egfr sirna  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc egfr sirna
    A , Autophagy was induced by <t>EGFR-TKIs</t> in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control <t>siRNA,</t> Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.
    Egfr Sirna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "EGFR Tyrosine Kinase Inhibitors Activate Autophagy as a Cytoprotective Response in Human Lung Cancer Cells"

    Article Title: EGFR Tyrosine Kinase Inhibitors Activate Autophagy as a Cytoprotective Response in Human Lung Cancer Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0018691

    A , Autophagy was induced by EGFR-TKIs in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.
    Figure Legend Snippet: A , Autophagy was induced by EGFR-TKIs in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.

    Techniques Used: Expressing, Incubation, Western Blot, MTT Assay, Transfection, Negative Control

    EGFR expression in A549 ( A ) or H1299 ( B ) cells transfected with control siRNA, EGFR siRNA1 or siRNA2 were determined by western blotting. LC3 expression in EGFR-TKIs treated A549 ( C ) or H1299 ( D ) cells with or without EGFR knockdown were determined by western blotting.
    Figure Legend Snippet: EGFR expression in A549 ( A ) or H1299 ( B ) cells transfected with control siRNA, EGFR siRNA1 or siRNA2 were determined by western blotting. LC3 expression in EGFR-TKIs treated A549 ( C ) or H1299 ( D ) cells with or without EGFR knockdown were determined by western blotting.

    Techniques Used: Expressing, Transfection, Western Blot

    egfr sirna  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc egfr sirna
    A , Autophagy was induced by <t>EGFR-TKIs</t> in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control <t>siRNA,</t> Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.
    Egfr Sirna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "EGFR Tyrosine Kinase Inhibitors Activate Autophagy as a Cytoprotective Response in Human Lung Cancer Cells"

    Article Title: EGFR Tyrosine Kinase Inhibitors Activate Autophagy as a Cytoprotective Response in Human Lung Cancer Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0018691

    A , Autophagy was induced by EGFR-TKIs in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.
    Figure Legend Snippet: A , Autophagy was induced by EGFR-TKIs in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.

    Techniques Used: Expressing, Incubation, Western Blot, MTT Assay, Transfection, Negative Control

    EGFR expression in A549 ( A ) or H1299 ( B ) cells transfected with control siRNA, EGFR siRNA1 or siRNA2 were determined by western blotting. LC3 expression in EGFR-TKIs treated A549 ( C ) or H1299 ( D ) cells with or without EGFR knockdown were determined by western blotting.
    Figure Legend Snippet: EGFR expression in A549 ( A ) or H1299 ( B ) cells transfected with control siRNA, EGFR siRNA1 or siRNA2 were determined by western blotting. LC3 expression in EGFR-TKIs treated A549 ( C ) or H1299 ( D ) cells with or without EGFR knockdown were determined by western blotting.

    Techniques Used: Expressing, Transfection, Western Blot

    small interfering rna sirna duplex  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc small interfering rna sirna duplex
    Small Interfering Rna Sirna Duplex, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    egf sirna  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc egf sirna
    Egf Sirna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    sirnas against egfr  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc sirnas against egfr
    Sirnas Against Egfr, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    sirnas against egfr  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc sirnas against egfr
    Sirnas Against Egfr, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    sirnas against egfr  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc sirnas against egfr
    Sirnas Against Egfr, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    egfr sirna  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc egfr sirna
    (A) Relative HPV16 infection of HaCaT cells in the presence of specific GFR and protein tyrosine kinase inhibitors. Subconfluent HaCaT cells were pre-treated 45 min with 1 µM AG1478, 100 nM PD168393, 100 µM genistein, 100 µM daidzein, 1 µM PD173074, or 100–600 nM cetuximab. Cells were exposed to HPV16 PsV at 100 vge/cell for 1 h at 4°C, then washed extensively and shifted to 37°C in the presence of the indicated inhibitor in CM for 24 h at which time they were analyzed for luciferase expression. Data are represented as mean ± SEM of 3 experiments. (B–C) <t>EGFR</t> knockdown in <t>EGFR-siRNA</t> transfected HaCaT cells was determined by immunoblot and compared by densitometry to EGFR levels in cells transfected with a negative control siRNA at 48 hours post transfection. Four separate transfections were analyzed (B) and HPV16 PsV infection levels were measured at 24 h post infection (48 h post transfection) (C). Error bars represent the average of triplicate luciferase readings from the four transfections. (D) HPV16 PsV infection levels (24 h post infection) in the presence of inhibitors following pre-treatment for 1 hr with 100 µM monastrol, pre-treatment with monastrol for 1 h plus 500 nM PD168393 for duration (monast.+PD), or pre-treatment with 500 nM PD168393 for 1 hr plus 100 µM monastrol for duration (PD+monast.). (E) Relative HPV16 infection is dependent upon medium constituents post primary HPV16 binding. HaCaT cells starved in SFM (4 h) were exposed to HPV16 in CM (positive control) or SFM. After washing away unbound virus, cells were incubated for 24 h in CM, SFM, syndecan-1-depleted CM (IP-snd), or EGF-depleted CM (IP-EGF). Infections were quantified by luciferase assay at 24 h post shift to 37°C. Data are represented as mean ± SEM of 3 experiments. (F) Relative HPV16 infection in SFM is enhanced by GFs. HaCaT cells starved in SFM were exposed to HPV16 in SFM for 1 h at 4°C. After washing away unbound virus, cells were incubated for 24 h in SFM, SFM containing GFs (concentrations indicated: ng/ml), or in CM. Infections were quantified by luciferase assay; bars represented the mean ± SEM of ≥3 individual experiments.
    Egfr Sirna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Essential Roles for Soluble Virion-Associated Heparan Sulfonated Proteoglycans and Growth Factors in Human Papillomavirus Infections"

    Article Title: Essential Roles for Soluble Virion-Associated Heparan Sulfonated Proteoglycans and Growth Factors in Human Papillomavirus Infections

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1002519

    (A) Relative HPV16 infection of HaCaT cells in the presence of specific GFR and protein tyrosine kinase inhibitors. Subconfluent HaCaT cells were pre-treated 45 min with 1 µM AG1478, 100 nM PD168393, 100 µM genistein, 100 µM daidzein, 1 µM PD173074, or 100–600 nM cetuximab. Cells were exposed to HPV16 PsV at 100 vge/cell for 1 h at 4°C, then washed extensively and shifted to 37°C in the presence of the indicated inhibitor in CM for 24 h at which time they were analyzed for luciferase expression. Data are represented as mean ± SEM of 3 experiments. (B–C) EGFR knockdown in EGFR-siRNA transfected HaCaT cells was determined by immunoblot and compared by densitometry to EGFR levels in cells transfected with a negative control siRNA at 48 hours post transfection. Four separate transfections were analyzed (B) and HPV16 PsV infection levels were measured at 24 h post infection (48 h post transfection) (C). Error bars represent the average of triplicate luciferase readings from the four transfections. (D) HPV16 PsV infection levels (24 h post infection) in the presence of inhibitors following pre-treatment for 1 hr with 100 µM monastrol, pre-treatment with monastrol for 1 h plus 500 nM PD168393 for duration (monast.+PD), or pre-treatment with 500 nM PD168393 for 1 hr plus 100 µM monastrol for duration (PD+monast.). (E) Relative HPV16 infection is dependent upon medium constituents post primary HPV16 binding. HaCaT cells starved in SFM (4 h) were exposed to HPV16 in CM (positive control) or SFM. After washing away unbound virus, cells were incubated for 24 h in CM, SFM, syndecan-1-depleted CM (IP-snd), or EGF-depleted CM (IP-EGF). Infections were quantified by luciferase assay at 24 h post shift to 37°C. Data are represented as mean ± SEM of 3 experiments. (F) Relative HPV16 infection in SFM is enhanced by GFs. HaCaT cells starved in SFM were exposed to HPV16 in SFM for 1 h at 4°C. After washing away unbound virus, cells were incubated for 24 h in SFM, SFM containing GFs (concentrations indicated: ng/ml), or in CM. Infections were quantified by luciferase assay; bars represented the mean ± SEM of ≥3 individual experiments.
    Figure Legend Snippet: (A) Relative HPV16 infection of HaCaT cells in the presence of specific GFR and protein tyrosine kinase inhibitors. Subconfluent HaCaT cells were pre-treated 45 min with 1 µM AG1478, 100 nM PD168393, 100 µM genistein, 100 µM daidzein, 1 µM PD173074, or 100–600 nM cetuximab. Cells were exposed to HPV16 PsV at 100 vge/cell for 1 h at 4°C, then washed extensively and shifted to 37°C in the presence of the indicated inhibitor in CM for 24 h at which time they were analyzed for luciferase expression. Data are represented as mean ± SEM of 3 experiments. (B–C) EGFR knockdown in EGFR-siRNA transfected HaCaT cells was determined by immunoblot and compared by densitometry to EGFR levels in cells transfected with a negative control siRNA at 48 hours post transfection. Four separate transfections were analyzed (B) and HPV16 PsV infection levels were measured at 24 h post infection (48 h post transfection) (C). Error bars represent the average of triplicate luciferase readings from the four transfections. (D) HPV16 PsV infection levels (24 h post infection) in the presence of inhibitors following pre-treatment for 1 hr with 100 µM monastrol, pre-treatment with monastrol for 1 h plus 500 nM PD168393 for duration (monast.+PD), or pre-treatment with 500 nM PD168393 for 1 hr plus 100 µM monastrol for duration (PD+monast.). (E) Relative HPV16 infection is dependent upon medium constituents post primary HPV16 binding. HaCaT cells starved in SFM (4 h) were exposed to HPV16 in CM (positive control) or SFM. After washing away unbound virus, cells were incubated for 24 h in CM, SFM, syndecan-1-depleted CM (IP-snd), or EGF-depleted CM (IP-EGF). Infections were quantified by luciferase assay at 24 h post shift to 37°C. Data are represented as mean ± SEM of 3 experiments. (F) Relative HPV16 infection in SFM is enhanced by GFs. HaCaT cells starved in SFM were exposed to HPV16 in SFM for 1 h at 4°C. After washing away unbound virus, cells were incubated for 24 h in SFM, SFM containing GFs (concentrations indicated: ng/ml), or in CM. Infections were quantified by luciferase assay; bars represented the mean ± SEM of ≥3 individual experiments.

    Techniques Used: Infection, Luciferase, Expressing, Transfection, Western Blot, Negative Control, Binding Assay, Positive Control, Incubation

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    Cell Signaling Technology Inc egfr sirna
    A , Autophagy was induced by <t>EGFR-TKIs</t> in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control <t>siRNA,</t> Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.
    Egfr Sirna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc small interfering rna sirna duplex
    A , Autophagy was induced by <t>EGFR-TKIs</t> in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control <t>siRNA,</t> Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.
    Small Interfering Rna Sirna Duplex, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/small interfering rna sirna duplex/product/Cell Signaling Technology Inc
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    Cell Signaling Technology Inc egf sirna
    A , Autophagy was induced by <t>EGFR-TKIs</t> in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control <t>siRNA,</t> Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.
    Egf Sirna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc sirnas against egfr
    A , Autophagy was induced by <t>EGFR-TKIs</t> in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control <t>siRNA,</t> Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.
    Sirnas Against Egfr, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    A , Autophagy was induced by EGFR-TKIs in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.

    Journal: PLoS ONE

    Article Title: EGFR Tyrosine Kinase Inhibitors Activate Autophagy as a Cytoprotective Response in Human Lung Cancer Cells

    doi: 10.1371/journal.pone.0018691

    Figure Lengend Snippet: A , Autophagy was induced by EGFR-TKIs in resistant but not sensitive lung cancer cells. LC3 expression in lung cancer cells incubated with 25 µM gefitinib or erlotinib for 24 h were analyzed by immunoblotting. B , The viability of cancer cells treated with 12.5 µM gefitinib or erlotinib for 48 h with or without 5 µM CQ were measured by MTT assay. C , The expression of ATG5 and ATG7 in A549 cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were determined by immunoblotting. D , Cells transiently transfected with negative control siRNA, Atg7 or Atg5 siRNA were treated with 12.5 µM gefitinib or 25 µM erlotinib for 48 h. The effect of EGFR-TKIs on cancer cells with or without ATG5 or ATG7 knockdown were analyzed by MTT assay. NC, Control siRNA. Data were expressed as the mean ± SD, and analyzed by Student's t test. * P<0.05, ** P<0.01.

    Article Snippet: Cells were transfected with either nonspecific siRNA (Qiagen, 1027280), ATG5 siRNA (Qiagen, SI02655310), ATG7 siRNA (Qiagen, SI02655373) or EGFR siRNA (Cell Signaling Technology, #6481) (siRNA final concentration, 100 nmol/L) via LipofectAMINE RNAi max (Invitrogen, 13778150) according to the manufacturer's instructions.

    Techniques: Expressing, Incubation, Western Blot, MTT Assay, Transfection, Negative Control

    EGFR expression in A549 ( A ) or H1299 ( B ) cells transfected with control siRNA, EGFR siRNA1 or siRNA2 were determined by western blotting. LC3 expression in EGFR-TKIs treated A549 ( C ) or H1299 ( D ) cells with or without EGFR knockdown were determined by western blotting.

    Journal: PLoS ONE

    Article Title: EGFR Tyrosine Kinase Inhibitors Activate Autophagy as a Cytoprotective Response in Human Lung Cancer Cells

    doi: 10.1371/journal.pone.0018691

    Figure Lengend Snippet: EGFR expression in A549 ( A ) or H1299 ( B ) cells transfected with control siRNA, EGFR siRNA1 or siRNA2 were determined by western blotting. LC3 expression in EGFR-TKIs treated A549 ( C ) or H1299 ( D ) cells with or without EGFR knockdown were determined by western blotting.

    Article Snippet: Cells were transfected with either nonspecific siRNA (Qiagen, 1027280), ATG5 siRNA (Qiagen, SI02655310), ATG7 siRNA (Qiagen, SI02655373) or EGFR siRNA (Cell Signaling Technology, #6481) (siRNA final concentration, 100 nmol/L) via LipofectAMINE RNAi max (Invitrogen, 13778150) according to the manufacturer's instructions.

    Techniques: Expressing, Transfection, Western Blot