cdk inhibitor ro-3306 Search Results


cdk inhibitor ro3306  (Enzo Biochem)
90
Enzo Biochem cdk inhibitor ro3306
a In vitro kinase assay: recombinant GST-Aurora B WT or KD proteins purified in the bacteria was incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. Incorporation of γ 32 P into Aurora B protein was visualized by autoradiography. Coomassie blue staining demonstrates equal protein loading. b Alignment of vertebrate Aurora B sequence from humans to mouse across a short region with the conserved GT motif (upper panel). In vitro kinase assay of phosphorylation mutants on the GST-Aurora B were incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. c Synchronized mitotic HeLa cells were treated with the PLK1 inhibitor BI2536 or DMSO for 30 min. Cells were then fixed and stained with anti-pThr236-Aurora B antibody (green), Aurora B (red), and DAPI (blue). Bars represent mean ± SEM from three independent experiments; DMSO n = 32, BI2536 n = 35 cells. *** p < 0.001 vs. DMSO by two-sided unpaired Student’s t -test. Scale bar, 5 μm. d HeLa cells synchronized to mitosis by Nocodazole were pre-treated with MG132 for 1 h and with BI2536, <t>Ro3306,</t> or DMSO for 30 min, followed by western blot analysis with the indicated antibodies. e RSF WT or RSF1 KO HeLa cells were synchronized to mitosis by Nocodazole, followed by western blotting analyzed by the indicated antibodies. f RSF WT or RSF1 KO HeLa cells were treated with nocodazole for 4 h. Mitotic cells were fixed with 4% paraformaldehyde and stained with anti-pT236-Aurora B (green) and anti-Aurora B (red) antibodies. Nucleus was stained with DAPI (blue). Bar represents mean ± SEM from three independent experiments; WT n = 27, RSF1 KO n = 44 cells. ** p < 0.005 vs. RSF1 WT by two-sided unpaired Student’s t -test. Scale bar, 5 μm. Data of a , b , d , e are representative of three independent experiments. Source data are provided as a Source Data file.
Cdk Inhibitor Ro3306, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cdk+inhibitor+ro-3306/pmc08505570-319-10-13?v=Enzo+Biochem
Average 90 stars, based on 1 article reviews
cdk inhibitor ro3306 - by Bioz Stars, 2026-07
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cdk inhibitor ro-3306  (Axon Medchem LLC)
90
Axon Medchem LLC cdk inhibitor ro-3306
a In vitro kinase assay: recombinant GST-Aurora B WT or KD proteins purified in the bacteria was incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. Incorporation of γ 32 P into Aurora B protein was visualized by autoradiography. Coomassie blue staining demonstrates equal protein loading. b Alignment of vertebrate Aurora B sequence from humans to mouse across a short region with the conserved GT motif (upper panel). In vitro kinase assay of phosphorylation mutants on the GST-Aurora B were incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. c Synchronized mitotic HeLa cells were treated with the PLK1 inhibitor BI2536 or DMSO for 30 min. Cells were then fixed and stained with anti-pThr236-Aurora B antibody (green), Aurora B (red), and DAPI (blue). Bars represent mean ± SEM from three independent experiments; DMSO n = 32, BI2536 n = 35 cells. *** p < 0.001 vs. DMSO by two-sided unpaired Student’s t -test. Scale bar, 5 μm. d HeLa cells synchronized to mitosis by Nocodazole were pre-treated with MG132 for 1 h and with BI2536, <t>Ro3306,</t> or DMSO for 30 min, followed by western blot analysis with the indicated antibodies. e RSF WT or RSF1 KO HeLa cells were synchronized to mitosis by Nocodazole, followed by western blotting analyzed by the indicated antibodies. f RSF WT or RSF1 KO HeLa cells were treated with nocodazole for 4 h. Mitotic cells were fixed with 4% paraformaldehyde and stained with anti-pT236-Aurora B (green) and anti-Aurora B (red) antibodies. Nucleus was stained with DAPI (blue). Bar represents mean ± SEM from three independent experiments; WT n = 27, RSF1 KO n = 44 cells. ** p < 0.005 vs. RSF1 WT by two-sided unpaired Student’s t -test. Scale bar, 5 μm. Data of a , b , d , e are representative of three independent experiments. Source data are provided as a Source Data file.
Cdk Inhibitor Ro 3306, supplied by Axon Medchem LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cdk+inhibitor+ro-3306/pm37347663-394-42-45?v=Axon+Medchem+LLC
Average 90 stars, based on 1 article reviews
cdk inhibitor ro-3306 - by Bioz Stars, 2026-07
90/100 stars
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cdk inhibitor ro 3306  (Selleck Chemicals)
96
Selleck Chemicals cdk inhibitor ro 3306
a In vitro kinase assay: recombinant GST-Aurora B WT or KD proteins purified in the bacteria was incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. Incorporation of γ 32 P into Aurora B protein was visualized by autoradiography. Coomassie blue staining demonstrates equal protein loading. b Alignment of vertebrate Aurora B sequence from humans to mouse across a short region with the conserved GT motif (upper panel). In vitro kinase assay of phosphorylation mutants on the GST-Aurora B were incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. c Synchronized mitotic HeLa cells were treated with the PLK1 inhibitor BI2536 or DMSO for 30 min. Cells were then fixed and stained with anti-pThr236-Aurora B antibody (green), Aurora B (red), and DAPI (blue). Bars represent mean ± SEM from three independent experiments; DMSO n = 32, BI2536 n = 35 cells. *** p < 0.001 vs. DMSO by two-sided unpaired Student’s t -test. Scale bar, 5 μm. d HeLa cells synchronized to mitosis by Nocodazole were pre-treated with MG132 for 1 h and with BI2536, <t>Ro3306,</t> or DMSO for 30 min, followed by western blot analysis with the indicated antibodies. e RSF WT or RSF1 KO HeLa cells were synchronized to mitosis by Nocodazole, followed by western blotting analyzed by the indicated antibodies. f RSF WT or RSF1 KO HeLa cells were treated with nocodazole for 4 h. Mitotic cells were fixed with 4% paraformaldehyde and stained with anti-pT236-Aurora B (green) and anti-Aurora B (red) antibodies. Nucleus was stained with DAPI (blue). Bar represents mean ± SEM from three independent experiments; WT n = 27, RSF1 KO n = 44 cells. ** p < 0.005 vs. RSF1 WT by two-sided unpaired Student’s t -test. Scale bar, 5 μm. Data of a , b , d , e are representative of three independent experiments. Source data are provided as a Source Data file.
Cdk Inhibitor Ro 3306, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cdk+inhibitor+ro-3306/pmc06011407-282-1-4?v=Selleck+Chemicals
Average 96 stars, based on 1 article reviews
cdk inhibitor ro 3306 - by Bioz Stars, 2026-07
96/100 stars
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cdk inhibitor ro3306  (Tocris)
95
Tocris cdk inhibitor ro3306
( A ) Schematic of DNA fiber analysis. Green tracks, CldU; red tracks, IdU. ( B ) Schematic drawing and representative images of two replication signals from DNA fibers. At the top, two DNA replication forks moved bidirectionally from an origin (indicated by the diverging black arrows) that was activated before the CIdU pulse. Each fork was labeled with both IdU (red) and CldU (green). At the bottom, the replication bubble resulting from an origin that was activated during the CldU pulse produces a green-only signal. ( C ) Summary of new origins fired during labeling with CldU. The frequency (as a percentage) was calculated as the number of green signals (b in panel B) divided by the total (a + b) of green (b) plus green/red signals (a in panel B). Results are from three independent experiment results ( T -test, * p < 0.05, ** p < 0.01). ( D ) CHK1 inhibition led to increased levels of nonextractable Cdc45 protein in MCF-7/C6 cells. The cells treated with AZD7762 (100 nM) for the indicated time were incubated with extraction buffer for 5 min on ice, and processed for Western blotting (top panel). The whole lysate protein is used as a control (bottom panel). ( E ) Measurement of Cdc45 chromatin loading after preextraction of cells with detergent by immunostaining. Cells presenting with Cdc45 staining were considered positive. The results are from three independent experiments. Error bars represent the SD of three independent experiments ( T -test, ** p < 0.01). ( F ) Representative Cdc45 staining (green) in MCF-7 and MCF-7/C6 cells are presented. Cell nuclei were stained with DAPI (blue). ( G )The effect of CHK1 inhibition on RS in RBCC depends on Cdk activity. Cdk activity was inhibited by inhibitor <t>Ro3306.</t>
Cdk Inhibitor Ro3306, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cdk+inhibitor+ro-3306/pmc05085184-206-1-7?v=Tocris
Average 95 stars, based on 1 article reviews
cdk inhibitor ro3306 - by Bioz Stars, 2026-07
95/100 stars
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Image Search Results


a In vitro kinase assay: recombinant GST-Aurora B WT or KD proteins purified in the bacteria was incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. Incorporation of γ 32 P into Aurora B protein was visualized by autoradiography. Coomassie blue staining demonstrates equal protein loading. b Alignment of vertebrate Aurora B sequence from humans to mouse across a short region with the conserved GT motif (upper panel). In vitro kinase assay of phosphorylation mutants on the GST-Aurora B were incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. c Synchronized mitotic HeLa cells were treated with the PLK1 inhibitor BI2536 or DMSO for 30 min. Cells were then fixed and stained with anti-pThr236-Aurora B antibody (green), Aurora B (red), and DAPI (blue). Bars represent mean ± SEM from three independent experiments; DMSO n = 32, BI2536 n = 35 cells. *** p < 0.001 vs. DMSO by two-sided unpaired Student’s t -test. Scale bar, 5 μm. d HeLa cells synchronized to mitosis by Nocodazole were pre-treated with MG132 for 1 h and with BI2536, Ro3306, or DMSO for 30 min, followed by western blot analysis with the indicated antibodies. e RSF WT or RSF1 KO HeLa cells were synchronized to mitosis by Nocodazole, followed by western blotting analyzed by the indicated antibodies. f RSF WT or RSF1 KO HeLa cells were treated with nocodazole for 4 h. Mitotic cells were fixed with 4% paraformaldehyde and stained with anti-pT236-Aurora B (green) and anti-Aurora B (red) antibodies. Nucleus was stained with DAPI (blue). Bar represents mean ± SEM from three independent experiments; WT n = 27, RSF1 KO n = 44 cells. ** p < 0.005 vs. RSF1 WT by two-sided unpaired Student’s t -test. Scale bar, 5 μm. Data of a , b , d , e are representative of three independent experiments. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Spatiotemporal coordination of the RSF1-PLK1-Aurora B cascade establishes mitotic signaling platforms

doi: 10.1038/s41467-021-26220-z

Figure Lengend Snippet: a In vitro kinase assay: recombinant GST-Aurora B WT or KD proteins purified in the bacteria was incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. Incorporation of γ 32 P into Aurora B protein was visualized by autoradiography. Coomassie blue staining demonstrates equal protein loading. b Alignment of vertebrate Aurora B sequence from humans to mouse across a short region with the conserved GT motif (upper panel). In vitro kinase assay of phosphorylation mutants on the GST-Aurora B were incubated with the active GST-PLK1 at 30 °C for 30 min in the presence of γ 32 P-ATP. c Synchronized mitotic HeLa cells were treated with the PLK1 inhibitor BI2536 or DMSO for 30 min. Cells were then fixed and stained with anti-pThr236-Aurora B antibody (green), Aurora B (red), and DAPI (blue). Bars represent mean ± SEM from three independent experiments; DMSO n = 32, BI2536 n = 35 cells. *** p < 0.001 vs. DMSO by two-sided unpaired Student’s t -test. Scale bar, 5 μm. d HeLa cells synchronized to mitosis by Nocodazole were pre-treated with MG132 for 1 h and with BI2536, Ro3306, or DMSO for 30 min, followed by western blot analysis with the indicated antibodies. e RSF WT or RSF1 KO HeLa cells were synchronized to mitosis by Nocodazole, followed by western blotting analyzed by the indicated antibodies. f RSF WT or RSF1 KO HeLa cells were treated with nocodazole for 4 h. Mitotic cells were fixed with 4% paraformaldehyde and stained with anti-pT236-Aurora B (green) and anti-Aurora B (red) antibodies. Nucleus was stained with DAPI (blue). Bar represents mean ± SEM from three independent experiments; WT n = 27, RSF1 KO n = 44 cells. ** p < 0.005 vs. RSF1 WT by two-sided unpaired Student’s t -test. Scale bar, 5 μm. Data of a , b , d , e are representative of three independent experiments. Source data are provided as a Source Data file.

Article Snippet: The following reagents were used: Aurora B inhibitor ZM447439 (Tocris), CDK inhibitor RO3306 (Enzo), Nocodazole (sigma), Paclitaxel (Tocris), PLK1 inhibitor IB2536 (Axonmedchem), and Puromycin Dihydrochloride (Invitrogen).

Techniques: In Vitro, Kinase Assay, Recombinant, Purification, Incubation, Autoradiography, Staining, Sequencing, Western Blot

( A ) Schematic of DNA fiber analysis. Green tracks, CldU; red tracks, IdU. ( B ) Schematic drawing and representative images of two replication signals from DNA fibers. At the top, two DNA replication forks moved bidirectionally from an origin (indicated by the diverging black arrows) that was activated before the CIdU pulse. Each fork was labeled with both IdU (red) and CldU (green). At the bottom, the replication bubble resulting from an origin that was activated during the CldU pulse produces a green-only signal. ( C ) Summary of new origins fired during labeling with CldU. The frequency (as a percentage) was calculated as the number of green signals (b in panel B) divided by the total (a + b) of green (b) plus green/red signals (a in panel B). Results are from three independent experiment results ( T -test, * p < 0.05, ** p < 0.01). ( D ) CHK1 inhibition led to increased levels of nonextractable Cdc45 protein in MCF-7/C6 cells. The cells treated with AZD7762 (100 nM) for the indicated time were incubated with extraction buffer for 5 min on ice, and processed for Western blotting (top panel). The whole lysate protein is used as a control (bottom panel). ( E ) Measurement of Cdc45 chromatin loading after preextraction of cells with detergent by immunostaining. Cells presenting with Cdc45 staining were considered positive. The results are from three independent experiments. Error bars represent the SD of three independent experiments ( T -test, ** p < 0.01). ( F ) Representative Cdc45 staining (green) in MCF-7 and MCF-7/C6 cells are presented. Cell nuclei were stained with DAPI (blue). ( G )The effect of CHK1 inhibition on RS in RBCC depends on Cdk activity. Cdk activity was inhibited by inhibitor Ro3306.

Journal: Oncotarget

Article Title: Targeting radioresistant breast cancer cells by single agent CHK1 inhibitor via enhancing replication stress

doi: 10.18632/oncotarget.9156

Figure Lengend Snippet: ( A ) Schematic of DNA fiber analysis. Green tracks, CldU; red tracks, IdU. ( B ) Schematic drawing and representative images of two replication signals from DNA fibers. At the top, two DNA replication forks moved bidirectionally from an origin (indicated by the diverging black arrows) that was activated before the CIdU pulse. Each fork was labeled with both IdU (red) and CldU (green). At the bottom, the replication bubble resulting from an origin that was activated during the CldU pulse produces a green-only signal. ( C ) Summary of new origins fired during labeling with CldU. The frequency (as a percentage) was calculated as the number of green signals (b in panel B) divided by the total (a + b) of green (b) plus green/red signals (a in panel B). Results are from three independent experiment results ( T -test, * p < 0.05, ** p < 0.01). ( D ) CHK1 inhibition led to increased levels of nonextractable Cdc45 protein in MCF-7/C6 cells. The cells treated with AZD7762 (100 nM) for the indicated time were incubated with extraction buffer for 5 min on ice, and processed for Western blotting (top panel). The whole lysate protein is used as a control (bottom panel). ( E ) Measurement of Cdc45 chromatin loading after preextraction of cells with detergent by immunostaining. Cells presenting with Cdc45 staining were considered positive. The results are from three independent experiments. Error bars represent the SD of three independent experiments ( T -test, ** p < 0.01). ( F ) Representative Cdc45 staining (green) in MCF-7 and MCF-7/C6 cells are presented. Cell nuclei were stained with DAPI (blue). ( G )The effect of CHK1 inhibition on RS in RBCC depends on Cdk activity. Cdk activity was inhibited by inhibitor Ro3306.

Article Snippet: The Cdk inhibitor Ro3306 was purchased from Tocris.

Techniques: Labeling, Inhibition, Incubation, Extraction, Western Blot, Control, Immunostaining, Staining, Activity Assay