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human genome u219 microarray platform  (Thermo Fisher)


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    Thermo Fisher human genome u219 microarray platform
    mTORC1 activity concurrent with enhanced metastatic potential. ( a ) Left panels, representative immunohistochemical scores (0, negative, to 3, highest expression) of pS6 staining in the tissue <t>microarray</t> (TMA) of primary breast tumors. Right panel, results for the association between pS6 staining and distant metastasis. ( b ) Increased expression of mTORC1 pathway components with enhanced metastatic potential of MDA-MB-231 cells. The loading control (α-tubulin, TUBA) is shown. Bottom panel, graph showing quantifications of protein levels relative to parental and TUBA (per sample). ( c ) Increased pS6 expression in lung metastases developed by LM2 cells. The arrows mark magnified fields. Right panel, box-and-whisker plots for the quantification (pixels/area, p/a) of pS6 intensity; three mice and three similar lung metastases were analyzed in each setting. The P -value of the two-tailed Mann–Whitney test is shown. ( d ) Left panel, graph showing the in vivo photon flux quantification in mice injected with LM2 and treated with DMSO or everolimus. Representative images from bioluminescence in lungs from DMSO- or everolimus-treated mice are shown. The scale bar depicts the range of photon flux values as a pseudo-color display, with red and blue representing high and low values, respectively. Right top panels, quantification of lung colonization (total metastasis area normalized per total lung area, based on HE). Right bottom panels, representative immunohistochemical results for pS6 and quantification of normalized intensities.
    Human Genome U219 Microarray Platform, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human genome u219 microarray platform/product/Thermo Fisher
    Average 86 stars, based on 1 article reviews
    human genome u219 microarray platform - by Bioz Stars, 2026-03
    86/100 stars

    Images

    1) Product Images from "Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition"

    Article Title: Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition

    Journal: Oncogene

    doi: 10.1038/onc.2016.427

    mTORC1 activity concurrent with enhanced metastatic potential. ( a ) Left panels, representative immunohistochemical scores (0, negative, to 3, highest expression) of pS6 staining in the tissue microarray (TMA) of primary breast tumors. Right panel, results for the association between pS6 staining and distant metastasis. ( b ) Increased expression of mTORC1 pathway components with enhanced metastatic potential of MDA-MB-231 cells. The loading control (α-tubulin, TUBA) is shown. Bottom panel, graph showing quantifications of protein levels relative to parental and TUBA (per sample). ( c ) Increased pS6 expression in lung metastases developed by LM2 cells. The arrows mark magnified fields. Right panel, box-and-whisker plots for the quantification (pixels/area, p/a) of pS6 intensity; three mice and three similar lung metastases were analyzed in each setting. The P -value of the two-tailed Mann–Whitney test is shown. ( d ) Left panel, graph showing the in vivo photon flux quantification in mice injected with LM2 and treated with DMSO or everolimus. Representative images from bioluminescence in lungs from DMSO- or everolimus-treated mice are shown. The scale bar depicts the range of photon flux values as a pseudo-color display, with red and blue representing high and low values, respectively. Right top panels, quantification of lung colonization (total metastasis area normalized per total lung area, based on HE). Right bottom panels, representative immunohistochemical results for pS6 and quantification of normalized intensities.
    Figure Legend Snippet: mTORC1 activity concurrent with enhanced metastatic potential. ( a ) Left panels, representative immunohistochemical scores (0, negative, to 3, highest expression) of pS6 staining in the tissue microarray (TMA) of primary breast tumors. Right panel, results for the association between pS6 staining and distant metastasis. ( b ) Increased expression of mTORC1 pathway components with enhanced metastatic potential of MDA-MB-231 cells. The loading control (α-tubulin, TUBA) is shown. Bottom panel, graph showing quantifications of protein levels relative to parental and TUBA (per sample). ( c ) Increased pS6 expression in lung metastases developed by LM2 cells. The arrows mark magnified fields. Right panel, box-and-whisker plots for the quantification (pixels/area, p/a) of pS6 intensity; three mice and three similar lung metastases were analyzed in each setting. The P -value of the two-tailed Mann–Whitney test is shown. ( d ) Left panel, graph showing the in vivo photon flux quantification in mice injected with LM2 and treated with DMSO or everolimus. Representative images from bioluminescence in lungs from DMSO- or everolimus-treated mice are shown. The scale bar depicts the range of photon flux values as a pseudo-color display, with red and blue representing high and low values, respectively. Right top panels, quantification of lung colonization (total metastasis area normalized per total lung area, based on HE). Right bottom panels, representative immunohistochemical results for pS6 and quantification of normalized intensities.

    Techniques Used: Activity Assay, Immunohistochemical staining, Expressing, Staining, Microarray, Whisker Assay, Two Tailed Test, MANN-WHITNEY, In Vivo, Injection

    EVI1 couples stemness, metastatic potential and resistance to mTOR inhibition. ( a ) TCGA network of significant co-expression (PCC P -values <0.05) between EVI1 and signatures derived from stem cell-like cells and/or metastatic settings . ( b ) Distributions of PCCs between EVI1 and the commonly overexpressed 79 genes across the studied models or the complete microarray gene list as background control. The P -value of the Mann–Whitney test for the comparison of the distributions is shown. ( c ) Reduced pS6 levels with EVI1 depletion in cell models. The quantification of pS6/S6 signal ratios is show at the bottom (relative to siControl). ( d ) Ectopic overexpression of GFP-EVI1 in MCF7 (left panels) and HCC1937 (right panels) cells provides higher viability upon exposure to everolimus, relative to GFP-only overexpression. Also shown are the western blot results for defined markers across the drug-exposed cell cultures. The quantification of pS6/S6 signal ratios is show at the bottom (relative to TUBA per sample). ( e ) Increased EVI1 binding at predicted target promoters/gene loci with adaptation to everolimus. The fold changes are relative to the immunoglobulin control and the promoter gene targets are shown in the X axis. ( f ) Relative overexpression of RAPTOR and/or RHEB with adaptation to everolimus in MCF7 and HCC1937 cells. The quantification is show at the bottom (relative to untreated and TUBA per sample). ( g ) Relative reduction of RAPTOR and RHEB expression following EVI1 depletion, in particular in the everolimus-adapted setting.
    Figure Legend Snippet: EVI1 couples stemness, metastatic potential and resistance to mTOR inhibition. ( a ) TCGA network of significant co-expression (PCC P -values <0.05) between EVI1 and signatures derived from stem cell-like cells and/or metastatic settings . ( b ) Distributions of PCCs between EVI1 and the commonly overexpressed 79 genes across the studied models or the complete microarray gene list as background control. The P -value of the Mann–Whitney test for the comparison of the distributions is shown. ( c ) Reduced pS6 levels with EVI1 depletion in cell models. The quantification of pS6/S6 signal ratios is show at the bottom (relative to siControl). ( d ) Ectopic overexpression of GFP-EVI1 in MCF7 (left panels) and HCC1937 (right panels) cells provides higher viability upon exposure to everolimus, relative to GFP-only overexpression. Also shown are the western blot results for defined markers across the drug-exposed cell cultures. The quantification of pS6/S6 signal ratios is show at the bottom (relative to TUBA per sample). ( e ) Increased EVI1 binding at predicted target promoters/gene loci with adaptation to everolimus. The fold changes are relative to the immunoglobulin control and the promoter gene targets are shown in the X axis. ( f ) Relative overexpression of RAPTOR and/or RHEB with adaptation to everolimus in MCF7 and HCC1937 cells. The quantification is show at the bottom (relative to untreated and TUBA per sample). ( g ) Relative reduction of RAPTOR and RHEB expression following EVI1 depletion, in particular in the everolimus-adapted setting.

    Techniques Used: Inhibition, Expressing, Derivative Assay, Microarray, MANN-WHITNEY, Over Expression, Western Blot, Binding Assay



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    Thermo Fisher human genome u219 microarray platform
    mTORC1 activity concurrent with enhanced metastatic potential. ( a ) Left panels, representative immunohistochemical scores (0, negative, to 3, highest expression) of pS6 staining in the tissue <t>microarray</t> (TMA) of primary breast tumors. Right panel, results for the association between pS6 staining and distant metastasis. ( b ) Increased expression of mTORC1 pathway components with enhanced metastatic potential of MDA-MB-231 cells. The loading control (α-tubulin, TUBA) is shown. Bottom panel, graph showing quantifications of protein levels relative to parental and TUBA (per sample). ( c ) Increased pS6 expression in lung metastases developed by LM2 cells. The arrows mark magnified fields. Right panel, box-and-whisker plots for the quantification (pixels/area, p/a) of pS6 intensity; three mice and three similar lung metastases were analyzed in each setting. The P -value of the two-tailed Mann–Whitney test is shown. ( d ) Left panel, graph showing the in vivo photon flux quantification in mice injected with LM2 and treated with DMSO or everolimus. Representative images from bioluminescence in lungs from DMSO- or everolimus-treated mice are shown. The scale bar depicts the range of photon flux values as a pseudo-color display, with red and blue representing high and low values, respectively. Right top panels, quantification of lung colonization (total metastasis area normalized per total lung area, based on HE). Right bottom panels, representative immunohistochemical results for pS6 and quantification of normalized intensities.
    Human Genome U219 Microarray Platform, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human genome u219 microarray platform/product/Thermo Fisher
    Average 86 stars, based on 1 article reviews
    human genome u219 microarray platform - by Bioz Stars, 2026-03
    86/100 stars
      Buy from Supplier

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    mTORC1 activity concurrent with enhanced metastatic potential. ( a ) Left panels, representative immunohistochemical scores (0, negative, to 3, highest expression) of pS6 staining in the tissue microarray (TMA) of primary breast tumors. Right panel, results for the association between pS6 staining and distant metastasis. ( b ) Increased expression of mTORC1 pathway components with enhanced metastatic potential of MDA-MB-231 cells. The loading control (α-tubulin, TUBA) is shown. Bottom panel, graph showing quantifications of protein levels relative to parental and TUBA (per sample). ( c ) Increased pS6 expression in lung metastases developed by LM2 cells. The arrows mark magnified fields. Right panel, box-and-whisker plots for the quantification (pixels/area, p/a) of pS6 intensity; three mice and three similar lung metastases were analyzed in each setting. The P -value of the two-tailed Mann–Whitney test is shown. ( d ) Left panel, graph showing the in vivo photon flux quantification in mice injected with LM2 and treated with DMSO or everolimus. Representative images from bioluminescence in lungs from DMSO- or everolimus-treated mice are shown. The scale bar depicts the range of photon flux values as a pseudo-color display, with red and blue representing high and low values, respectively. Right top panels, quantification of lung colonization (total metastasis area normalized per total lung area, based on HE). Right bottom panels, representative immunohistochemical results for pS6 and quantification of normalized intensities.

    Journal: Oncogene

    Article Title: Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition

    doi: 10.1038/onc.2016.427

    Figure Lengend Snippet: mTORC1 activity concurrent with enhanced metastatic potential. ( a ) Left panels, representative immunohistochemical scores (0, negative, to 3, highest expression) of pS6 staining in the tissue microarray (TMA) of primary breast tumors. Right panel, results for the association between pS6 staining and distant metastasis. ( b ) Increased expression of mTORC1 pathway components with enhanced metastatic potential of MDA-MB-231 cells. The loading control (α-tubulin, TUBA) is shown. Bottom panel, graph showing quantifications of protein levels relative to parental and TUBA (per sample). ( c ) Increased pS6 expression in lung metastases developed by LM2 cells. The arrows mark magnified fields. Right panel, box-and-whisker plots for the quantification (pixels/area, p/a) of pS6 intensity; three mice and three similar lung metastases were analyzed in each setting. The P -value of the two-tailed Mann–Whitney test is shown. ( d ) Left panel, graph showing the in vivo photon flux quantification in mice injected with LM2 and treated with DMSO or everolimus. Representative images from bioluminescence in lungs from DMSO- or everolimus-treated mice are shown. The scale bar depicts the range of photon flux values as a pseudo-color display, with red and blue representing high and low values, respectively. Right top panels, quantification of lung colonization (total metastasis area normalized per total lung area, based on HE). Right bottom panels, representative immunohistochemical results for pS6 and quantification of normalized intensities.

    Article Snippet: The RNAs were amplified using the Ribo-SPIA system (NuGEN Technologies Inc., San Carlos, CA, USA) and subsequently hybridized on the Human Genome U219 microarray platform (Affymetrix, Santa Clara, CA, USA; IRB Core Facility, Barcelona, Spain).

    Techniques: Activity Assay, Immunohistochemical staining, Expressing, Staining, Microarray, Whisker Assay, Two Tailed Test, MANN-WHITNEY, In Vivo, Injection

    EVI1 couples stemness, metastatic potential and resistance to mTOR inhibition. ( a ) TCGA network of significant co-expression (PCC P -values <0.05) between EVI1 and signatures derived from stem cell-like cells and/or metastatic settings . ( b ) Distributions of PCCs between EVI1 and the commonly overexpressed 79 genes across the studied models or the complete microarray gene list as background control. The P -value of the Mann–Whitney test for the comparison of the distributions is shown. ( c ) Reduced pS6 levels with EVI1 depletion in cell models. The quantification of pS6/S6 signal ratios is show at the bottom (relative to siControl). ( d ) Ectopic overexpression of GFP-EVI1 in MCF7 (left panels) and HCC1937 (right panels) cells provides higher viability upon exposure to everolimus, relative to GFP-only overexpression. Also shown are the western blot results for defined markers across the drug-exposed cell cultures. The quantification of pS6/S6 signal ratios is show at the bottom (relative to TUBA per sample). ( e ) Increased EVI1 binding at predicted target promoters/gene loci with adaptation to everolimus. The fold changes are relative to the immunoglobulin control and the promoter gene targets are shown in the X axis. ( f ) Relative overexpression of RAPTOR and/or RHEB with adaptation to everolimus in MCF7 and HCC1937 cells. The quantification is show at the bottom (relative to untreated and TUBA per sample). ( g ) Relative reduction of RAPTOR and RHEB expression following EVI1 depletion, in particular in the everolimus-adapted setting.

    Journal: Oncogene

    Article Title: Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition

    doi: 10.1038/onc.2016.427

    Figure Lengend Snippet: EVI1 couples stemness, metastatic potential and resistance to mTOR inhibition. ( a ) TCGA network of significant co-expression (PCC P -values <0.05) between EVI1 and signatures derived from stem cell-like cells and/or metastatic settings . ( b ) Distributions of PCCs between EVI1 and the commonly overexpressed 79 genes across the studied models or the complete microarray gene list as background control. The P -value of the Mann–Whitney test for the comparison of the distributions is shown. ( c ) Reduced pS6 levels with EVI1 depletion in cell models. The quantification of pS6/S6 signal ratios is show at the bottom (relative to siControl). ( d ) Ectopic overexpression of GFP-EVI1 in MCF7 (left panels) and HCC1937 (right panels) cells provides higher viability upon exposure to everolimus, relative to GFP-only overexpression. Also shown are the western blot results for defined markers across the drug-exposed cell cultures. The quantification of pS6/S6 signal ratios is show at the bottom (relative to TUBA per sample). ( e ) Increased EVI1 binding at predicted target promoters/gene loci with adaptation to everolimus. The fold changes are relative to the immunoglobulin control and the promoter gene targets are shown in the X axis. ( f ) Relative overexpression of RAPTOR and/or RHEB with adaptation to everolimus in MCF7 and HCC1937 cells. The quantification is show at the bottom (relative to untreated and TUBA per sample). ( g ) Relative reduction of RAPTOR and RHEB expression following EVI1 depletion, in particular in the everolimus-adapted setting.

    Article Snippet: The RNAs were amplified using the Ribo-SPIA system (NuGEN Technologies Inc., San Carlos, CA, USA) and subsequently hybridized on the Human Genome U219 microarray platform (Affymetrix, Santa Clara, CA, USA; IRB Core Facility, Barcelona, Spain).

    Techniques: Inhibition, Expressing, Derivative Assay, Microarray, MANN-WHITNEY, Over Expression, Western Blot, Binding Assay