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human atg5 shrna plasmids  (Genechem)
86
Genechem human atg5 shrna plasmids
Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three <t>ATG5-targeting</t> shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Human Atg5 Shrna Plasmids, supplied by Genechem, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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lentiviral plasmids encoding shrnas for atg5 tl314610  (OriGene)
90
OriGene lentiviral plasmids encoding shrnas for atg5 tl314610
Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three <t>ATG5-targeting</t> shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Lentiviral Plasmids Encoding Shrnas For Atg5 Tl314610, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atg5 short hairpin rna (shrna) lentiviruses  (Shanghai GenePharma)
90
Shanghai GenePharma atg5 short hairpin rna (shrna) lentiviruses
Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three <t>ATG5-targeting</t> shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Atg5 Short Hairpin Rna (Shrna) Lentiviruses, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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lentivirus containing atg5 shrna  (biolasco taiwan)
90
biolasco taiwan lentivirus containing atg5 shrna
Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three <t>ATG5-targeting</t> shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Lentivirus Containing Atg5 Shrna, supplied by biolasco taiwan, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pglvh1/gfp + puro vectors carrying atg5 shrna or nonsense control (nc) shrna  (Shanghai GenePharma)
90
Shanghai GenePharma pglvh1/gfp + puro vectors carrying atg5 shrna or nonsense control (nc) shrna
Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three <t>ATG5-targeting</t> shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Pglvh1/Gfp + Puro Vectors Carrying Atg5 Shrna Or Nonsense Control (Nc) Shrna, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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recombinant adeno-associated virus 9 expressing control, shrna-atg5 or atg5  (Shandong Weizhen Food Co Ltd)
90
Shandong Weizhen Food Co Ltd recombinant adeno-associated virus 9 expressing control, shrna-atg5 or atg5
Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three <t>ATG5-targeting</t> shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Recombinant Adeno Associated Virus 9 Expressing Control, Shrna Atg5 Or Atg5, supplied by Shandong Weizhen Food Co Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atg 5  (OriGene)
94
OriGene atg 5
Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three <t>ATG5-targeting</t> shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Atg 5, supplied by OriGene, 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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Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three ATG5-targeting shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.

Journal: Acta Biochimica et Biophysica Sinica

Article Title: Autophagy-dependent sensitization effects of PARP inhibitors on recurrent nasopharyngeal carcinoma treated with carbon ion and photon irradiation

doi: 10.3724/abbs.2025130

Figure Lengend Snippet: Autophagy inhibition attenuates the radiation-sensitizing effect of olaparib (A) HK-1 cells were plated in 96-well plates and treated with X-ray or C-ion irradiation, with or without olaparib (5 μM), in the presence of different cell death inhibitors. Z-VAD (15 μM), Nec-1 (15 μM) and Fer-1 (5 μM) were added 24 h before radiation exposure, and 3-MA (5 μM) was added 2 h before radiation. All the inhibitors were incubated for 24 h postirradiation. The morphology of the cells was observed and imaged 48 h after irradiation via an inverted microscope (20× magnification; scale bar: 100 μm). (B,C) HK-1 cells were treated as described in (A). Left panel: Cell survival was assessed via CCK-8 assay 48 h after X-ray or C-ion exposure, with the values normalized to those of the nonirradiated control of the corresponding drug group. Right panel: The proportion of surviving cells rescued by each inhibitor in the X-ray + olaparib or C-ion + olaparib combination treatment group was calculated and is presented as a pie chart. The “other” category represents additional cell death mechanisms, determined as one minus the sum of the cell survival fractions rescued by the four inhibitors. (D) The gene knockdown efficiency of three ATG5-targeting shRNAs was confirmed via western blot analysis. GAPDH served as the loading control. Sh-ATG5-67 clones were selected for subsequent studies. (E) Cells transfected with sh-ATG5 or sh-NC were treated with olaparib and/or radiation, and their autophagy levels were measured by flow cytometry 48 h after irradiation. (F,G) ATG5 knockdown significantly increased the HK-1 cell survival rate following X-ray or C-ion irradiation, with or without olaparib (5 μM). The numbers in parentheses indicate the number of cells plated per well for each dose group. Survival curves were generated for the X-ray (H) and C-ion (I) groups, with the values normalized to those of the nonirradiated group. Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.

Article Snippet: For ATG5 knockdown, three human ATG5 shRNA plasmids constructed by GeneChem were used: shATG5-65: 5′-GATTCATGGAATTGAGCCAAT-3′; shATG5-66: 5′-CCTTTCATTCAGAAGCTGTTT-3′; shATG5-67: 5′-CCTGAACAGAATCATCCTTAA-3′.

Techniques: Inhibition, Irradiation, Incubation, Inverted Microscopy, CCK-8 Assay, Control, Knockdown, Western Blot, Clone Assay, Transfection, Flow Cytometry, Generated