), phospho-MK2 (Thr334), HSP27, and phospho-HSP27 (Ser82) in H460 cells transduced with the WIP1-overexpressing plasmid (WIP1) or vector control (pLV). c , d A sphere formation assay was performed with H1299 (top graphs) and H460 (bottom graphs) cells transduced with the WIP1-overexpressing (WIP1) or vector control (pLV) plasmid. Quantifications of sphere sizes ( d ) and numbers ( e ) are shown in bar graphs. The data are presented as the mean ± SD of three independent experiments. * indicates P

    Techniques Used: Expressing, Western Blot, Transduction, Plasmid Preparation, Tube Formation Assay

    Related Articles

    Staining:

    Article Title: WIP1 promotes cancer stem cell properties by inhibiting p38 MAPK in NSCLC
    Article Snippet: .. H & E and immunohistochemical staining were performed according to previously described protocols, using a 1:1000 dilution of an anti-WIP1 antibody (Abcam, ab31270), 1:100 dilution of an anti-phospho-p38 MAPK antibody (Cell Signaling Technology, #4511), 1:100 dilution of an anti-SOX2 antibody (Proteintech, 11064-1), and 1:100 dilution of an anti-ALDH1A1 antibody (Santa Cruz, sc-374149). .. The images were acquired with an optical microscope fitted with a camera (Olympus, Japan).

    Immunohistochemistry:

    Article Title: WIP1 promotes cancer stem cell properties by inhibiting p38 MAPK in NSCLC
    Article Snippet: .. H & E and immunohistochemical staining were performed according to previously described protocols, using a 1:1000 dilution of an anti-WIP1 antibody (Abcam, ab31270), 1:100 dilution of an anti-phospho-p38 MAPK antibody (Cell Signaling Technology, #4511), 1:100 dilution of an anti-SOX2 antibody (Proteintech, 11064-1), and 1:100 dilution of an anti-ALDH1A1 antibody (Santa Cruz, sc-374149). .. The images were acquired with an optical microscope fitted with a camera (Olympus, Japan).

    Similar Products

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  • 93
    Proteintech sox2 antibodies
    BmK AGAP inhibits the growth of breast xenograft tumors, stem-like features and epithelial-mesenchymal transition in a mouse model. (A) Weight changes in rBmK AGAP-treated and untreated tumor model mice. BALB/c nude mice were treated with rBmK AGAP or saline and the changes in body weight of mice bearing xenograft tumors were examined for 20 days. (B) Tumor volume of tumors from rBmK AGAP-treated and untreated tumor model mice. Xenograft tumor volume were calculated from measuring the length, height and width of tumors using digital caliper following rBmK AGAP treatment. (C) Image of excised xenograft tumors from the different treatment groups after 20 days of tumor implantation. (D) Quantitative analysis of excised tumor weight. Tumors excised from tumor-bearing mice sacrificed after day 20 were weighed on a digital weighting apparatus. (E) Immunohistochemical assessment of stemness, EMT, and inflammation markers in excised tumor tissues. Xenograft tumor tissues were stained with antibodies against Nav 1.5, PTX3, Oct4, <t>Sox2,</t> E-cadherin, N-cadherin, and p65/NF-κB and examined by immunohistochemical staining (Scale bars = 100 μm; magnification, 200x). (F) Protein expression assessment of PTX3, stemness, EMT, Wnt/β-catenin pathway and NF-κB, in excised tumors. Xenograft tumor tissues from rBmK AGAP-treated and untreated mice were lyse. Equal amount of protein samples were subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, pGSK3-β, GSK3-β, p65/NF-κB, and β-catenin. GAPDH was used as an internal control. The data was statistically significant at * P
    Sox2 Antibodies, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sox2 antibodies/product/Proteintech
    Average 93 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    sox2 antibodies - by Bioz Stars, 2020-09
    93/100 stars
      Buy from Supplier

    99
    Cell Signaling Technology Inc rabbit anti sox2
    Representative figure of Western blot analysis of OCT4 ( a ), <t>SOX2</t> ( b ) and b-actin ( c ) proteins, and relative expression of OCT4 and SOX2. Samples 1 CD tissue, 2 CD blood, 3 UC tissue, 4 UC blood. *p
    Rabbit Anti Sox2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti sox2/product/Cell Signaling Technology Inc
    Average 99 stars, based on 45 article reviews
    Price from $9.99 to $1999.99
    rabbit anti sox2 - by Bioz Stars, 2020-09
    99/100 stars
      Buy from Supplier

    Image Search Results


    BmK AGAP inhibits the growth of breast xenograft tumors, stem-like features and epithelial-mesenchymal transition in a mouse model. (A) Weight changes in rBmK AGAP-treated and untreated tumor model mice. BALB/c nude mice were treated with rBmK AGAP or saline and the changes in body weight of mice bearing xenograft tumors were examined for 20 days. (B) Tumor volume of tumors from rBmK AGAP-treated and untreated tumor model mice. Xenograft tumor volume were calculated from measuring the length, height and width of tumors using digital caliper following rBmK AGAP treatment. (C) Image of excised xenograft tumors from the different treatment groups after 20 days of tumor implantation. (D) Quantitative analysis of excised tumor weight. Tumors excised from tumor-bearing mice sacrificed after day 20 were weighed on a digital weighting apparatus. (E) Immunohistochemical assessment of stemness, EMT, and inflammation markers in excised tumor tissues. Xenograft tumor tissues were stained with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and p65/NF-κB and examined by immunohistochemical staining (Scale bars = 100 μm; magnification, 200x). (F) Protein expression assessment of PTX3, stemness, EMT, Wnt/β-catenin pathway and NF-κB, in excised tumors. Xenograft tumor tissues from rBmK AGAP-treated and untreated mice were lyse. Equal amount of protein samples were subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, pGSK3-β, GSK3-β, p65/NF-κB, and β-catenin. GAPDH was used as an internal control. The data was statistically significant at * P

    Journal: Frontiers in Oncology

    Article Title: Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

    doi: 10.3389/fonc.2019.00021

    Figure Lengend Snippet: BmK AGAP inhibits the growth of breast xenograft tumors, stem-like features and epithelial-mesenchymal transition in a mouse model. (A) Weight changes in rBmK AGAP-treated and untreated tumor model mice. BALB/c nude mice were treated with rBmK AGAP or saline and the changes in body weight of mice bearing xenograft tumors were examined for 20 days. (B) Tumor volume of tumors from rBmK AGAP-treated and untreated tumor model mice. Xenograft tumor volume were calculated from measuring the length, height and width of tumors using digital caliper following rBmK AGAP treatment. (C) Image of excised xenograft tumors from the different treatment groups after 20 days of tumor implantation. (D) Quantitative analysis of excised tumor weight. Tumors excised from tumor-bearing mice sacrificed after day 20 were weighed on a digital weighting apparatus. (E) Immunohistochemical assessment of stemness, EMT, and inflammation markers in excised tumor tissues. Xenograft tumor tissues were stained with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and p65/NF-κB and examined by immunohistochemical staining (Scale bars = 100 μm; magnification, 200x). (F) Protein expression assessment of PTX3, stemness, EMT, Wnt/β-catenin pathway and NF-κB, in excised tumors. Xenograft tumor tissues from rBmK AGAP-treated and untreated mice were lyse. Equal amount of protein samples were subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, pGSK3-β, GSK3-β, p65/NF-κB, and β-catenin. GAPDH was used as an internal control. The data was statistically significant at * P

    Article Snippet: The sources of antibodies and reagents were: PTX3 antibodies #13797-1-AP (proteintech, China); Oct4 antibodies # 11263-1-AP (proteintech, China); Sox2 antibodies #11064-1-AP (Proteintech, China); Nanog antibodies #14295-1-AP (proteintech, China); E-cadherin antibodies #20874-1-AP (proteintech, China); N-cadherin antibodies #22018-1-AP (Proteintech, China); Snai1 antibodies #13099-1-AP (proteintech, China); Vimentin antibodies #10366-1-AP (Proteintech, China); Nav 1.5 antibody #23016-1-AP (Proteintech, China); NF-κB antibodies (Selleck, USA); p65/NF-κB # 10745-1-AP and p-p65 antibodies (Proteintech, China); IKKα and IκBα antibodies (Selleck, USA); pGSK3-β antibodies (Abcam, USA); GSK3-β antibodies (Abcam, USA); β-catenin antibodies # 51067-2-AP (proteintech, China); TNF-α (Proteintech, China); Peroxidase-conjugated goat anti-rabbit IgG (Proteintech, China); PRAP antibodies (Proteintech, China) and GAPDH antibodies (Proteintech, China).

    Techniques: Mouse Assay, Tumor Implantation, Immunohistochemistry, Staining, Expressing, SDS Page, Western Blot

    PTX3 expression in breast cancer cells is associated with stem-like features and epithelial-mesenchymal transition. (A) Tumorsphere formation of MCF-7 and MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated with siPTX3 or rhPTX3 for 14 days, and tumor spheres expansion were analyzed at 40x magnification under a microscope (bar = 50 μm; magnification, 400x). (B) PTX3 promotes cell migration and invasion in breast cancer. MCF-7 and MDA-MB-231 cells were treated with either siPTX3 or rhPTX3. The migration and invasion abilities of the cells were examined by migration and invasion assay (Transwell assay). (C,D) Effect of PTX3 on stem-like features and epithelial-mesenchymal transition markers. siPTX3 or rhPTX3-treated MDA-MB-231 and MCF-7 cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and Snail. GAPDH was used as an internal control. The data was statistically significant at * P

    Journal: Frontiers in Oncology

    Article Title: Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

    doi: 10.3389/fonc.2019.00021

    Figure Lengend Snippet: PTX3 expression in breast cancer cells is associated with stem-like features and epithelial-mesenchymal transition. (A) Tumorsphere formation of MCF-7 and MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated with siPTX3 or rhPTX3 for 14 days, and tumor spheres expansion were analyzed at 40x magnification under a microscope (bar = 50 μm; magnification, 400x). (B) PTX3 promotes cell migration and invasion in breast cancer. MCF-7 and MDA-MB-231 cells were treated with either siPTX3 or rhPTX3. The migration and invasion abilities of the cells were examined by migration and invasion assay (Transwell assay). (C,D) Effect of PTX3 on stem-like features and epithelial-mesenchymal transition markers. siPTX3 or rhPTX3-treated MDA-MB-231 and MCF-7 cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and Snail. GAPDH was used as an internal control. The data was statistically significant at * P

    Article Snippet: The sources of antibodies and reagents were: PTX3 antibodies #13797-1-AP (proteintech, China); Oct4 antibodies # 11263-1-AP (proteintech, China); Sox2 antibodies #11064-1-AP (Proteintech, China); Nanog antibodies #14295-1-AP (proteintech, China); E-cadherin antibodies #20874-1-AP (proteintech, China); N-cadherin antibodies #22018-1-AP (Proteintech, China); Snai1 antibodies #13099-1-AP (proteintech, China); Vimentin antibodies #10366-1-AP (Proteintech, China); Nav 1.5 antibody #23016-1-AP (Proteintech, China); NF-κB antibodies (Selleck, USA); p65/NF-κB # 10745-1-AP and p-p65 antibodies (Proteintech, China); IKKα and IκBα antibodies (Selleck, USA); pGSK3-β antibodies (Abcam, USA); GSK3-β antibodies (Abcam, USA); β-catenin antibodies # 51067-2-AP (proteintech, China); TNF-α (Proteintech, China); Peroxidase-conjugated goat anti-rabbit IgG (Proteintech, China); PRAP antibodies (Proteintech, China) and GAPDH antibodies (Proteintech, China).

    Techniques: Expressing, Multiple Displacement Amplification, Microscopy, Migration, Invasion Assay, Transwell Assay, SDS Page, Western Blot

    BmK AGAP inhibits the growth of breast xenograft tumors, stem-like features and epithelial-mesenchymal transition in a mouse model. (A) Weight changes in rBmK AGAP-treated and untreated tumor model mice. BALB/c nude mice were treated with rBmK AGAP or saline and the changes in body weight of mice bearing xenograft tumors were examined for 20 days. (B) Tumor volume of tumors from rBmK AGAP-treated and untreated tumor model mice. Xenograft tumor volume were calculated from measuring the length, height and width of tumors using digital caliper following rBmK AGAP treatment. (C) Image of excised xenograft tumors from the different treatment groups after 20 days of tumor implantation. (D) Quantitative analysis of excised tumor weight. Tumors excised from tumor-bearing mice sacrificed after day 20 were weighed on a digital weighting apparatus. (E) Immunohistochemical assessment of stemness, EMT, and inflammation markers in excised tumor tissues. Xenograft tumor tissues were stained with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and p65/NF-κB and examined by immunohistochemical staining (Scale bars = 100 μm; magnification, 200x). (F) Protein expression assessment of PTX3, stemness, EMT, Wnt/β-catenin pathway and NF-κB, in excised tumors. Xenograft tumor tissues from rBmK AGAP-treated and untreated mice were lyse. Equal amount of protein samples were subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, pGSK3-β, GSK3-β, p65/NF-κB, and β-catenin. GAPDH was used as an internal control. The data was statistically significant at * P

    Journal: Frontiers in Oncology

    Article Title: Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

    doi: 10.3389/fonc.2019.00021

    Figure Lengend Snippet: BmK AGAP inhibits the growth of breast xenograft tumors, stem-like features and epithelial-mesenchymal transition in a mouse model. (A) Weight changes in rBmK AGAP-treated and untreated tumor model mice. BALB/c nude mice were treated with rBmK AGAP or saline and the changes in body weight of mice bearing xenograft tumors were examined for 20 days. (B) Tumor volume of tumors from rBmK AGAP-treated and untreated tumor model mice. Xenograft tumor volume were calculated from measuring the length, height and width of tumors using digital caliper following rBmK AGAP treatment. (C) Image of excised xenograft tumors from the different treatment groups after 20 days of tumor implantation. (D) Quantitative analysis of excised tumor weight. Tumors excised from tumor-bearing mice sacrificed after day 20 were weighed on a digital weighting apparatus. (E) Immunohistochemical assessment of stemness, EMT, and inflammation markers in excised tumor tissues. Xenograft tumor tissues were stained with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and p65/NF-κB and examined by immunohistochemical staining (Scale bars = 100 μm; magnification, 200x). (F) Protein expression assessment of PTX3, stemness, EMT, Wnt/β-catenin pathway and NF-κB, in excised tumors. Xenograft tumor tissues from rBmK AGAP-treated and untreated mice were lyse. Equal amount of protein samples were subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, pGSK3-β, GSK3-β, p65/NF-κB, and β-catenin. GAPDH was used as an internal control. The data was statistically significant at * P

    Article Snippet: Antibodies and Reagents The sources of antibodies and reagents were: PTX3 antibodies #13797-1-AP (proteintech, China); Oct4 antibodies # 11263-1-AP (proteintech, China); Sox2 antibodies #11064-1-AP (Proteintech, China); Nanog antibodies #14295-1-AP (proteintech, China); E-cadherin antibodies #20874-1-AP (proteintech, China); N-cadherin antibodies #22018-1-AP (Proteintech, China); Snai1 antibodies #13099-1-AP (proteintech, China); Vimentin antibodies #10366-1-AP (Proteintech, China); Nav 1.5 antibody #23016-1-AP (Proteintech, China); NF-κB antibodies (Selleck, USA); p65/NF-κB # 10745-1-AP and p-p65 antibodies (Proteintech, China); IKKα and IκBα antibodies (Selleck, USA); pGSK3-β antibodies (Abcam, USA); GSK3-β antibodies (Abcam, USA); β-catenin antibodies # 51067-2-AP (proteintech, China); TNF-α (Proteintech, China); Peroxidase-conjugated goat anti-rabbit IgG (Proteintech, China); PRAP antibodies (Proteintech, China) and GAPDH antibodies (Proteintech, China).

    Techniques: Mouse Assay, Tumor Implantation, Immunohistochemistry, Staining, Expressing, SDS Page, Western Blot

    PTX3 expression in breast cancer cells is associated with stem-like features and epithelial-mesenchymal transition. (A) Tumorsphere formation of MCF-7 and MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated with siPTX3 or rhPTX3 for 14 days, and tumor spheres expansion were analyzed at 40x magnification under a microscope (bar = 50 μm; magnification, 400x). (B) PTX3 promotes cell migration and invasion in breast cancer. MCF-7 and MDA-MB-231 cells were treated with either siPTX3 or rhPTX3. The migration and invasion abilities of the cells were examined by migration and invasion assay (Transwell assay). (C,D) Effect of PTX3 on stem-like features and epithelial-mesenchymal transition markers. siPTX3 or rhPTX3-treated MDA-MB-231 and MCF-7 cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and Snail. GAPDH was used as an internal control. The data was statistically significant at * P

    Journal: Frontiers in Oncology

    Article Title: Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

    doi: 10.3389/fonc.2019.00021

    Figure Lengend Snippet: PTX3 expression in breast cancer cells is associated with stem-like features and epithelial-mesenchymal transition. (A) Tumorsphere formation of MCF-7 and MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated with siPTX3 or rhPTX3 for 14 days, and tumor spheres expansion were analyzed at 40x magnification under a microscope (bar = 50 μm; magnification, 400x). (B) PTX3 promotes cell migration and invasion in breast cancer. MCF-7 and MDA-MB-231 cells were treated with either siPTX3 or rhPTX3. The migration and invasion abilities of the cells were examined by migration and invasion assay (Transwell assay). (C,D) Effect of PTX3 on stem-like features and epithelial-mesenchymal transition markers. siPTX3 or rhPTX3-treated MDA-MB-231 and MCF-7 cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and Snail. GAPDH was used as an internal control. The data was statistically significant at * P

    Article Snippet: Antibodies and Reagents The sources of antibodies and reagents were: PTX3 antibodies #13797-1-AP (proteintech, China); Oct4 antibodies # 11263-1-AP (proteintech, China); Sox2 antibodies #11064-1-AP (Proteintech, China); Nanog antibodies #14295-1-AP (proteintech, China); E-cadherin antibodies #20874-1-AP (proteintech, China); N-cadherin antibodies #22018-1-AP (Proteintech, China); Snai1 antibodies #13099-1-AP (proteintech, China); Vimentin antibodies #10366-1-AP (Proteintech, China); Nav 1.5 antibody #23016-1-AP (Proteintech, China); NF-κB antibodies (Selleck, USA); p65/NF-κB # 10745-1-AP and p-p65 antibodies (Proteintech, China); IKKα and IκBα antibodies (Selleck, USA); pGSK3-β antibodies (Abcam, USA); GSK3-β antibodies (Abcam, USA); β-catenin antibodies # 51067-2-AP (proteintech, China); TNF-α (Proteintech, China); Peroxidase-conjugated goat anti-rabbit IgG (Proteintech, China); PRAP antibodies (Proteintech, China) and GAPDH antibodies (Proteintech, China).

    Techniques: Expressing, Multiple Displacement Amplification, Microscopy, Migration, Invasion Assay, Transwell Assay, SDS Page, Western Blot

    Ectopic expression of WIP1 reduces the levels of activated p38 and enhances stemness-related protein expression and CSC properties in NSCLC cells. a Western blotting was used to analyze the expression of WIP1, phospho-p38, p38, SOX2, OCT4, NANOG, and ALDH1A1 in H1299 (left panels) and H460 (right panels) cells transduced with a WIP1-overexpressing plasmid (WIP1) or vector control (pLV). Arrows indicate the positions of p38 isoforms. b Western blotting was used to analyze MK2, phospho-MK2 (Thr222), phospho-MK2 (Thr334), HSP27, and phospho-HSP27 (Ser82) in H460 cells transduced with the WIP1-overexpressing plasmid (WIP1) or vector control (pLV). c , d A sphere formation assay was performed with H1299 (top graphs) and H460 (bottom graphs) cells transduced with the WIP1-overexpressing (WIP1) or vector control (pLV) plasmid. Quantifications of sphere sizes ( d ) and numbers ( e ) are shown in bar graphs. The data are presented as the mean ± SD of three independent experiments. * indicates P

    Journal: Signal Transduction and Targeted Therapy

    Article Title: WIP1 promotes cancer stem cell properties by inhibiting p38 MAPK in NSCLC

    doi: 10.1038/s41392-020-0126-x

    Figure Lengend Snippet: Ectopic expression of WIP1 reduces the levels of activated p38 and enhances stemness-related protein expression and CSC properties in NSCLC cells. a Western blotting was used to analyze the expression of WIP1, phospho-p38, p38, SOX2, OCT4, NANOG, and ALDH1A1 in H1299 (left panels) and H460 (right panels) cells transduced with a WIP1-overexpressing plasmid (WIP1) or vector control (pLV). Arrows indicate the positions of p38 isoforms. b Western blotting was used to analyze MK2, phospho-MK2 (Thr222), phospho-MK2 (Thr334), HSP27, and phospho-HSP27 (Ser82) in H460 cells transduced with the WIP1-overexpressing plasmid (WIP1) or vector control (pLV). c , d A sphere formation assay was performed with H1299 (top graphs) and H460 (bottom graphs) cells transduced with the WIP1-overexpressing (WIP1) or vector control (pLV) plasmid. Quantifications of sphere sizes ( d ) and numbers ( e ) are shown in bar graphs. The data are presented as the mean ± SD of three independent experiments. * indicates P

    Article Snippet: The antibodies used in this study included anti-WIP1 (Abcam, USA, ab31270), anti-p38 (Abcam, ab32142), anti-phospho-p38 MAPK (Cell Signaling Technology, USA, #4511), anti-MAPKAPK-2 (Cell Signaling Technology, #3042), anti-phospho-MAPKAPK-2 (Thr222) (Cell Signaling Technology, #3316), anti-phospho-MAPKAPK-2 (Thr334) (Cell Signaling Technology, #3041), anti-HSP27 (Cell Signaling Technology, #2402), anti-phospho-HSP27 (Ser82) (Cell Signaling Technology, #9709), anti-SOX2 (Proteintech, USA, 11064-1), anti-OCT4 (Proteintech, 11263-1), anti-NANOG (Proteintech, 14295-1), anti-ALDH1A1 (Santa Cruz, USA, sc-374149), and anti-β-actin (Santa Cruz, sc-47778).

    Techniques: Expressing, Western Blot, Transduction, Plasmid Preparation, Tube Formation Assay

    Representative figure of Western blot analysis of OCT4 ( a ), SOX2 ( b ) and b-actin ( c ) proteins, and relative expression of OCT4 and SOX2. Samples 1 CD tissue, 2 CD blood, 3 UC tissue, 4 UC blood. *p

    Journal: Gut Pathogens

    Article Title: Specific detection of OCT4 isoforms in inflammatory bowel disease

    doi: 10.1186/s13099-015-0073-1

    Figure Lengend Snippet: Representative figure of Western blot analysis of OCT4 ( a ), SOX2 ( b ) and b-actin ( c ) proteins, and relative expression of OCT4 and SOX2. Samples 1 CD tissue, 2 CD blood, 3 UC tissue, 4 UC blood. *p

    Article Snippet: The primary antibodies used in the current study were: rabbit anti-OCT4 (1:1000, Proteintech, 11263-1-AP), rabbit anti-SOX2 (1:1000, Cell Signalling Technology, 2748) and rabbit anti-beta actin (1:1000, Rockland antibodies & assays, 600-401-886), and the secondary antibody: anti-rabbit HRP (1:1000, Lifespan Biosciences, LS-C56309).

    Techniques: Western Blot, Expressing