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ha tagged cdk12 expression vectors  (Addgene inc)


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    Structured Review

    Addgene inc ha tagged cdk12 expression vectors
    ( A ) Chemical structure of CTX-439. ( B ) Kinome tree illustrating the selectivity profile of CTX-439. Binding affinity of CTX-439 was screened by scanMAX kinase panel and the Kd values for CDKs and the other top 6 kinases were evaluated. For CASK, DCAMKL3, DYRK2, MAP3K15, JNK3, JNK1, RSK4, ERK8, ERN1, RSK3 and CLK1, CTX-439 showed weak inhibitory effects of 50-65% at 30 nM, but it is not included in the kinome tree. ( C ) Inhibitory activities of CTX-439, THZ531 and SR4835 on transcription-related CDK kinases. ( D ) Western blot analysis of <t>CDK12</t> and Pol II CTD phosphorylation in SUM149PT cells treated with the indicated concentration of CTX-439 for 6 h. ( E ) RT-qPCR analyses of BRCA1 and BRCA2 in SUM149PT cells treated with CTX-439 for 6h. ( F ) Western blot analysis of DDR proteins and apoptosis markers in SUM149PT cells treated with CTX-439 for 24h. ( G ) Drug response assay in SUM149PT cells treated with CTX-439 for 72h. ( H ) in vivo anti-tumor efficacy of CTX-439 in mice bearing SUM149PT xenografts treated with the indicated dose twice weekly (biw). ( I ) in vivo anti-tumor efficacy of CTX-439 in TNBC PDX model mice treated with the indicated dose. * p <0.05, ** p <0.01 ** p <0.001 by Dunnett’s test. Data are shown as mean ± SD (n=3, E ; n=6, H and I ).
    Ha Tagged Cdk12 Expression Vectors, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ha+tagged+cdk12+expression+vectors/bio_rxiv__64898__2026__02__20__706902-287-2-16?v=Addgene+inc
    Average 93 stars, based on 3 article reviews
    ha tagged cdk12 expression vectors - by Bioz Stars, 2026-07
    93/100 stars

    Images

    1) Product Images from "CDK12/13 inhibitor, CTX-439, suppresses tumor growth and potentiates BCL-2 family blockade"

    Article Title: CDK12/13 inhibitor, CTX-439, suppresses tumor growth and potentiates BCL-2 family blockade

    Journal: bioRxiv

    doi: 10.64898/2026.02.20.706902

    ( A ) Chemical structure of CTX-439. ( B ) Kinome tree illustrating the selectivity profile of CTX-439. Binding affinity of CTX-439 was screened by scanMAX kinase panel and the Kd values for CDKs and the other top 6 kinases were evaluated. For CASK, DCAMKL3, DYRK2, MAP3K15, JNK3, JNK1, RSK4, ERK8, ERN1, RSK3 and CLK1, CTX-439 showed weak inhibitory effects of 50-65% at 30 nM, but it is not included in the kinome tree. ( C ) Inhibitory activities of CTX-439, THZ531 and SR4835 on transcription-related CDK kinases. ( D ) Western blot analysis of CDK12 and Pol II CTD phosphorylation in SUM149PT cells treated with the indicated concentration of CTX-439 for 6 h. ( E ) RT-qPCR analyses of BRCA1 and BRCA2 in SUM149PT cells treated with CTX-439 for 6h. ( F ) Western blot analysis of DDR proteins and apoptosis markers in SUM149PT cells treated with CTX-439 for 24h. ( G ) Drug response assay in SUM149PT cells treated with CTX-439 for 72h. ( H ) in vivo anti-tumor efficacy of CTX-439 in mice bearing SUM149PT xenografts treated with the indicated dose twice weekly (biw). ( I ) in vivo anti-tumor efficacy of CTX-439 in TNBC PDX model mice treated with the indicated dose. * p <0.05, ** p <0.01 ** p <0.001 by Dunnett’s test. Data are shown as mean ± SD (n=3, E ; n=6, H and I ).
    Figure Legend Snippet: ( A ) Chemical structure of CTX-439. ( B ) Kinome tree illustrating the selectivity profile of CTX-439. Binding affinity of CTX-439 was screened by scanMAX kinase panel and the Kd values for CDKs and the other top 6 kinases were evaluated. For CASK, DCAMKL3, DYRK2, MAP3K15, JNK3, JNK1, RSK4, ERK8, ERN1, RSK3 and CLK1, CTX-439 showed weak inhibitory effects of 50-65% at 30 nM, but it is not included in the kinome tree. ( C ) Inhibitory activities of CTX-439, THZ531 and SR4835 on transcription-related CDK kinases. ( D ) Western blot analysis of CDK12 and Pol II CTD phosphorylation in SUM149PT cells treated with the indicated concentration of CTX-439 for 6 h. ( E ) RT-qPCR analyses of BRCA1 and BRCA2 in SUM149PT cells treated with CTX-439 for 6h. ( F ) Western blot analysis of DDR proteins and apoptosis markers in SUM149PT cells treated with CTX-439 for 24h. ( G ) Drug response assay in SUM149PT cells treated with CTX-439 for 72h. ( H ) in vivo anti-tumor efficacy of CTX-439 in mice bearing SUM149PT xenografts treated with the indicated dose twice weekly (biw). ( I ) in vivo anti-tumor efficacy of CTX-439 in TNBC PDX model mice treated with the indicated dose. * p <0.05, ** p <0.01 ** p <0.001 by Dunnett’s test. Data are shown as mean ± SD (n=3, E ; n=6, H and I ).

    Techniques Used: Binding Assay, Western Blot, Phospho-proteomics, Concentration Assay, Quantitative RT-PCR, In Vivo

    ( A ) Western blot analysis of cells expressing the indicated cDNA and sgRNA. mtCDK12 carries the combined mutations of TA770FL, D817N and E1041AG. ( B ) Western blot analysis showing that pS2 was maintained in mtCDK12-expressing cells under the treatment of CTX-439. ( C ) Cell survival assay. Cells with endogenous, or exogenous wt or mt CDK12 were tested. ( D ) Western blot analysis. Cells with endogenous (E), or exogenous wt or mt CDK12 were treated with the indicated drug(s) for 8h. Note that MCL1 downregulation was suppressed by mt CDK12. ( E ) RT-qPCR analysis of MCL1 expression in the nucleus. Note that nuclear MCL1 transcript upregulation was suppressed by mt CDK12. ( F-G ) RT-qPCR analyses of MCL1 ( F ) and TUBB4B readthrough ( G ) in the nucleus. Readthrough was detected in mt CDK12-expressing cells, but their level is far below than that in cells with endogenous or exogenous wt CDK12. Data are shown as mean ± SD (n=3, E-G ). * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001 by Student’s t- test.
    Figure Legend Snippet: ( A ) Western blot analysis of cells expressing the indicated cDNA and sgRNA. mtCDK12 carries the combined mutations of TA770FL, D817N and E1041AG. ( B ) Western blot analysis showing that pS2 was maintained in mtCDK12-expressing cells under the treatment of CTX-439. ( C ) Cell survival assay. Cells with endogenous, or exogenous wt or mt CDK12 were tested. ( D ) Western blot analysis. Cells with endogenous (E), or exogenous wt or mt CDK12 were treated with the indicated drug(s) for 8h. Note that MCL1 downregulation was suppressed by mt CDK12. ( E ) RT-qPCR analysis of MCL1 expression in the nucleus. Note that nuclear MCL1 transcript upregulation was suppressed by mt CDK12. ( F-G ) RT-qPCR analyses of MCL1 ( F ) and TUBB4B readthrough ( G ) in the nucleus. Readthrough was detected in mt CDK12-expressing cells, but their level is far below than that in cells with endogenous or exogenous wt CDK12. Data are shown as mean ± SD (n=3, E-G ). * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001 by Student’s t- test.

    Techniques Used: Western Blot, Expressing, Clonogenic Cell Survival Assay, Quantitative RT-PCR



    Similar Products

    ha tagged cdk12 expression vectors  (Addgene inc)
    93
    Addgene inc ha tagged cdk12 expression vectors
    ( A ) Chemical structure of CTX-439. ( B ) Kinome tree illustrating the selectivity profile of CTX-439. Binding affinity of CTX-439 was screened by scanMAX kinase panel and the Kd values for CDKs and the other top 6 kinases were evaluated. For CASK, DCAMKL3, DYRK2, MAP3K15, JNK3, JNK1, RSK4, ERK8, ERN1, RSK3 and CLK1, CTX-439 showed weak inhibitory effects of 50-65% at 30 nM, but it is not included in the kinome tree. ( C ) Inhibitory activities of CTX-439, THZ531 and SR4835 on transcription-related CDK kinases. ( D ) Western blot analysis of <t>CDK12</t> and Pol II CTD phosphorylation in SUM149PT cells treated with the indicated concentration of CTX-439 for 6 h. ( E ) RT-qPCR analyses of BRCA1 and BRCA2 in SUM149PT cells treated with CTX-439 for 6h. ( F ) Western blot analysis of DDR proteins and apoptosis markers in SUM149PT cells treated with CTX-439 for 24h. ( G ) Drug response assay in SUM149PT cells treated with CTX-439 for 72h. ( H ) in vivo anti-tumor efficacy of CTX-439 in mice bearing SUM149PT xenografts treated with the indicated dose twice weekly (biw). ( I ) in vivo anti-tumor efficacy of CTX-439 in TNBC PDX model mice treated with the indicated dose. * p <0.05, ** p <0.01 ** p <0.001 by Dunnett’s test. Data are shown as mean ± SD (n=3, E ; n=6, H and I ).
    Ha Tagged Cdk12 Expression Vectors, supplied by Addgene 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/product/ha+tagged+cdk12+expression+vectors/bio_rxiv__64898__2026__02__20__706902-287-2-16?v=Addgene+inc
    Average 93 stars, based on 1 article reviews
    ha tagged cdk12 expression vectors - by Bioz Stars, 2026-07
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    ( A ) Chemical structure of CTX-439. ( B ) Kinome tree illustrating the selectivity profile of CTX-439. Binding affinity of CTX-439 was screened by scanMAX kinase panel and the Kd values for CDKs and the other top 6 kinases were evaluated. For CASK, DCAMKL3, DYRK2, MAP3K15, JNK3, JNK1, RSK4, ERK8, ERN1, RSK3 and CLK1, CTX-439 showed weak inhibitory effects of 50-65% at 30 nM, but it is not included in the kinome tree. ( C ) Inhibitory activities of CTX-439, THZ531 and SR4835 on transcription-related CDK kinases. ( D ) Western blot analysis of CDK12 and Pol II CTD phosphorylation in SUM149PT cells treated with the indicated concentration of CTX-439 for 6 h. ( E ) RT-qPCR analyses of BRCA1 and BRCA2 in SUM149PT cells treated with CTX-439 for 6h. ( F ) Western blot analysis of DDR proteins and apoptosis markers in SUM149PT cells treated with CTX-439 for 24h. ( G ) Drug response assay in SUM149PT cells treated with CTX-439 for 72h. ( H ) in vivo anti-tumor efficacy of CTX-439 in mice bearing SUM149PT xenografts treated with the indicated dose twice weekly (biw). ( I ) in vivo anti-tumor efficacy of CTX-439 in TNBC PDX model mice treated with the indicated dose. * p <0.05, ** p <0.01 ** p <0.001 by Dunnett’s test. Data are shown as mean ± SD (n=3, E ; n=6, H and I ).

    Journal: bioRxiv

    Article Title: CDK12/13 inhibitor, CTX-439, suppresses tumor growth and potentiates BCL-2 family blockade

    doi: 10.64898/2026.02.20.706902

    Figure Lengend Snippet: ( A ) Chemical structure of CTX-439. ( B ) Kinome tree illustrating the selectivity profile of CTX-439. Binding affinity of CTX-439 was screened by scanMAX kinase panel and the Kd values for CDKs and the other top 6 kinases were evaluated. For CASK, DCAMKL3, DYRK2, MAP3K15, JNK3, JNK1, RSK4, ERK8, ERN1, RSK3 and CLK1, CTX-439 showed weak inhibitory effects of 50-65% at 30 nM, but it is not included in the kinome tree. ( C ) Inhibitory activities of CTX-439, THZ531 and SR4835 on transcription-related CDK kinases. ( D ) Western blot analysis of CDK12 and Pol II CTD phosphorylation in SUM149PT cells treated with the indicated concentration of CTX-439 for 6 h. ( E ) RT-qPCR analyses of BRCA1 and BRCA2 in SUM149PT cells treated with CTX-439 for 6h. ( F ) Western blot analysis of DDR proteins and apoptosis markers in SUM149PT cells treated with CTX-439 for 24h. ( G ) Drug response assay in SUM149PT cells treated with CTX-439 for 72h. ( H ) in vivo anti-tumor efficacy of CTX-439 in mice bearing SUM149PT xenografts treated with the indicated dose twice weekly (biw). ( I ) in vivo anti-tumor efficacy of CTX-439 in TNBC PDX model mice treated with the indicated dose. * p <0.05, ** p <0.01 ** p <0.001 by Dunnett’s test. Data are shown as mean ± SD (n=3, E ; n=6, H and I ).

    Article Snippet: To construct HA-tagged CDK12 expression vectors, CDK12 cDNA fragment was first generated by PCR using pHAGE-CDK12 (Addgene #116723) as a template.

    Techniques: Binding Assay, Western Blot, Phospho-proteomics, Concentration Assay, Quantitative RT-PCR, In Vivo

    ( A ) Western blot analysis of cells expressing the indicated cDNA and sgRNA. mtCDK12 carries the combined mutations of TA770FL, D817N and E1041AG. ( B ) Western blot analysis showing that pS2 was maintained in mtCDK12-expressing cells under the treatment of CTX-439. ( C ) Cell survival assay. Cells with endogenous, or exogenous wt or mt CDK12 were tested. ( D ) Western blot analysis. Cells with endogenous (E), or exogenous wt or mt CDK12 were treated with the indicated drug(s) for 8h. Note that MCL1 downregulation was suppressed by mt CDK12. ( E ) RT-qPCR analysis of MCL1 expression in the nucleus. Note that nuclear MCL1 transcript upregulation was suppressed by mt CDK12. ( F-G ) RT-qPCR analyses of MCL1 ( F ) and TUBB4B readthrough ( G ) in the nucleus. Readthrough was detected in mt CDK12-expressing cells, but their level is far below than that in cells with endogenous or exogenous wt CDK12. Data are shown as mean ± SD (n=3, E-G ). * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001 by Student’s t- test.

    Journal: bioRxiv

    Article Title: CDK12/13 inhibitor, CTX-439, suppresses tumor growth and potentiates BCL-2 family blockade

    doi: 10.64898/2026.02.20.706902

    Figure Lengend Snippet: ( A ) Western blot analysis of cells expressing the indicated cDNA and sgRNA. mtCDK12 carries the combined mutations of TA770FL, D817N and E1041AG. ( B ) Western blot analysis showing that pS2 was maintained in mtCDK12-expressing cells under the treatment of CTX-439. ( C ) Cell survival assay. Cells with endogenous, or exogenous wt or mt CDK12 were tested. ( D ) Western blot analysis. Cells with endogenous (E), or exogenous wt or mt CDK12 were treated with the indicated drug(s) for 8h. Note that MCL1 downregulation was suppressed by mt CDK12. ( E ) RT-qPCR analysis of MCL1 expression in the nucleus. Note that nuclear MCL1 transcript upregulation was suppressed by mt CDK12. ( F-G ) RT-qPCR analyses of MCL1 ( F ) and TUBB4B readthrough ( G ) in the nucleus. Readthrough was detected in mt CDK12-expressing cells, but their level is far below than that in cells with endogenous or exogenous wt CDK12. Data are shown as mean ± SD (n=3, E-G ). * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001 by Student’s t- test.

    Article Snippet: To construct HA-tagged CDK12 expression vectors, CDK12 cDNA fragment was first generated by PCR using pHAGE-CDK12 (Addgene #116723) as a template.

    Techniques: Western Blot, Expressing, Clonogenic Cell Survival Assay, Quantitative RT-PCR