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monoclonal rabbit anti human cdk9 antibody (Cell Signaling Technology Inc)

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Cell Signaling Technology Inc monoclonal rabbit anti human cdk9 antibody

Higher expression of <t>CDK9</t> was present in the resistant ovarian cancer cell line compared to the parental sensitive cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of paclitaxel for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of paclitaxel for five days. ( C ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription in SKOV3TR and OVCAR8TR, and parental sensitive cell lines SKOV3 and OVCAR8 were determined by Western blot. There are 2 isoforms of the CDK9 protein: the 42 kDa CDK9 isoform and the 55 kDa isoform. The smaller 42 kDa isoform was the first identified isoform. The larger, 55 kDa isoform has a characteristic 117 residue terminal expansion. ( D ) Relative expression of both CDK9 isoforms and α-Tubulin in the ovarian cancer cell lines. ** P < 0.01.

Monoclonal Rabbit Anti Human Cdk9 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti+cdk9/pmc13062015-156-1-9
Average 86 stars, based on 1 article reviews

monoclonal rabbit anti human cdk9 antibody - by Bioz Stars, 2026-09

86/100 stars

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1) Product Images from "Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel"

Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

Journal: Scientific Reports

doi: 10.1038/s41598-026-47843-6

Higher expression of CDK9 was present in the resistant ovarian cancer cell line compared to the parental sensitive cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of paclitaxel for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of paclitaxel for five days. ( C ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription in SKOV3TR and OVCAR8TR, and parental sensitive cell lines SKOV3 and OVCAR8 were determined by Western blot. There are 2 isoforms of the CDK9 protein: the 42 kDa CDK9 isoform and the 55 kDa isoform. The smaller 42 kDa isoform was the first identified isoform. The larger, 55 kDa isoform has a characteristic 117 residue terminal expansion. ( D ) Relative expression of both CDK9 isoforms and α-Tubulin in the ovarian cancer cell lines. ** P < 0.01.

Figure Legend Snippet: Higher expression of CDK9 was present in the resistant ovarian cancer cell line compared to the parental sensitive cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of paclitaxel for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of paclitaxel for five days. ( C ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription in SKOV3TR and OVCAR8TR, and parental sensitive cell lines SKOV3 and OVCAR8 were determined by Western blot. There are 2 isoforms of the CDK9 protein: the 42 kDa CDK9 isoform and the 55 kDa isoform. The smaller 42 kDa isoform was the first identified isoform. The larger, 55 kDa isoform has a characteristic 117 residue terminal expansion. ( D ) Relative expression of both CDK9 isoforms and α-Tubulin in the ovarian cancer cell lines. ** P < 0.01.

Techniques Used: Expressing, Incubation, Concentration Assay, Western Blot, Residue

CDK9 knockdown by siRNA transfection enhanced paclitaxel sensitivity in resistant ovarian cancer cells. ( A and B ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription and apoptosis after transfection of CDK9 siRNA and nonspecific siRNA in SKOV3TR and OVCAR8TR cell lines by Western blot. ( C and D ) MTT assay revealed enhanced sensitivity to paclitaxel of SKOV3TR and OVCAR8TR cells after CDK9 siRNA transfection. ** P < 0.01 indicates that the observed results of CDK9 knockdown by siRNA transfection enhanced paclitaxel sensitivity in drug resistant SKOV3TR or OVCAR8TR cell lines are highly statistically significant as compared with the same non-transfected cell lines or nonspecific siRNA transfected cell lines.

Figure Legend Snippet: CDK9 knockdown by siRNA transfection enhanced paclitaxel sensitivity in resistant ovarian cancer cells. ( A and B ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription and apoptosis after transfection of CDK9 siRNA and nonspecific siRNA in SKOV3TR and OVCAR8TR cell lines by Western blot. ( C and D ) MTT assay revealed enhanced sensitivity to paclitaxel of SKOV3TR and OVCAR8TR cells after CDK9 siRNA transfection. ** P < 0.01 indicates that the observed results of CDK9 knockdown by siRNA transfection enhanced paclitaxel sensitivity in drug resistant SKOV3TR or OVCAR8TR cell lines are highly statistically significant as compared with the same non-transfected cell lines or nonspecific siRNA transfected cell lines.

Techniques Used: Knockdown, Transfection, Expressing, Western Blot, MTT Assay

Effects of combination treatment with paclitaxel and CDK9 inhibitor LDC067 on the viability of multidrug resistant ovarian cancer cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( C and D ) Relative cell viability of SKOV3TR and OVCAR8TR cells in combination with paclitaxel and CDK9 inhibitor LDC067 for five days. N.S. indicates that the observed data for paclitaxel and LDC067 alone treated groups are not statistically significant as compared with untreated groups; * P < 0.05, the observed data for paclitaxel and LDC067 combinatorial treated groups are statistically significant as compared with the untreated groups; ** P < 0.01, the observed results for paclitaxel and LDC067 combinatorial treated groups are highly statistically significant as compared with the untreated groups.

Figure Legend Snippet: Effects of combination treatment with paclitaxel and CDK9 inhibitor LDC067 on the viability of multidrug resistant ovarian cancer cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( C and D ) Relative cell viability of SKOV3TR and OVCAR8TR cells in combination with paclitaxel and CDK9 inhibitor LDC067 for five days. N.S. indicates that the observed data for paclitaxel and LDC067 alone treated groups are not statistically significant as compared with untreated groups; * P < 0.05, the observed data for paclitaxel and LDC067 combinatorial treated groups are statistically significant as compared with the untreated groups; ** P < 0.01, the observed results for paclitaxel and LDC067 combinatorial treated groups are highly statistically significant as compared with the untreated groups.

Techniques Used: Incubation, Concentration Assay

Effects of treatment with paclitaxel and CDK9 inhibitor LDC067 on the transcription and apoptosis in multidrug resistant ovarian cancer cell line. ( A and B ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription and apoptosis after treatment with paclitaxel and CDK9 inhibitor LDC067 in SKOV3TR and OVCAR8TR cell lines by Western blot.

Figure Legend Snippet: Effects of treatment with paclitaxel and CDK9 inhibitor LDC067 on the transcription and apoptosis in multidrug resistant ovarian cancer cell line. ( A and B ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription and apoptosis after treatment with paclitaxel and CDK9 inhibitor LDC067 in SKOV3TR and OVCAR8TR cell lines by Western blot.

Techniques Used: Expressing, Western Blot

Inhibition of CDK9 suppressed drug resistant ovarian cancer cell spheroid growth, and clonogenicity formation. ( A ) Representative images of drug resistant ovarian cancer cells SKOV3TR and OVCAR8TR after treatment with the CDK9 inhibitor LDC067 at different time points (5 days, 10 days, and 15 days). ( B ) The relative diameters of spheroids in SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group. ( C ) Representative images of drug resistant ovarian cancer cells SKOV3TR and OVCAR8TR colony formation after incubation with different concentrations of LDC067 (0, 5, 10 µM) for 14 days. ( D ) Quantification of clonogenicity formation of SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group.

Figure Legend Snippet: Inhibition of CDK9 suppressed drug resistant ovarian cancer cell spheroid growth, and clonogenicity formation. ( A ) Representative images of drug resistant ovarian cancer cells SKOV3TR and OVCAR8TR after treatment with the CDK9 inhibitor LDC067 at different time points (5 days, 10 days, and 15 days). ( B ) The relative diameters of spheroids in SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group. ( C ) Representative images of drug resistant ovarian cancer cells SKOV3TR and OVCAR8TR colony formation after incubation with different concentrations of LDC067 (0, 5, 10 µM) for 14 days. ( D ) Quantification of clonogenicity formation of SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group.

Techniques Used: Inhibition, Incubation

Effect of treatment with CDK9 inhibitor LDC067 on the migratory activity of multidrug resistant ovarian cancer cell line. ( A and B ) Relative migration distance of SKOV3TR and OVCAR8TR cells at different time points (0 h, 24 h, 48 h, 72 h) when treated with the CDK9 inhibitor LDC067. ( C and D ) Quantification of cell migration distance of SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group.

Figure Legend Snippet: Effect of treatment with CDK9 inhibitor LDC067 on the migratory activity of multidrug resistant ovarian cancer cell line. ( A and B ) Relative migration distance of SKOV3TR and OVCAR8TR cells at different time points (0 h, 24 h, 48 h, 72 h) when treated with the CDK9 inhibitor LDC067. ( C and D ) Quantification of cell migration distance of SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group.

Techniques Used: Activity Assay, Migration

other:

Article Title: Discovery of Potent and Selective CDK9 Degraders for Targeting Transcription Regulation in Triple-Negative Breast Cancer.
Article Snippet: Antibody Dilution Company Cat No. Rabbit anti-CDK9 1:200 CST 2316 Mouse anti-CDK7 1:400 CST 2916S Rabbit anti-Ki67 1:400 CST 9027 Rabbit anti-c-Myc 1:1800 JieHao Biotech MM-0141 S11 Molecular Docking Study.

Membrane:

Article Title: Targeting CDK9 in Cancer: An Integrated Approach of Combining In Silico Screening with Experimental Validation for Novel Degraders
Article Snippet: The gel was run at 125 V for 60–90 min and then electro-transferred onto PVDF (Bio-Rad, Hercules, CA, USA, Cat # 162-0177). .. After transfer, the membrane was blocked with 5% dry-milk powder (Boston Bioproducts, Milford, MA, USA, Cat # P-1400) and developed using a combination of rabbit anti-CDK9 (Cell Signaling Technology, Cat # 2316S) and anti-myosin light-chain monoclonal antibodies (Cell Signaling Technology, Cat # 8505S), used at 1:1500 dilution and 1:5000, respectively, followed by goat anti-rabbit antibody conjugated with HRP (Cell Signaling Technology, Cat # 7074S) at 1:10,000 dilution. .. Bands on the membrane were visualized and imaged by chemiluminescence (Aplegen, Omega Lum G) using an ECL reagent (Thermo Scientific, Cat # A38554) [ , ].

Bioprocessing:

Western Blot:

Article Title: Regulated induced proximity targeting chimeras-RIPTACs-A heterobifunctional small molecule strategy for cancer selective therapies.
Article Snippet: In brief Raina et al. present a proof-of-concept approach to modulate protein-protein interaction (PPI) with heterobifunctional regulated induced proximity targeting chimeras (RIPTACs) that induce an enduring interaction between target proteins (TPs) and effector proteins (EPs).. The RIPTACs arrest cancer cell growth by selectively inhibiting a pan-essential effector protein in ternary complex with target proteins expressed at elevated levels in cancer cells.

Article Title: Pseudouridylation of 7SK by PUS7 regulates Pol II transcription elongation.
Article Snippet: .. The antibodies used in this study are listedbelow in the formatof name (supplier, catalog): Rabbit anti-β-Tubulin (Cell Signaling Technology, 2128); Rabbit anti-SNRP70 (abcam, ab83306); Rabbit anti-H3 (Cell Signaling Technology, 9715); Rabbit anti-PUS7 for PAR-CLIP and western blot (Bethyl Laboratories, A305-146A-T (thermo fisher)); Rabbit anti-GAPDH (Cell Signaling Technology, 2118); Rabbit anti-DKC1 (Cell Signaling Technology, 53234); Rabbit anti-LARP7 (Proteintech, 17067- 1-AP); Rabbit anti-MEPCE (Proteintech, 14917-1-AP); Rabbit anti-HEXIM1 for immunoprecipitation (Cell Signaling Technology, 12604); Mouse anti-HEXIM1 for western blot (Proteintech, 66311-1-Ig); Rabbit antiCDK9 (Proteintech, 11705-1-AP); Rabbit anti-ARID1A (Cell Signaling Technology, 12354); Rabbit anti-ARID2 (Cell Signaling Technology, 82342); Rabbit anti-CDK9 (Cell Signaling Technology, 53234); Mouse anti-Pol II (Biolegend, 664906); Rabbit Anti-KLF6 (Invitrogen, PA587561(thermo fisher)); Mouse anti-DDIT3 (Cell Signaling Technology, 2895); Goat anti-rabbit lgG-HRP (Cell Signaling Technology, 7074); Goat Anti-Mouse IgG H&L (Alexa Fluor® 488, abcam, ab150113); Goat Anti-Rabbit IgG H&L (Alexa Fluor® 594, abcam, ab150080); Horse antimouse lgG-HRP (Cell Signaling Technology, 7076). .. Cells were lysed in RIPA Buffer (Thermo Scientific) containing 1x protease inhibitor cocktail (Roche) on ice for at least 15min.

Immunoprecipitation:

Image Search Results

Journal: Scientific Reports

Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

doi: 10.1038/s41598-026-47843-6

Figure Lengend Snippet: Higher expression of CDK9 was present in the resistant ovarian cancer cell line compared to the parental sensitive cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of paclitaxel for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of paclitaxel for five days. ( C ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription in SKOV3TR and OVCAR8TR, and parental sensitive cell lines SKOV3 and OVCAR8 were determined by Western blot. There are 2 isoforms of the CDK9 protein: the 42 kDa CDK9 isoform and the 55 kDa isoform. The smaller 42 kDa isoform was the first identified isoform. The larger, 55 kDa isoform has a characteristic 117 residue terminal expansion. ( D ) Relative expression of both CDK9 isoforms and α-Tubulin in the ovarian cancer cell lines. ** P < 0.01.

Article Snippet: The monoclonal rabbit anti-human CDK9 antibody was purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Expressing, Incubation, Concentration Assay, Western Blot, Residue

Journal: Scientific Reports

Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

doi: 10.1038/s41598-026-47843-6

Figure Lengend Snippet: CDK9 knockdown by siRNA transfection enhanced paclitaxel sensitivity in resistant ovarian cancer cells. ( A and B ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription and apoptosis after transfection of CDK9 siRNA and nonspecific siRNA in SKOV3TR and OVCAR8TR cell lines by Western blot. ( C and D ) MTT assay revealed enhanced sensitivity to paclitaxel of SKOV3TR and OVCAR8TR cells after CDK9 siRNA transfection. ** P < 0.01 indicates that the observed results of CDK9 knockdown by siRNA transfection enhanced paclitaxel sensitivity in drug resistant SKOV3TR or OVCAR8TR cell lines are highly statistically significant as compared with the same non-transfected cell lines or nonspecific siRNA transfected cell lines.

Article Snippet: The monoclonal rabbit anti-human CDK9 antibody was purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Knockdown, Transfection, Expressing, Western Blot, MTT Assay

Journal: Scientific Reports

Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

doi: 10.1038/s41598-026-47843-6

Figure Lengend Snippet: Effects of combination treatment with paclitaxel and CDK9 inhibitor LDC067 on the viability of multidrug resistant ovarian cancer cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( C and D ) Relative cell viability of SKOV3TR and OVCAR8TR cells in combination with paclitaxel and CDK9 inhibitor LDC067 for five days. N.S. indicates that the observed data for paclitaxel and LDC067 alone treated groups are not statistically significant as compared with untreated groups; * P < 0.05, the observed data for paclitaxel and LDC067 combinatorial treated groups are statistically significant as compared with the untreated groups; ** P < 0.01, the observed results for paclitaxel and LDC067 combinatorial treated groups are highly statistically significant as compared with the untreated groups.

Article Snippet: The monoclonal rabbit anti-human CDK9 antibody was purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Incubation, Concentration Assay

Journal: Scientific Reports

Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

doi: 10.1038/s41598-026-47843-6

Figure Lengend Snippet: Effects of treatment with paclitaxel and CDK9 inhibitor LDC067 on the transcription and apoptosis in multidrug resistant ovarian cancer cell line. ( A and B ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription and apoptosis after treatment with paclitaxel and CDK9 inhibitor LDC067 in SKOV3TR and OVCAR8TR cell lines by Western blot.

Article Snippet: The monoclonal rabbit anti-human CDK9 antibody was purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Expressing, Western Blot

Journal: Scientific Reports

Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

doi: 10.1038/s41598-026-47843-6

Figure Lengend Snippet: Inhibition of CDK9 suppressed drug resistant ovarian cancer cell spheroid growth, and clonogenicity formation. ( A ) Representative images of drug resistant ovarian cancer cells SKOV3TR and OVCAR8TR after treatment with the CDK9 inhibitor LDC067 at different time points (5 days, 10 days, and 15 days). ( B ) The relative diameters of spheroids in SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group. ( C ) Representative images of drug resistant ovarian cancer cells SKOV3TR and OVCAR8TR colony formation after incubation with different concentrations of LDC067 (0, 5, 10 µM) for 14 days. ( D ) Quantification of clonogenicity formation of SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group.

Article Snippet: The monoclonal rabbit anti-human CDK9 antibody was purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Inhibition, Incubation

Journal: Scientific Reports

Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

doi: 10.1038/s41598-026-47843-6

Figure Lengend Snippet: Effect of treatment with CDK9 inhibitor LDC067 on the migratory activity of multidrug resistant ovarian cancer cell line. ( A and B ) Relative migration distance of SKOV3TR and OVCAR8TR cells at different time points (0 h, 24 h, 48 h, 72 h) when treated with the CDK9 inhibitor LDC067. ( C and D ) Quantification of cell migration distance of SKOV3TR and OVCAR8TR cells after LDC067 treatment. ** P < 0.01 compared with the cell only group.

Article Snippet: The monoclonal rabbit anti-human CDK9 antibody was purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Activity Assay, Migration

The kinase activity of CDK9 is required for HIV gene activation following CDK12/CCNK targeting by SR-4835 HIV GKO infected Jurkat T cells were sorted for those where HIV is latent [(GFP(-);mKO2(+)] and then treated with SR-4835 (0.5µM) alone, or in combination with the CDK9 Flavopiridol (1µM) for 24 hours. HIV gene expression was monitored by measuring GFP expression by FACS. Data represent mean ± SD from three independent experiments. Statistical significance was assessed using an unpaired two-tailed t-test. **** P < 0.001.

Journal: bioRxiv

Article Title: Targeting CDK12/CYCLIN K induces HIV gene activation and latency reversal which is mediated by P-TEFb

doi: 10.64898/2026.02.10.705011

Figure Lengend Snippet: The kinase activity of CDK9 is required for HIV gene activation following CDK12/CCNK targeting by SR-4835 HIV GKO infected Jurkat T cells were sorted for those where HIV is latent [(GFP(-);mKO2(+)] and then treated with SR-4835 (0.5µM) alone, or in combination with the CDK9 Flavopiridol (1µM) for 24 hours. HIV gene expression was monitored by measuring GFP expression by FACS. Data represent mean ± SD from three independent experiments. Statistical significance was assessed using an unpaired two-tailed t-test. **** P < 0.001.

Article Snippet: Antibodies were used for western blotting and cut and run: Anti-rabbit (Jackson Immunoresearch, Lot# 168738); anti-actin (Sigma, A5441, Lot # 030M4788); Anti-mouse(Jackson Immuno-research #115-035-062); Cyclin T1 (abcam, ab27963); Cyclin K (Cell Signaling #19472S); CDK12 (abcam-EPR29009-30 ab317746); Pol II CTD (Cell Signaling #2629S); Pol II CTD Ser2 (Cell Signaling #13499S); Pol II CTD Ser5 (Cell Signaling #13523S); CDK9 (Cell Signaling #2316S); H3K27ac (Cell Signaling #8173S).

Techniques: Activity Assay, Activation Assay, Infection, Gene Expression, Expressing, Two Tailed Test

$CDK12/CCNK targeting disrupts the association of CDK9 and CYCLIN T1 with HEXIM1. Jurkat T cells were treated with SR-4835 (0.5µM) or remained untreated for 24 hours, followed by immunoprecipitation with an anti-HEXIM1 IgG ( A ), or anti-CDK9 IgG ( B ). Co-IP fractions were analyzed by Western Blotting analysis for HEXIM1, CDK9 and CYCLIN T1.$

Journal: bioRxiv

Article Title: Targeting CDK12/CYCLIN K induces HIV gene activation and latency reversal which is mediated by P-TEFb

doi: 10.64898/2026.02.10.705011

Figure Lengend Snippet: CDK12/CCNK targeting disrupts the association of CDK9 and CYCLIN T1 with HEXIM1. Jurkat T cells were treated with SR-4835 (0.5µM) or remained untreated for 24 hours, followed by immunoprecipitation with an anti-HEXIM1 IgG ( A ), or anti-CDK9 IgG ( B ). Co-IP fractions were analyzed by Western Blotting analysis for HEXIM1, CDK9 and CYCLIN T1.

Techniques: Immunoprecipitation, Co-Immunoprecipitation Assay, Western Blot

Targeting CDK12/CCNK induces HIV specific and global gene activation A. ChIP-qPCR analysis of Jurkat HIV transduced T cells treated with SR-4835 for 24 hours. ChIP qPCR was analyzed on ChIP material from SR-4835 treated, or untreated cells using the indicated antibodies. Data is presented as percentage of input relative to IgG as a negative control. Statistical significance is based on calculating mean ± SD from three independent experiments using One-way ANOVA. ** P <0.01. B. CUT&RUN analysis shows global increase levels in gene promoters and gene bodies of CDK9 total RNA Pol II and well specific CTD Ser2-P and Ser5-P levels following SR-4835 treatment. Experiments were performed as described in the Methods based on Epicipher protocols.

Journal: bioRxiv

Article Title: Targeting CDK12/CYCLIN K induces HIV gene activation and latency reversal which is mediated by P-TEFb

doi: 10.64898/2026.02.10.705011

Figure Lengend Snippet: Targeting CDK12/CCNK induces HIV specific and global gene activation A. ChIP-qPCR analysis of Jurkat HIV transduced T cells treated with SR-4835 for 24 hours. ChIP qPCR was analyzed on ChIP material from SR-4835 treated, or untreated cells using the indicated antibodies. Data is presented as percentage of input relative to IgG as a negative control. Statistical significance is based on calculating mean ± SD from three independent experiments using One-way ANOVA. ** P <0.01. B. CUT&RUN analysis shows global increase levels in gene promoters and gene bodies of CDK9 total RNA Pol II and well specific CTD Ser2-P and Ser5-P levels following SR-4835 treatment. Experiments were performed as described in the Methods based on Epicipher protocols.

Techniques: Activation Assay, ChIP-qPCR, Negative Control

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monoclonal rabbit anti human cdk9 antibody (Cell Signaling Technology Inc)

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