9 research outputs found

    Additional file 4: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

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    CAL33-shControl cells untreated or treated with MK-2206 and CAL33-shAKT1.1 and 1.2 cells electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 220 kb

    Additional file 8: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

    No full text
    Detroit562 cells untreated or treated with MK-2206 or Rapamycin electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 213 kb

    Additional file 13: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

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    Figure S4 Analysis of e-cadherin expression and localization by immunofluorescence in CAL27 and Detroit562 cells. Immunostaining of e-cadherin (green) and Alexa555-phalloidin (red) staining of the actin cytoskeleton (F-actin) in CAL27 and Detroit562 cells treated with the pan-AKT inhibitor MK-2206 (MK), Rapamycin (Rapa) or Erlotinib (Erlo). Nuclear DNA was counterstained with Hoechst 33,342 (blue). (PDF 247 kb

    Additional file 1: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

    No full text
    CAL33-shControl cells treated with Erlotinib, Rapamycin and MK-2206 electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 432 kb

    Additional file 9: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

    No full text
    Electrical data used to generate the figures. The ECIS measurements of resistance in MΩ at a frequency of 4000 Hz were normalized to the first measurement and plotted in the Graphpad Prism software to generate the traces shown in Figs. 3a-c and 4a. The quantification data were obtained by measuring the mean resistance increase during the cell attachment phase (from 4 to 8 h after cell spreading). (XLSX 140 kb

    Additional file 5: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

    No full text
    CAL33-shControl cells untreated or treated with MK-2206 and CAL33-shAKT1.1 and 1.2 cells electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 86 kb

    Additional file 2: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

    No full text
    CAL33-shControl cells untreated or treated with Rapamycin and MK-2206 electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 213 kb

    Additional file 10: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

    No full text
    Figure S1. AKT1 and AKT2 isoform expression in CAL33, Detroit562 and CAL27 cells. AKT1 and AKT2 expression levels were evaluated by immunoblot with specific anti-AKT antibody in CAL33 cells expressing a control shRNA (shCont), two independent shRNA sequences targeting AKT1 (sh1.1 and sh1.2) and in Detroit562 and CAL27 cells. GAPDH was used as a loading control. (PDF 26 kb

    Additional file 3: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

    No full text
    CAL33-shControl cells untreated or treated with MK-2206 and CAL33-shAKT1.1 and 1.2 cells electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 147 kb
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