human bladder cancer line t24 Search Results


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European Collection of Authenticated Cell Cultures plc/prf/5 cell line
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Pro-cell Co Ltd human embryonic kidney (hek) 293 t cells
Human Embryonic Kidney (Hek) 293 T Cells, supplied by Pro-cell 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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China Center for Type Culture Collection human bladder cancer biu-87 and t24 cells
The validation of recombinant adenovirus BMP9 and siBMP9. ( A ) The expression of BMP9 in normal bladder mucosa ( n = 126), superficial bladder cancer ( n = 68), and infiltrating bladder cancer ( n = 62) in the Lee Bladder database. p = 0.007; ( B ) The expression levels of BMP9 in <t>T24</t> and BIU-87 cells were detected by western blot; ( C ) The BMP9 was up-regulated in BIU-87 cells after being transfected with AdBMP9 compared to the control group; ( D ) The BMP9 was down-regulated in T24 cells after being transfected with AdsiBMP9 compared to the control group. Data are shown as mean ± SD. ** p < 0.01.
Human Bladder Cancer Biu 87 And T24 Cells, supplied by China Center for Type Culture Collection, 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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human bladder cancer biu-87 and t24 cells - by Bioz Stars, 2026-03
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Verrica Pharmaceuticals human bladder cancer t24 cells
The validation of recombinant adenovirus BMP9 and siBMP9. ( A ) The expression of BMP9 in normal bladder mucosa ( n = 126), superficial bladder cancer ( n = 68), and infiltrating bladder cancer ( n = 62) in the Lee Bladder database. p = 0.007; ( B ) The expression levels of BMP9 in <t>T24</t> and BIU-87 cells were detected by western blot; ( C ) The BMP9 was up-regulated in BIU-87 cells after being transfected with AdBMP9 compared to the control group; ( D ) The BMP9 was down-regulated in T24 cells after being transfected with AdsiBMP9 compared to the control group. Data are shown as mean ± SD. ** p < 0.01.
Human Bladder Cancer T24 Cells, supplied by Verrica Pharmaceuticals, 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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Shanghai GenePharma human bladder cancer cell lines t24, biu-87 and 5637
The validation of recombinant adenovirus BMP9 and siBMP9. ( A ) The expression of BMP9 in normal bladder mucosa ( n = 126), superficial bladder cancer ( n = 68), and infiltrating bladder cancer ( n = 62) in the Lee Bladder database. p = 0.007; ( B ) The expression levels of BMP9 in <t>T24</t> and BIU-87 cells were detected by western blot; ( C ) The BMP9 was up-regulated in BIU-87 cells after being transfected with AdBMP9 compared to the control group; ( D ) The BMP9 was down-regulated in T24 cells after being transfected with AdsiBMP9 compared to the control group. Data are shown as mean ± SD. ** p < 0.01.
Human Bladder Cancer Cell Lines T24, Biu 87 And 5637, 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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Keygen Biotech human bladder cancer cells t24
The validation of recombinant adenovirus BMP9 and siBMP9. ( A ) The expression of BMP9 in normal bladder mucosa ( n = 126), superficial bladder cancer ( n = 68), and infiltrating bladder cancer ( n = 62) in the Lee Bladder database. p = 0.007; ( B ) The expression levels of BMP9 in <t>T24</t> and BIU-87 cells were detected by western blot; ( C ) The BMP9 was up-regulated in BIU-87 cells after being transfected with AdBMP9 compared to the control group; ( D ) The BMP9 was down-regulated in T24 cells after being transfected with AdsiBMP9 compared to the control group. Data are shown as mean ± SD. ** p < 0.01.
Human Bladder Cancer Cells T24, supplied by Keygen Biotech, 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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Coriell Institute for Medical Research t24 human urinary bladder cancer cells
( a ) <t>T24</t> bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.
T24 Human Urinary Bladder Cancer Cells, supplied by Coriell Institute for Medical Research, 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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tiangen biotech co human invasive bladder cancer (t24, ht-1376, j82, umuc-3, rt4 and tccsup) cell lines
( a ) <t>T24</t> bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.
Human Invasive Bladder Cancer (T24, Ht 1376, J82, Umuc 3, Rt4 And Tccsup) Cell Lines, supplied by tiangen biotech co, 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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human invasive bladder cancer (t24, ht-1376, j82, umuc-3, rt4 and tccsup) cell lines - by Bioz Stars, 2026-03
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Bionova Inc urothelial carcinoma cells from human bladder cancer t24 cells ep-cl-0227
( a ) <t>T24</t> bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.
Urothelial Carcinoma Cells From Human Bladder Cancer T24 Cells Ep Cl 0227, supplied by Bionova Inc, 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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AllBio Science Inc t24 human bladder carcinoma cell line
( a ) <t>T24</t> bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.
T24 Human Bladder Carcinoma Cell Line, supplied by AllBio Science Inc, 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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t24 human bladder carcinoma cell line - by Bioz Stars, 2026-03
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BioResource International Inc human bladder cancer cell lines t24 and jmsu1
( a ) <t>T24</t> bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.
Human Bladder Cancer Cell Lines T24 And Jmsu1, supplied by BioResource International Inc, 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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human bladder cancer cell lines t24 and jmsu1 - by Bioz Stars, 2026-03
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Keygen Biotech human bladder cancer cell line t24 cells
( a ) <t>T24</t> bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.
Human Bladder Cancer Cell Line T24 Cells, supplied by Keygen Biotech, 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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The validation of recombinant adenovirus BMP9 and siBMP9. ( A ) The expression of BMP9 in normal bladder mucosa ( n = 126), superficial bladder cancer ( n = 68), and infiltrating bladder cancer ( n = 62) in the Lee Bladder database. p = 0.007; ( B ) The expression levels of BMP9 in T24 and BIU-87 cells were detected by western blot; ( C ) The BMP9 was up-regulated in BIU-87 cells after being transfected with AdBMP9 compared to the control group; ( D ) The BMP9 was down-regulated in T24 cells after being transfected with AdsiBMP9 compared to the control group. Data are shown as mean ± SD. ** p < 0.01.

Journal: International Journal of Molecular Sciences

Article Title: BMP9 Promotes the Proliferation and Migration of Bladder Cancer Cells through Up-Regulating lncRNA UCA1

doi: 10.3390/ijms19041116

Figure Lengend Snippet: The validation of recombinant adenovirus BMP9 and siBMP9. ( A ) The expression of BMP9 in normal bladder mucosa ( n = 126), superficial bladder cancer ( n = 68), and infiltrating bladder cancer ( n = 62) in the Lee Bladder database. p = 0.007; ( B ) The expression levels of BMP9 in T24 and BIU-87 cells were detected by western blot; ( C ) The BMP9 was up-regulated in BIU-87 cells after being transfected with AdBMP9 compared to the control group; ( D ) The BMP9 was down-regulated in T24 cells after being transfected with AdsiBMP9 compared to the control group. Data are shown as mean ± SD. ** p < 0.01.

Article Snippet: Human bladder cancer BIU-87 and T24 cells were obtained from the China Center for Type Culture Collection (CCTCC).

Techniques: Biomarker Discovery, Recombinant, Expressing, Western Blot, Transfection, Control

BMP9 up-regulated the expression of lncRNA UCA1 in bladder cancer cells. ( A ) Five common lncRNA were screened in BIU-87 cells after transfected with AdBMP9 by RT-PCR; ( B ) The expression of lncRNA UCA1 were verified in BIU-87 cells after transfected with AdBMP9 by RT-PCR; ( C ) The expression of lncRNA UCA1 were tested in T24 cells after being transfected with AdsiBMP9 by RT-PCR; ( D ) The inhibitory effect of siUCA1 were analyzed by RT-PCR in BIU-87 cells after being co-transfected with AdBMP9 and siUCA1. Data are shown as mean ± SD. ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, vs. control groups.

Journal: International Journal of Molecular Sciences

Article Title: BMP9 Promotes the Proliferation and Migration of Bladder Cancer Cells through Up-Regulating lncRNA UCA1

doi: 10.3390/ijms19041116

Figure Lengend Snippet: BMP9 up-regulated the expression of lncRNA UCA1 in bladder cancer cells. ( A ) Five common lncRNA were screened in BIU-87 cells after transfected with AdBMP9 by RT-PCR; ( B ) The expression of lncRNA UCA1 were verified in BIU-87 cells after transfected with AdBMP9 by RT-PCR; ( C ) The expression of lncRNA UCA1 were tested in T24 cells after being transfected with AdsiBMP9 by RT-PCR; ( D ) The inhibitory effect of siUCA1 were analyzed by RT-PCR in BIU-87 cells after being co-transfected with AdBMP9 and siUCA1. Data are shown as mean ± SD. ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, vs. control groups.

Article Snippet: Human bladder cancer BIU-87 and T24 cells were obtained from the China Center for Type Culture Collection (CCTCC).

Techniques: Expressing, Transfection, Reverse Transcription Polymerase Chain Reaction, Control

( a ) T24 bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.

Journal: PLoS Genetics

Article Title: The Splicing Efficiency of Activating HRAS Mutations Can Determine Costello Syndrome Phenotype and Frequency in Cancer

doi: 10.1371/journal.pgen.1006039

Figure Lengend Snippet: ( a ) T24 bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.

Article Snippet: T24 human urinary bladder cancer cells were obtained from Coriell Institute ( https://catalog.coriell.org/ ).

Techniques: Mutagenesis, Transfection, Control, Western Blot, WST-1 Assay

( a , b ) HepG2 ( top ) or T24 ( bottom ) cells were transfected with HRAS minigenes harboring different sequence variants in positions c.34-38. The frequencies of the mutations in Costello syndrome according to Giannoulatou and co-workers and in cancer according to Cosmic database are displayed. For cancer the numbers are displayed with skin cancers included or excluded due to the extremely high occurrence of the c.37G>C mutation in skin cancer. The original scoring of the transforming potential of the mutants in two studies are displayed—A is from Seeburg and co-workers ; B is from Fasano and co-workers . Quantitative data for exon 2 inclusion (molar ratio) were obtained from triplicates of duplicate transfections using the Agilent 2100 Bioanalyzer. It is worth noting that there is a clear difference in the overall splicing efficiency between T24 cells and HepG2 cells, which is consistent with the reported low levels of hnRNPF in HepG2 cells .

Journal: PLoS Genetics

Article Title: The Splicing Efficiency of Activating HRAS Mutations Can Determine Costello Syndrome Phenotype and Frequency in Cancer

doi: 10.1371/journal.pgen.1006039

Figure Lengend Snippet: ( a , b ) HepG2 ( top ) or T24 ( bottom ) cells were transfected with HRAS minigenes harboring different sequence variants in positions c.34-38. The frequencies of the mutations in Costello syndrome according to Giannoulatou and co-workers and in cancer according to Cosmic database are displayed. For cancer the numbers are displayed with skin cancers included or excluded due to the extremely high occurrence of the c.37G>C mutation in skin cancer. The original scoring of the transforming potential of the mutants in two studies are displayed—A is from Seeburg and co-workers ; B is from Fasano and co-workers . Quantitative data for exon 2 inclusion (molar ratio) were obtained from triplicates of duplicate transfections using the Agilent 2100 Bioanalyzer. It is worth noting that there is a clear difference in the overall splicing efficiency between T24 cells and HepG2 cells, which is consistent with the reported low levels of hnRNPF in HepG2 cells .

Article Snippet: T24 human urinary bladder cancer cells were obtained from Coriell Institute ( https://catalog.coriell.org/ ).

Techniques: Transfection, Sequencing, Mutagenesis