cell signal 26 Search Results


lysotracker green dnd 26  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc lysotracker green dnd 26
Lysotracker Green Dnd 26, supplied by Cell Signaling Technology Inc, 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/result/lysotracker green dnd 26/product/Cell Signaling Technology Inc
Average 95 stars, based on 1 article reviews
lysotracker green dnd 26 - by Bioz Stars, 2026-04
95/100 stars
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phospho histone h3  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc phospho histone h3
( a ) Cartoon showing that TPX2 and RAN act sequentially to activate AURKA, a known regulator of mitosis. RAN prevents the inhibitory interaction of Importins on TPX2, allowing it to activate AURKA for mitotic spindle assembly. ( b ) Immunoblot analysis confirms that three of the four siRNAs greatly reduce TPX2 protein levels in NCI-H1819 cell lysates 3 days after transfecting the cells. ( c ) Five days after transfecting NCI-H1819 cells with non-targeting or individual siRNAs targeting TPX2, cell viability was measured with a CellTiter-Glo viability assay. PLK1 was depleted as the positive control. NT=nontargeting. ** indicates statistical significance ( P <0.001). Statistical significance was assessed by one-way ANOVA and post hoc Dunnett's multiple comparison tests. ( d ) The effect of individual siRNAs on NCI-H1819 cells was measured by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone <t>H3</t> and β-Actin as a loading control 3 days after transfecting the cells with either non-targeting or TPX2-targeting siRNAs. Cleaved PARP indicated an active apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate experiments. ( e ) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNAs #5 and #6 targeting TPX2, cell viability was measured with a CellTiter-Glo assay that measure cellular ATP as a surrogate for cell proliferation or survival. PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates.
Phospho Histone H3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/phospho histone h3/product/Cell Signaling Technology Inc
Average 93 stars, based on 1 article reviews
phospho histone h3 - by Bioz Stars, 2026-04
93/100 stars
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fuel cell for radar set an/tps-26 (xn-1)  (Signal Research)
90
Signal Research fuel cell for radar set an/tps-26 (xn-1)
( a ) Cartoon showing that TPX2 and RAN act sequentially to activate AURKA, a known regulator of mitosis. RAN prevents the inhibitory interaction of Importins on TPX2, allowing it to activate AURKA for mitotic spindle assembly. ( b ) Immunoblot analysis confirms that three of the four siRNAs greatly reduce TPX2 protein levels in NCI-H1819 cell lysates 3 days after transfecting the cells. ( c ) Five days after transfecting NCI-H1819 cells with non-targeting or individual siRNAs targeting TPX2, cell viability was measured with a CellTiter-Glo viability assay. PLK1 was depleted as the positive control. NT=nontargeting. ** indicates statistical significance ( P <0.001). Statistical significance was assessed by one-way ANOVA and post hoc Dunnett's multiple comparison tests. ( d ) The effect of individual siRNAs on NCI-H1819 cells was measured by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone <t>H3</t> and β-Actin as a loading control 3 days after transfecting the cells with either non-targeting or TPX2-targeting siRNAs. Cleaved PARP indicated an active apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate experiments. ( e ) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNAs #5 and #6 targeting TPX2, cell viability was measured with a CellTiter-Glo assay that measure cellular ATP as a surrogate for cell proliferation or survival. PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates.
Fuel Cell For Radar Set An/Tps 26 (Xn 1), supplied by Signal Research, 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/result/fuel cell for radar set an/tps-26 (xn-1)/product/Signal Research
Average 90 stars, based on 1 article reviews
fuel cell for radar set an/tps-26 (xn-1) - by Bioz Stars, 2026-04
90/100 stars
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Image Search Results


( a ) Cartoon showing that TPX2 and RAN act sequentially to activate AURKA, a known regulator of mitosis. RAN prevents the inhibitory interaction of Importins on TPX2, allowing it to activate AURKA for mitotic spindle assembly. ( b ) Immunoblot analysis confirms that three of the four siRNAs greatly reduce TPX2 protein levels in NCI-H1819 cell lysates 3 days after transfecting the cells. ( c ) Five days after transfecting NCI-H1819 cells with non-targeting or individual siRNAs targeting TPX2, cell viability was measured with a CellTiter-Glo viability assay. PLK1 was depleted as the positive control. NT=nontargeting. ** indicates statistical significance ( P <0.001). Statistical significance was assessed by one-way ANOVA and post hoc Dunnett's multiple comparison tests. ( d ) The effect of individual siRNAs on NCI-H1819 cells was measured by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone H3 and β-Actin as a loading control 3 days after transfecting the cells with either non-targeting or TPX2-targeting siRNAs. Cleaved PARP indicated an active apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate experiments. ( e ) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNAs #5 and #6 targeting TPX2, cell viability was measured with a CellTiter-Glo assay that measure cellular ATP as a surrogate for cell proliferation or survival. PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates.

Journal: Nature Communications

Article Title: SMARCA4 -inactivating mutations increase sensitivity to Aurora kinase A inhibitor VX-680 in non-small cell lung cancers

doi: 10.1038/ncomms14098

Figure Lengend Snippet: ( a ) Cartoon showing that TPX2 and RAN act sequentially to activate AURKA, a known regulator of mitosis. RAN prevents the inhibitory interaction of Importins on TPX2, allowing it to activate AURKA for mitotic spindle assembly. ( b ) Immunoblot analysis confirms that three of the four siRNAs greatly reduce TPX2 protein levels in NCI-H1819 cell lysates 3 days after transfecting the cells. ( c ) Five days after transfecting NCI-H1819 cells with non-targeting or individual siRNAs targeting TPX2, cell viability was measured with a CellTiter-Glo viability assay. PLK1 was depleted as the positive control. NT=nontargeting. ** indicates statistical significance ( P <0.001). Statistical significance was assessed by one-way ANOVA and post hoc Dunnett's multiple comparison tests. ( d ) The effect of individual siRNAs on NCI-H1819 cells was measured by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone H3 and β-Actin as a loading control 3 days after transfecting the cells with either non-targeting or TPX2-targeting siRNAs. Cleaved PARP indicated an active apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate experiments. ( e ) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNAs #5 and #6 targeting TPX2, cell viability was measured with a CellTiter-Glo assay that measure cellular ATP as a surrogate for cell proliferation or survival. PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates.

Article Snippet: TPX2 (Biolegend, mouse mAb, 628001, 1:1,000 dilution), AURKA (Cell Signaling, rabbit mAb, 4718, 1:1,000 dilution), Phospho-Histone H3 (Cell Signaling, rabbit mAb, 33770, 1:1,000 dilution), cleaved PARP (Cell Signaling, rabbit mAb, 9541, 1:1,000 dilution), FLAG (Cell Signaling, rabbit mAb, 2368, 1:1,000 dilution), SMARCA4/BRG1 (EMD Millipore, rat mAb, MABE60, 1:1,000 dilution), DLG7/HURP (Bethyl Laboratory, A300-852A, 1:1,000 dilution), c-MYC (Santa Cruz Biotechnology, mouse mAb, sc-40, 1:1,000 dilution) and β-Actin (MP Biomedicals, mouse mAb, 69100, 1:10,000 dilution) antibodies were used for immunoblotting assays.

Techniques: Western Blot, Viability Assay, Positive Control, Comparison, Bioprocessing, Control, Glo Assay

( a ) NCI-H1819 cell lysates were collected 3 days after transfecting the cells with either non-targeting or AURKA-targeting siRNAs and were immunoblotted to monitor AURKA protein levels. ( b ) Five days after transfecting NCI-H1819 cells with individual siRNAs, cell viability was measured with a CellTiter-Glo assay on triplicate biological replicates. PLK1 knockdowns were used as the positive control. Means with s.d. are shown on the graphs. * indicates statistical significance ( P <0.001) and ** indicates statistical significance ( P <0.001) combined with higher biological significance (viability<50%). ( c ) The response to depletion of AURKA was assessed by immunoblotting with monoclonal antibodies to cleaved PARP, phospho-Histone H3 and β-Actin. ( d ) Five days after depleting AURKA in NCI-H1819, NCI-H1819-pBABE and NCI-H1819-pBABE-SMARCA4-FLAG cells, cell viability was measured with a CellTiter-Glo assay as in part ( b ). ( e ) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNA #28 targeting AURKA, cell viability was measured with a CellTiter-Glo viability assay as in . PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates. Statistical significance on graphs was assessed by one-way ANOVA and post hoc Dunnett's multiple comparison tests.

Journal: Nature Communications

Article Title: SMARCA4 -inactivating mutations increase sensitivity to Aurora kinase A inhibitor VX-680 in non-small cell lung cancers

doi: 10.1038/ncomms14098

Figure Lengend Snippet: ( a ) NCI-H1819 cell lysates were collected 3 days after transfecting the cells with either non-targeting or AURKA-targeting siRNAs and were immunoblotted to monitor AURKA protein levels. ( b ) Five days after transfecting NCI-H1819 cells with individual siRNAs, cell viability was measured with a CellTiter-Glo assay on triplicate biological replicates. PLK1 knockdowns were used as the positive control. Means with s.d. are shown on the graphs. * indicates statistical significance ( P <0.001) and ** indicates statistical significance ( P <0.001) combined with higher biological significance (viability<50%). ( c ) The response to depletion of AURKA was assessed by immunoblotting with monoclonal antibodies to cleaved PARP, phospho-Histone H3 and β-Actin. ( d ) Five days after depleting AURKA in NCI-H1819, NCI-H1819-pBABE and NCI-H1819-pBABE-SMARCA4-FLAG cells, cell viability was measured with a CellTiter-Glo assay as in part ( b ). ( e ) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNA #28 targeting AURKA, cell viability was measured with a CellTiter-Glo viability assay as in . PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates. Statistical significance on graphs was assessed by one-way ANOVA and post hoc Dunnett's multiple comparison tests.

Article Snippet: TPX2 (Biolegend, mouse mAb, 628001, 1:1,000 dilution), AURKA (Cell Signaling, rabbit mAb, 4718, 1:1,000 dilution), Phospho-Histone H3 (Cell Signaling, rabbit mAb, 33770, 1:1,000 dilution), cleaved PARP (Cell Signaling, rabbit mAb, 9541, 1:1,000 dilution), FLAG (Cell Signaling, rabbit mAb, 2368, 1:1,000 dilution), SMARCA4/BRG1 (EMD Millipore, rat mAb, MABE60, 1:1,000 dilution), DLG7/HURP (Bethyl Laboratory, A300-852A, 1:1,000 dilution), c-MYC (Santa Cruz Biotechnology, mouse mAb, sc-40, 1:1,000 dilution) and β-Actin (MP Biomedicals, mouse mAb, 69100, 1:10,000 dilution) antibodies were used for immunoblotting assays.

Techniques: Glo Assay, Positive Control, Western Blot, Bioprocessing, Viability Assay, Comparison

( a ) The response to depleting HURP with a pool of four individual siRNAs was measured with monoclonal antibodies to HURP, cleaved PARP (indicating apoptosis) and phospho-Histone H3 (indicating cells engaged in mitosis). ( b ) Five days after depleting HURP in NCI-H1819, NCI-H1819-pBABE and NCI-H1819-pBABE-SMARCA4-FLAG cells and ( c ) in NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells, cell viability was measured with a CellTiter-Glo assay as in and . PLK1 was depleted as the positive control. Data are means with s.d. of triplicate biological replicates and representative of triplicate experiments. ( d ) Cell lysates of NCI-H1819, NCI-H1819-pBABE and NCI-H1819-pBABE-SMARCA4-FLAG cells were immunoblotted with monoclonal antibodies to HURP. ( e ) HURP expression was measured in a panel of SMARCA4 -mutant or wild-type NSCLCs and HBECs by immunoblotting. ( f ) HURP protein band intensities were measured with the ImageQuant software and graphed. Horizontal bars indicate means and s.e.m. of sample groups. Statistical significance on graphs was assessed by one-way ANOVA and post hoc Dunnet's multiple comparison tests.

Journal: Nature Communications

Article Title: SMARCA4 -inactivating mutations increase sensitivity to Aurora kinase A inhibitor VX-680 in non-small cell lung cancers

doi: 10.1038/ncomms14098

Figure Lengend Snippet: ( a ) The response to depleting HURP with a pool of four individual siRNAs was measured with monoclonal antibodies to HURP, cleaved PARP (indicating apoptosis) and phospho-Histone H3 (indicating cells engaged in mitosis). ( b ) Five days after depleting HURP in NCI-H1819, NCI-H1819-pBABE and NCI-H1819-pBABE-SMARCA4-FLAG cells and ( c ) in NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells, cell viability was measured with a CellTiter-Glo assay as in and . PLK1 was depleted as the positive control. Data are means with s.d. of triplicate biological replicates and representative of triplicate experiments. ( d ) Cell lysates of NCI-H1819, NCI-H1819-pBABE and NCI-H1819-pBABE-SMARCA4-FLAG cells were immunoblotted with monoclonal antibodies to HURP. ( e ) HURP expression was measured in a panel of SMARCA4 -mutant or wild-type NSCLCs and HBECs by immunoblotting. ( f ) HURP protein band intensities were measured with the ImageQuant software and graphed. Horizontal bars indicate means and s.e.m. of sample groups. Statistical significance on graphs was assessed by one-way ANOVA and post hoc Dunnet's multiple comparison tests.

Article Snippet: TPX2 (Biolegend, mouse mAb, 628001, 1:1,000 dilution), AURKA (Cell Signaling, rabbit mAb, 4718, 1:1,000 dilution), Phospho-Histone H3 (Cell Signaling, rabbit mAb, 33770, 1:1,000 dilution), cleaved PARP (Cell Signaling, rabbit mAb, 9541, 1:1,000 dilution), FLAG (Cell Signaling, rabbit mAb, 2368, 1:1,000 dilution), SMARCA4/BRG1 (EMD Millipore, rat mAb, MABE60, 1:1,000 dilution), DLG7/HURP (Bethyl Laboratory, A300-852A, 1:1,000 dilution), c-MYC (Santa Cruz Biotechnology, mouse mAb, sc-40, 1:1,000 dilution) and β-Actin (MP Biomedicals, mouse mAb, 69100, 1:10,000 dilution) antibodies were used for immunoblotting assays.

Techniques: Bioprocessing, Glo Assay, Positive Control, Expressing, Mutagenesis, Western Blot, Software, Comparison