annexin v  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin v
    Annexin V, 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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    annexin v  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin v
    Annexin V, 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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    fitc labeled anti annexin v antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc fitc labeled anti annexin v antibody
    Fitc Labeled Anti Annexin V Antibody, 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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    apoptosis detection kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc apoptosis detection kit
    Apoptosis Detection Kit, 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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    annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease <t>apoptosis,</t> which is related to radioresistance
    Annexin Green Apoptosis Cell Detection Reagent Kit, 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/annexin green apoptosis cell detection reagent kit/product/Cell Signaling Technology Inc
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    1) Product Images from "Interleukin‐6 production mediated by the IRE 1‐ XBP 1 pathway confers radioresistance in human papillomavirus‐negative oropharyngeal carcinoma"

    Article Title: Interleukin‐6 production mediated by the IRE 1‐ XBP 1 pathway confers radioresistance in human papillomavirus‐negative oropharyngeal carcinoma

    Journal: Cancer Science

    doi: 10.1111/cas.14094

    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance
    Figure Legend Snippet: Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance

    Techniques Used: Irradiation, Expressing

    annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    EGFR regulates the radiosensitivity of OSCC cells via ERS and is associated with <t>apoptosis,</t> DSB repair, and autophagy. A, γ‐H2AX foci formation and B, LC3 immunopositive dots in control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells followed by irradiation (5 Gy, 2 h). C, DNA‐PKcs, LC3B (LC3B‐II/β‐actin), Atg3, and cleaved caspase 3 levels in control and EGFR siRNA transfected OSCC cells pre‐treated with or without 100 µg/L cetuximab, 10 µmol/L salubrinal, or 1.0 µg/mL tunicamycin for 12 h followed by 5 Gy of irradiation. D, Also shown, cleaved caspase 3 and cleaved PARP in FaDuR, Detroit562R, FaDuP, and Detroit562P cells pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. E, FACS analysis by AnnexinV/PI double staining of control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells, pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. Note: * denotes P < 0.05 compared to the control group
    Annexin Green Apoptosis Cell Detection Reagent Kit, 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 confers radioresistance in human oropharyngeal carcinoma by activating endoplasmic reticulum stress signaling PERK‐eIF2α‐GRP94 and IRE1α‐XBP1‐GRP78"

    Article Title: EGFR confers radioresistance in human oropharyngeal carcinoma by activating endoplasmic reticulum stress signaling PERK‐eIF2α‐GRP94 and IRE1α‐XBP1‐GRP78

    Journal: Cancer Medicine

    doi: 10.1002/cam4.1862

    EGFR regulates the radiosensitivity of OSCC cells via ERS and is associated with apoptosis, DSB repair, and autophagy. A, γ‐H2AX foci formation and B, LC3 immunopositive dots in control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells followed by irradiation (5 Gy, 2 h). C, DNA‐PKcs, LC3B (LC3B‐II/β‐actin), Atg3, and cleaved caspase 3 levels in control and EGFR siRNA transfected OSCC cells pre‐treated with or without 100 µg/L cetuximab, 10 µmol/L salubrinal, or 1.0 µg/mL tunicamycin for 12 h followed by 5 Gy of irradiation. D, Also shown, cleaved caspase 3 and cleaved PARP in FaDuR, Detroit562R, FaDuP, and Detroit562P cells pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. E, FACS analysis by AnnexinV/PI double staining of control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells, pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. Note: * denotes P < 0.05 compared to the control group
    Figure Legend Snippet: EGFR regulates the radiosensitivity of OSCC cells via ERS and is associated with apoptosis, DSB repair, and autophagy. A, γ‐H2AX foci formation and B, LC3 immunopositive dots in control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells followed by irradiation (5 Gy, 2 h). C, DNA‐PKcs, LC3B (LC3B‐II/β‐actin), Atg3, and cleaved caspase 3 levels in control and EGFR siRNA transfected OSCC cells pre‐treated with or without 100 µg/L cetuximab, 10 µmol/L salubrinal, or 1.0 µg/mL tunicamycin for 12 h followed by 5 Gy of irradiation. D, Also shown, cleaved caspase 3 and cleaved PARP in FaDuR, Detroit562R, FaDuP, and Detroit562P cells pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. E, FACS analysis by AnnexinV/PI double staining of control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells, pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. Note: * denotes P < 0.05 compared to the control group

    Techniques Used: Transfection, Irradiation, Double Staining

    annexin v pi early apoptosis detection kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin v pi early apoptosis detection kit
    The combinatorial miR treatment induced strong cytotoxic and apoptotic effect, along with Caspase activation ( A ) Potential synergism is illustrated by the combination’s (Combo) cytotoxicity being larger than the addition of the cytotoxicity of the individual miRs alone. Fluorescence intensity, which correlates to number of dead cells, was measured till 33 h post transfection. Lipofectamine with Scramble (Lipo), and untreated cells (Control) were used as negative controls. Positive control (Positive) was provided by the vendor. *p < 0.05 of combo vs. Control, miR-143, miR-506. ( B ) FACS Annexin V/PI analysis of cell <t>apoptosis</t> treated with individual mimics, and combination at 24 and 48 h compared to untreated cells. ( C ) Caspase-3/7 activity of A549 cells treated with individual and combination of miR, at 24 h. Cells without any treatment (Negative control-NC), with Lipofectamine, and with no-target control miRNA (scramble) were used as experimental controls. Doxorubicin (DOX, equimolar) was used as positive control. **p < 0.01 relative to NC. ( D ) <t>Annexin</t> <t>V</t> positive A549 cells, following transfection with miR-143 and/or miR-506 at 24 and 48 h post transfection.
    Annexin V Pi Early Apoptosis Detection Kit, 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 "Multipronged activity of combinatorial miR-143 and miR-506 inhibits Lung Cancer cell cycle progression and angiogenesis in vitro"

    Article Title: Multipronged activity of combinatorial miR-143 and miR-506 inhibits Lung Cancer cell cycle progression and angiogenesis in vitro

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-28872-2

    The combinatorial miR treatment induced strong cytotoxic and apoptotic effect, along with Caspase activation ( A ) Potential synergism is illustrated by the combination’s (Combo) cytotoxicity being larger than the addition of the cytotoxicity of the individual miRs alone. Fluorescence intensity, which correlates to number of dead cells, was measured till 33 h post transfection. Lipofectamine with Scramble (Lipo), and untreated cells (Control) were used as negative controls. Positive control (Positive) was provided by the vendor. *p < 0.05 of combo vs. Control, miR-143, miR-506. ( B ) FACS Annexin V/PI analysis of cell apoptosis treated with individual mimics, and combination at 24 and 48 h compared to untreated cells. ( C ) Caspase-3/7 activity of A549 cells treated with individual and combination of miR, at 24 h. Cells without any treatment (Negative control-NC), with Lipofectamine, and with no-target control miRNA (scramble) were used as experimental controls. Doxorubicin (DOX, equimolar) was used as positive control. **p < 0.01 relative to NC. ( D ) Annexin V positive A549 cells, following transfection with miR-143 and/or miR-506 at 24 and 48 h post transfection.
    Figure Legend Snippet: The combinatorial miR treatment induced strong cytotoxic and apoptotic effect, along with Caspase activation ( A ) Potential synergism is illustrated by the combination’s (Combo) cytotoxicity being larger than the addition of the cytotoxicity of the individual miRs alone. Fluorescence intensity, which correlates to number of dead cells, was measured till 33 h post transfection. Lipofectamine with Scramble (Lipo), and untreated cells (Control) were used as negative controls. Positive control (Positive) was provided by the vendor. *p < 0.05 of combo vs. Control, miR-143, miR-506. ( B ) FACS Annexin V/PI analysis of cell apoptosis treated with individual mimics, and combination at 24 and 48 h compared to untreated cells. ( C ) Caspase-3/7 activity of A549 cells treated with individual and combination of miR, at 24 h. Cells without any treatment (Negative control-NC), with Lipofectamine, and with no-target control miRNA (scramble) were used as experimental controls. Doxorubicin (DOX, equimolar) was used as positive control. **p < 0.01 relative to NC. ( D ) Annexin V positive A549 cells, following transfection with miR-143 and/or miR-506 at 24 and 48 h post transfection.

    Techniques Used: Activation Assay, Fluorescence, Transfection, Positive Control, Activity Assay, Negative Control

    Annexin V/PI  apoptosis  analysis of A549 cell populations, as determined by flow-cytometric quantification (Average of triplicates ± SEM).
    Figure Legend Snippet: Annexin V/PI apoptosis analysis of A549 cell populations, as determined by flow-cytometric quantification (Average of triplicates ± SEM).

    Techniques Used:

    Genes and their activity on the cell cycle, which demonstrated >10% up-/down-regulation, as identified by the microarray analysis of A549 cells transfected with miR-143/506, for 24 and/or 48 h post transfection, compared to control.
    Figure Legend Snippet: Genes and their activity on the cell cycle, which demonstrated >10% up-/down-regulation, as identified by the microarray analysis of A549 cells transfected with miR-143/506, for 24 and/or 48 h post transfection, compared to control.

    Techniques Used: Activity Assay, Microarray, Transfection, Over Expression, Migration

    annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    (A) Silencing GRP78 inhibited the radiation-induced (5 Gy, 12 h) expression of the DNA double-strand break repair protein DNA-PK and increased the phosphorylation level of ATM. Silencing GRP78 also inhibited the radiation-induced expression of the autophagy-related proteins LC3B (LC3B-II/β-actin) and Atg16L1 and increased the expression of the <t>apoptosis</t> marker protein cleaved caspase-3 and cleaved PARP. (B) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ-H2AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ-H2AX foci). In addition, the effect of radiation after GRP78 silencing was more evident than that of simple radiation. (C) Immunofluorescence studies by LC3B staining also showed autophagy regions in the nucleus after 5 Gy radiation for 1 h (the blue background indicates the cell nucleus, and light green dots indicate LC3B foci), which was reversed after GRP78 silencing. The oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with 5 Gy of radiation. Compared with the IR group, *P < 0.05. For (A), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.
    Annexin Green Apoptosis Cell Detection Reagent Kit, 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/annexin green apoptosis cell detection reagent kit/product/Cell Signaling Technology Inc
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    1) Product Images from "Inhibition of GRP78 abrogates radioresistance in oropharyngeal carcinoma cells after EGFR inhibition by cetuximab"

    Article Title: Inhibition of GRP78 abrogates radioresistance in oropharyngeal carcinoma cells after EGFR inhibition by cetuximab

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0188932

    (A) Silencing GRP78 inhibited the radiation-induced (5 Gy, 12 h) expression of the DNA double-strand break repair protein DNA-PK and increased the phosphorylation level of ATM. Silencing GRP78 also inhibited the radiation-induced expression of the autophagy-related proteins LC3B (LC3B-II/β-actin) and Atg16L1 and increased the expression of the apoptosis marker protein cleaved caspase-3 and cleaved PARP. (B) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ-H2AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ-H2AX foci). In addition, the effect of radiation after GRP78 silencing was more evident than that of simple radiation. (C) Immunofluorescence studies by LC3B staining also showed autophagy regions in the nucleus after 5 Gy radiation for 1 h (the blue background indicates the cell nucleus, and light green dots indicate LC3B foci), which was reversed after GRP78 silencing. The oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with 5 Gy of radiation. Compared with the IR group, *P < 0.05. For (A), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.
    Figure Legend Snippet: (A) Silencing GRP78 inhibited the radiation-induced (5 Gy, 12 h) expression of the DNA double-strand break repair protein DNA-PK and increased the phosphorylation level of ATM. Silencing GRP78 also inhibited the radiation-induced expression of the autophagy-related proteins LC3B (LC3B-II/β-actin) and Atg16L1 and increased the expression of the apoptosis marker protein cleaved caspase-3 and cleaved PARP. (B) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ-H2AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ-H2AX foci). In addition, the effect of radiation after GRP78 silencing was more evident than that of simple radiation. (C) Immunofluorescence studies by LC3B staining also showed autophagy regions in the nucleus after 5 Gy radiation for 1 h (the blue background indicates the cell nucleus, and light green dots indicate LC3B foci), which was reversed after GRP78 silencing. The oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with 5 Gy of radiation. Compared with the IR group, *P < 0.05. For (A), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.

    Techniques Used: Expressing, Marker, Immunofluorescence, Staining, Software, Negative Control

    Oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with different doses of radiation. (A) The results of cloning showed that Ly294002 and 3-MA could increase the radiosensitivity of oropharyngeal carcinoma cells. Additionally, radiation parameters were fitted to a classic multitarget single hit model as shown in the table. (B) Western blot analysis showed that Ly294002 and 3-MA increased the radiation-induced protein expression of cleaved PARP and inhibited the radiation-induced expression of the anti-apoptotic protein Bcl-2 and the cell proliferation regulatory protein EGR1. (C) At 48 h after irradiation, CCK-8 analysis showed that Ly294002 and 3-MA further reduced the proliferation of cells inhibited by radiation alone. (D) At 48 h after irradiation, apoptosis was detected by flow cytometry after Annexin V/PI staining. The results showed that Ly294002 and 3-MA increased radiation-induced apoptosis. For (C) and (D), compared with the IR group, *P < 0.05. For (B), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.
    Figure Legend Snippet: Oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with different doses of radiation. (A) The results of cloning showed that Ly294002 and 3-MA could increase the radiosensitivity of oropharyngeal carcinoma cells. Additionally, radiation parameters were fitted to a classic multitarget single hit model as shown in the table. (B) Western blot analysis showed that Ly294002 and 3-MA increased the radiation-induced protein expression of cleaved PARP and inhibited the radiation-induced expression of the anti-apoptotic protein Bcl-2 and the cell proliferation regulatory protein EGR1. (C) At 48 h after irradiation, CCK-8 analysis showed that Ly294002 and 3-MA further reduced the proliferation of cells inhibited by radiation alone. (D) At 48 h after irradiation, apoptosis was detected by flow cytometry after Annexin V/PI staining. The results showed that Ly294002 and 3-MA increased radiation-induced apoptosis. For (C) and (D), compared with the IR group, *P < 0.05. For (B), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.

    Techniques Used: Clone Assay, Western Blot, Expressing, Irradiation, CCK-8 Assay, Flow Cytometry, Staining, Software, Negative Control

    Oropharyngeal carcinoma cells transfected with siRNA to silence GRP78 or negative siRNA were treated with 50 μg/mL cetuximab for 12 h and then irradiated. (A) Colony formation experiments showed that cetuximab inhibited the colony formation of FaDu cells, which was further enhanced by silencing GRP78. In contrast, cetuximab alone did not affect the colony formation of Detroit562 cells, which was reversed by the silencing of GRP78. (B) Cetuximab weakened the radiation-mediated inhibition of FaDu cell proliferation, which was further enhanced by the silencing of GRP78. In addition, cetuximab had no significant effects on the radiation-mediated inhibition of Detroit562 cell proliferation, which was reversed by the silencing of GRP78. (C) Cetuximab increased the radiation-induced apoptosis of FaDu cells, which was further enhanced by the silencing of GRP78. The effect of cetuximab on the apoptosis of Detroit562 cells was not obvious, and this changed after GRP78 was silenced. Note: CTX = cetuximab, Neg = negative. *P < 0.05 Compared with Negative siRNA + IR; ΔP < 0.01 Compared with Negative siRNA + IR + CTX; ФP = 0.05 Compared with Negative siRNA + IR + CTX.
    Figure Legend Snippet: Oropharyngeal carcinoma cells transfected with siRNA to silence GRP78 or negative siRNA were treated with 50 μg/mL cetuximab for 12 h and then irradiated. (A) Colony formation experiments showed that cetuximab inhibited the colony formation of FaDu cells, which was further enhanced by silencing GRP78. In contrast, cetuximab alone did not affect the colony formation of Detroit562 cells, which was reversed by the silencing of GRP78. (B) Cetuximab weakened the radiation-mediated inhibition of FaDu cell proliferation, which was further enhanced by the silencing of GRP78. In addition, cetuximab had no significant effects on the radiation-mediated inhibition of Detroit562 cell proliferation, which was reversed by the silencing of GRP78. (C) Cetuximab increased the radiation-induced apoptosis of FaDu cells, which was further enhanced by the silencing of GRP78. The effect of cetuximab on the apoptosis of Detroit562 cells was not obvious, and this changed after GRP78 was silenced. Note: CTX = cetuximab, Neg = negative. *P < 0.05 Compared with Negative siRNA + IR; ΔP < 0.01 Compared with Negative siRNA + IR + CTX; ФP = 0.05 Compared with Negative siRNA + IR + CTX.

    Techniques Used: Transfection, Irradiation, Inhibition

    cellsimple annexin v early apoptosis detection kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cellsimple annexin v early apoptosis detection kit
    Cellsimple Annexin V Early Apoptosis Detection Kit, 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/cellsimple annexin v early apoptosis detection kit/product/Cell Signaling Technology Inc
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    annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    eIF 2α regulated radioresistance in oropharyngeal carcinoma cells by activating the NF ‐κB pathway. Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy X‐ray. (a) Cells were collected after 24 h to detect <t>apoptosis</t> using <t>Annexin</t> V/ PI staining followed by flow cytometry analysis. (b) Cells were collected after 48 h to identify the cell cycle using PI staining followed by flow cytometry. The results are expressed as the mean ± SD of three independent experiments. Compared with the IR group, * P < 0.05, # P < 0.01. (c) Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy for 12 h. Nuclear and cytoplasm proteins were extracted to detect the expression of phospho‐p65 and its downstream protein HIF ‐1α. Total protein was extracted to evaluate the expression of Rad50, Mre11, Nbs1 and phospho‐ ATM proteins. Western blot results showed that eIF 2α silencing inhibited radiation‐induced nuclear phospho‐p65 protein expression. Conversely, radiation inhibited cytoplasmic p65 protein phosphorylation, whereas eIF 2α silencing reversed this function. These results indicated that eIF 2α silencing inhibited radiation‐induced p65 nuclear translocation. In addition, eIF 2α silencing inhibited the radiation‐induced HIF ‐1α, Rad50 and Nbs1 expression, increased radiation‐induced phospho‐ ATM expression, and did not affect Mre11 protein expression. (d) After eIF 2α was silenced by si RNA transfection, the cells were irradiated (5 Gy, 1 h). The real‐time quantitative PCR results showed that eIF 2α silencing decreased the radiation‐induced expression of p65 mRNA expression. Compared to the irradiated group, * P < 0.05 and # P < 0.01. (e) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ‐H2 AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ‐H2 AX foci). In addition, the effect of radiation after eIF 2α silencing was more evident than that of simple radiation. (f) The western blot results showed that eIF 2α silencing inhibited radiation (5 Gy, 12 h)‐induced phospho‐cdc2, Cyclin B, Bcl‐2 and Bcl‐ xL protein expression and increased radiation‐induced cleaved‐Caspase 3 and cleaved‐ PARP protein expression. The above functions were inhibited by pretreatment of the oropharyngeal carcinoma cells with the NF ‐κB activator TNF α (10 ng/mL) and the ATM inhibitor Ku55933 (10 μmol/L) for 12 h. Bands were quantified using ImageJ software and normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. NA, not applicable.
    Annexin Green Apoptosis Cell Detection Reagent Kit, 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/annexin green apoptosis cell detection reagent kit/product/Cell Signaling Technology Inc
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    Images

    1) Product Images from "Endoplasmic reticulum stress pathway PERK ‐ eIF 2α confers radioresistance in oropharyngeal carcinoma by activating NF ‐κB"

    Article Title: Endoplasmic reticulum stress pathway PERK ‐ eIF 2α confers radioresistance in oropharyngeal carcinoma by activating NF ‐κB

    Journal: Cancer Science

    doi: 10.1111/cas.13260

    eIF 2α regulated radioresistance in oropharyngeal carcinoma cells by activating the NF ‐κB pathway. Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy X‐ray. (a) Cells were collected after 24 h to detect apoptosis using Annexin V/ PI staining followed by flow cytometry analysis. (b) Cells were collected after 48 h to identify the cell cycle using PI staining followed by flow cytometry. The results are expressed as the mean ± SD of three independent experiments. Compared with the IR group, * P < 0.05, # P < 0.01. (c) Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy for 12 h. Nuclear and cytoplasm proteins were extracted to detect the expression of phospho‐p65 and its downstream protein HIF ‐1α. Total protein was extracted to evaluate the expression of Rad50, Mre11, Nbs1 and phospho‐ ATM proteins. Western blot results showed that eIF 2α silencing inhibited radiation‐induced nuclear phospho‐p65 protein expression. Conversely, radiation inhibited cytoplasmic p65 protein phosphorylation, whereas eIF 2α silencing reversed this function. These results indicated that eIF 2α silencing inhibited radiation‐induced p65 nuclear translocation. In addition, eIF 2α silencing inhibited the radiation‐induced HIF ‐1α, Rad50 and Nbs1 expression, increased radiation‐induced phospho‐ ATM expression, and did not affect Mre11 protein expression. (d) After eIF 2α was silenced by si RNA transfection, the cells were irradiated (5 Gy, 1 h). The real‐time quantitative PCR results showed that eIF 2α silencing decreased the radiation‐induced expression of p65 mRNA expression. Compared to the irradiated group, * P < 0.05 and # P < 0.01. (e) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ‐H2 AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ‐H2 AX foci). In addition, the effect of radiation after eIF 2α silencing was more evident than that of simple radiation. (f) The western blot results showed that eIF 2α silencing inhibited radiation (5 Gy, 12 h)‐induced phospho‐cdc2, Cyclin B, Bcl‐2 and Bcl‐ xL protein expression and increased radiation‐induced cleaved‐Caspase 3 and cleaved‐ PARP protein expression. The above functions were inhibited by pretreatment of the oropharyngeal carcinoma cells with the NF ‐κB activator TNF α (10 ng/mL) and the ATM inhibitor Ku55933 (10 μmol/L) for 12 h. Bands were quantified using ImageJ software and normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. NA, not applicable.
    Figure Legend Snippet: eIF 2α regulated radioresistance in oropharyngeal carcinoma cells by activating the NF ‐κB pathway. Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy X‐ray. (a) Cells were collected after 24 h to detect apoptosis using Annexin V/ PI staining followed by flow cytometry analysis. (b) Cells were collected after 48 h to identify the cell cycle using PI staining followed by flow cytometry. The results are expressed as the mean ± SD of three independent experiments. Compared with the IR group, * P < 0.05, # P < 0.01. (c) Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy for 12 h. Nuclear and cytoplasm proteins were extracted to detect the expression of phospho‐p65 and its downstream protein HIF ‐1α. Total protein was extracted to evaluate the expression of Rad50, Mre11, Nbs1 and phospho‐ ATM proteins. Western blot results showed that eIF 2α silencing inhibited radiation‐induced nuclear phospho‐p65 protein expression. Conversely, radiation inhibited cytoplasmic p65 protein phosphorylation, whereas eIF 2α silencing reversed this function. These results indicated that eIF 2α silencing inhibited radiation‐induced p65 nuclear translocation. In addition, eIF 2α silencing inhibited the radiation‐induced HIF ‐1α, Rad50 and Nbs1 expression, increased radiation‐induced phospho‐ ATM expression, and did not affect Mre11 protein expression. (d) After eIF 2α was silenced by si RNA transfection, the cells were irradiated (5 Gy, 1 h). The real‐time quantitative PCR results showed that eIF 2α silencing decreased the radiation‐induced expression of p65 mRNA expression. Compared to the irradiated group, * P < 0.05 and # P < 0.01. (e) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ‐H2 AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ‐H2 AX foci). In addition, the effect of radiation after eIF 2α silencing was more evident than that of simple radiation. (f) The western blot results showed that eIF 2α silencing inhibited radiation (5 Gy, 12 h)‐induced phospho‐cdc2, Cyclin B, Bcl‐2 and Bcl‐ xL protein expression and increased radiation‐induced cleaved‐Caspase 3 and cleaved‐ PARP protein expression. The above functions were inhibited by pretreatment of the oropharyngeal carcinoma cells with the NF ‐κB activator TNF α (10 ng/mL) and the ATM inhibitor Ku55933 (10 μmol/L) for 12 h. Bands were quantified using ImageJ software and normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. NA, not applicable.

    Techniques Used: Transfection, Irradiation, Staining, Flow Cytometry, Expressing, Western Blot, Translocation Assay, Real-time Polymerase Chain Reaction, Immunofluorescence, Software, Negative Control

    pe annexin v apoptosis detection kit  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc pe annexin v apoptosis detection kit
    IVC induces apoptotic death. a MHCC97H cells were incubated with IVC at indicated doses for 24 h, and Annexin V-PE and 7-AAD stained cells were sorted by flow cytometry. b Distribution of cell <t>apoptosis</t> was analyzed. c Protein expressions of Caspase3, Cleaved Caspase3, PARP and Bcl-2 were detected by western blot. d The relative protein level in each condition was quantitated using Image J. Experiments were repeated three times, and similar results were obtained. Data are expressed as mean ± S.E. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the control
    Pe Annexin V Apoptosis Detection Kit, 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/pe annexin v apoptosis detection kit/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pe annexin v apoptosis detection kit - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Incarvine C suppresses proliferation and vasculogenic mimicry of hepatocellular carcinoma cells via targeting ROCK inhibition"

    Article Title: Incarvine C suppresses proliferation and vasculogenic mimicry of hepatocellular carcinoma cells via targeting ROCK inhibition

    Journal: BMC Cancer

    doi: 10.1186/s12885-015-1809-5

    IVC induces apoptotic death. a MHCC97H cells were incubated with IVC at indicated doses for 24 h, and Annexin V-PE and 7-AAD stained cells were sorted by flow cytometry. b Distribution of cell apoptosis was analyzed. c Protein expressions of Caspase3, Cleaved Caspase3, PARP and Bcl-2 were detected by western blot. d The relative protein level in each condition was quantitated using Image J. Experiments were repeated three times, and similar results were obtained. Data are expressed as mean ± S.E. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the control
    Figure Legend Snippet: IVC induces apoptotic death. a MHCC97H cells were incubated with IVC at indicated doses for 24 h, and Annexin V-PE and 7-AAD stained cells were sorted by flow cytometry. b Distribution of cell apoptosis was analyzed. c Protein expressions of Caspase3, Cleaved Caspase3, PARP and Bcl-2 were detected by western blot. d The relative protein level in each condition was quantitated using Image J. Experiments were repeated three times, and similar results were obtained. Data are expressed as mean ± S.E. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the control

    Techniques Used: Incubation, Staining, Flow Cytometry, Western Blot

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    Cell Signaling Technology Inc annexin v
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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease <t>apoptosis,</t> which is related to radioresistance
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    The combinatorial miR treatment induced strong cytotoxic and apoptotic effect, along with Caspase activation ( A ) Potential synergism is illustrated by the combination’s (Combo) cytotoxicity being larger than the addition of the cytotoxicity of the individual miRs alone. Fluorescence intensity, which correlates to number of dead cells, was measured till 33 h post transfection. Lipofectamine with Scramble (Lipo), and untreated cells (Control) were used as negative controls. Positive control (Positive) was provided by the vendor. *p < 0.05 of combo vs. Control, miR-143, miR-506. ( B ) FACS Annexin V/PI analysis of cell <t>apoptosis</t> treated with individual mimics, and combination at 24 and 48 h compared to untreated cells. ( C ) Caspase-3/7 activity of A549 cells treated with individual and combination of miR, at 24 h. Cells without any treatment (Negative control-NC), with Lipofectamine, and with no-target control miRNA (scramble) were used as experimental controls. Doxorubicin (DOX, equimolar) was used as positive control. **p < 0.01 relative to NC. ( D ) <t>Annexin</t> <t>V</t> positive A549 cells, following transfection with miR-143 and/or miR-506 at 24 and 48 h post transfection.
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    The combinatorial miR treatment induced strong cytotoxic and apoptotic effect, along with Caspase activation ( A ) Potential synergism is illustrated by the combination’s (Combo) cytotoxicity being larger than the addition of the cytotoxicity of the individual miRs alone. Fluorescence intensity, which correlates to number of dead cells, was measured till 33 h post transfection. Lipofectamine with Scramble (Lipo), and untreated cells (Control) were used as negative controls. Positive control (Positive) was provided by the vendor. *p < 0.05 of combo vs. Control, miR-143, miR-506. ( B ) FACS Annexin V/PI analysis of cell <t>apoptosis</t> treated with individual mimics, and combination at 24 and 48 h compared to untreated cells. ( C ) Caspase-3/7 activity of A549 cells treated with individual and combination of miR, at 24 h. Cells without any treatment (Negative control-NC), with Lipofectamine, and with no-target control miRNA (scramble) were used as experimental controls. Doxorubicin (DOX, equimolar) was used as positive control. **p < 0.01 relative to NC. ( D ) <t>Annexin</t> <t>V</t> positive A549 cells, following transfection with miR-143 and/or miR-506 at 24 and 48 h post transfection.
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    Cell Signaling Technology Inc pe annexin v apoptosis detection kit
    IVC induces apoptotic death. a MHCC97H cells were incubated with IVC at indicated doses for 24 h, and Annexin V-PE and 7-AAD stained cells were sorted by flow cytometry. b Distribution of cell <t>apoptosis</t> was analyzed. c Protein expressions of Caspase3, Cleaved Caspase3, PARP and Bcl-2 were detected by western blot. d The relative protein level in each condition was quantitated using Image J. Experiments were repeated three times, and similar results were obtained. Data are expressed as mean ± S.E. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the control
    Pe Annexin V Apoptosis Detection Kit, 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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    Image Search Results


    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance

    Journal: Cancer Science

    Article Title: Interleukin‐6 production mediated by the IRE 1‐ XBP 1 pathway confers radioresistance in human papillomavirus‐negative oropharyngeal carcinoma

    doi: 10.1111/cas.14094

    Figure Lengend Snippet: Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance

    Article Snippet: Experiments were performed according to the protocol supplied with the Annexin‐Green Apoptosis cell detection reagent kit (Cell Signaling Technology).

    Techniques: Irradiation, Expressing

    The combinatorial miR treatment induced strong cytotoxic and apoptotic effect, along with Caspase activation ( A ) Potential synergism is illustrated by the combination’s (Combo) cytotoxicity being larger than the addition of the cytotoxicity of the individual miRs alone. Fluorescence intensity, which correlates to number of dead cells, was measured till 33 h post transfection. Lipofectamine with Scramble (Lipo), and untreated cells (Control) were used as negative controls. Positive control (Positive) was provided by the vendor. *p < 0.05 of combo vs. Control, miR-143, miR-506. ( B ) FACS Annexin V/PI analysis of cell apoptosis treated with individual mimics, and combination at 24 and 48 h compared to untreated cells. ( C ) Caspase-3/7 activity of A549 cells treated with individual and combination of miR, at 24 h. Cells without any treatment (Negative control-NC), with Lipofectamine, and with no-target control miRNA (scramble) were used as experimental controls. Doxorubicin (DOX, equimolar) was used as positive control. **p < 0.01 relative to NC. ( D ) Annexin V positive A549 cells, following transfection with miR-143 and/or miR-506 at 24 and 48 h post transfection.

    Journal: Scientific Reports

    Article Title: Multipronged activity of combinatorial miR-143 and miR-506 inhibits Lung Cancer cell cycle progression and angiogenesis in vitro

    doi: 10.1038/s41598-018-28872-2

    Figure Lengend Snippet: The combinatorial miR treatment induced strong cytotoxic and apoptotic effect, along with Caspase activation ( A ) Potential synergism is illustrated by the combination’s (Combo) cytotoxicity being larger than the addition of the cytotoxicity of the individual miRs alone. Fluorescence intensity, which correlates to number of dead cells, was measured till 33 h post transfection. Lipofectamine with Scramble (Lipo), and untreated cells (Control) were used as negative controls. Positive control (Positive) was provided by the vendor. *p < 0.05 of combo vs. Control, miR-143, miR-506. ( B ) FACS Annexin V/PI analysis of cell apoptosis treated with individual mimics, and combination at 24 and 48 h compared to untreated cells. ( C ) Caspase-3/7 activity of A549 cells treated with individual and combination of miR, at 24 h. Cells without any treatment (Negative control-NC), with Lipofectamine, and with no-target control miRNA (scramble) were used as experimental controls. Doxorubicin (DOX, equimolar) was used as positive control. **p < 0.01 relative to NC. ( D ) Annexin V positive A549 cells, following transfection with miR-143 and/or miR-506 at 24 and 48 h post transfection.

    Article Snippet: We evaluated the capacity of the combinatorial treatment to induce apoptotic activity against A549 lung cancer cells, using a Annexin V/PI Early Apoptosis Detection Kit (Cell Signaling), following an established protocol .

    Techniques: Activation Assay, Fluorescence, Transfection, Positive Control, Activity Assay, Negative Control

    Annexin V/PI  apoptosis  analysis of A549 cell populations, as determined by flow-cytometric quantification (Average of triplicates ± SEM).

    Journal: Scientific Reports

    Article Title: Multipronged activity of combinatorial miR-143 and miR-506 inhibits Lung Cancer cell cycle progression and angiogenesis in vitro

    doi: 10.1038/s41598-018-28872-2

    Figure Lengend Snippet: Annexin V/PI apoptosis analysis of A549 cell populations, as determined by flow-cytometric quantification (Average of triplicates ± SEM).

    Article Snippet: We evaluated the capacity of the combinatorial treatment to induce apoptotic activity against A549 lung cancer cells, using a Annexin V/PI Early Apoptosis Detection Kit (Cell Signaling), following an established protocol .

    Techniques:

    Genes and their activity on the cell cycle, which demonstrated >10% up-/down-regulation, as identified by the microarray analysis of A549 cells transfected with miR-143/506, for 24 and/or 48 h post transfection, compared to control.

    Journal: Scientific Reports

    Article Title: Multipronged activity of combinatorial miR-143 and miR-506 inhibits Lung Cancer cell cycle progression and angiogenesis in vitro

    doi: 10.1038/s41598-018-28872-2

    Figure Lengend Snippet: Genes and their activity on the cell cycle, which demonstrated >10% up-/down-regulation, as identified by the microarray analysis of A549 cells transfected with miR-143/506, for 24 and/or 48 h post transfection, compared to control.

    Article Snippet: We evaluated the capacity of the combinatorial treatment to induce apoptotic activity against A549 lung cancer cells, using a Annexin V/PI Early Apoptosis Detection Kit (Cell Signaling), following an established protocol .

    Techniques: Activity Assay, Microarray, Transfection, Over Expression, Migration

    IVC induces apoptotic death. a MHCC97H cells were incubated with IVC at indicated doses for 24 h, and Annexin V-PE and 7-AAD stained cells were sorted by flow cytometry. b Distribution of cell apoptosis was analyzed. c Protein expressions of Caspase3, Cleaved Caspase3, PARP and Bcl-2 were detected by western blot. d The relative protein level in each condition was quantitated using Image J. Experiments were repeated three times, and similar results were obtained. Data are expressed as mean ± S.E. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the control

    Journal: BMC Cancer

    Article Title: Incarvine C suppresses proliferation and vasculogenic mimicry of hepatocellular carcinoma cells via targeting ROCK inhibition

    doi: 10.1186/s12885-015-1809-5

    Figure Lengend Snippet: IVC induces apoptotic death. a MHCC97H cells were incubated with IVC at indicated doses for 24 h, and Annexin V-PE and 7-AAD stained cells were sorted by flow cytometry. b Distribution of cell apoptosis was analyzed. c Protein expressions of Caspase3, Cleaved Caspase3, PARP and Bcl-2 were detected by western blot. d The relative protein level in each condition was quantitated using Image J. Experiments were repeated three times, and similar results were obtained. Data are expressed as mean ± S.E. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the control

    Article Snippet: Chemicals and antibodies used in this study include Matrigel (BD Biosciences); cell culture media (RPMI 1640, DMEM and MEM), fetal bovine serum (FBS) and antibiotics (Gibco); Y27632 and other chemicals (Sigma-Aldrich); anti-VE-cadherin, MYPT-1 and p-MYPT-1(Thr853) antibodies (Cell Signaling); PE Annexin V Apoptosis Detection Kit and PI/RNase Staining Buffer (BD PharmingenTM).

    Techniques: Incubation, Staining, Flow Cytometry, Western Blot