Journal:

Article Title: The Histidine Triad Protein Hint Is Not Required for Murine Development or Cdk7 Function

doi: 10.1128/MCB.23.11.3929-3935.2003

Figure Lengend Snippet: Characterization of Cdk7 function in Hint−/− MEFs. (A) Western blotting analysis of endogenous Hint, Cdk7, cyclin H, Mat1, and actin from protein lysates from wild-type and Hint null MEFs. (B) In vitro Cdk7 kinase activity from Hint wild-type and Hint null MEFs assayed by using GST-CTD and GST-Cdk2 as substrates following anti-Cdk7 immunoprecipitation (IP). (C) Western blotting analysis from protein lysates of wild-type, Hint heterozygous, and Hint null MEFs with RNA Pol II large-subunit antibody 8WG16 recognizing nonphosphorylated Ser-2 (RNA Pol II), antibody H5, recognizing Pol II phosphorylated on serine 2 (p-Ser-2) of the CTD repeat, and antibody H14, recognizing Pol II phosphorylated on serine 5 (p-Ser-5) of the CTD repeat. (D) Western blot analysis of protein lysates from two independent cultures of wild-type and Hint null MEFs with a Cdk2 antibody recognizing total Cdk2 levels. In vitro Cdk2 kinase activity from unsynchronized Hint wild-type and Hint null MEFs was assayed by using histone H1 (H1) as a substrate following anti-Cdk2 immunoprecipitation. (E) [3H]thymidine incorporation of wild-type and Hint null MEFs labeled at different times after release to G1 by readdition of serum to starved cells. Standard deviations (error bars) originate from duplicates of three independent primary cultures for each genotype.

Article Snippet: Primary antibodies were rabbit polyclonal antibodies against Hint (hPKCI, 1:1,000; a kind gift from Bernard Weinstein) ( 13 ), cyclin H (1:1,000, FL323; Santa Cruz), Mat1 (FL309, 1:1,000; Santa Cruz), and Cdk2 (sc-169, 1:1,000; Santa Cruz) and mouse monoclonal antibodies against Cdk7 (sc-7344, 1:500; Santa Cruz), actin (AC-40, 1:1,000; Sigma), and RNA Pol II epitopes H5, H14, and 8WG16 (all 1:500; Research Diagnostics).

Techniques: Western Blot, In Vitro, Activity Assay, Immunoprecipitation, Labeling

Journal: bioRxiv

Article Title: Transcriptional control of DNA repair networks by CDK7 regulates sensitivity to radiation in Myc-driven Medulloblastoma

doi: 10.1101/2020.04.30.069237

Figure Lengend Snippet: CDK7 expression in medulloblastoma enhanced in group 3 tumors. (A) Methodological graphic of the crispr-cas9 druggable kinase screen performed on three group 3 medulloblastoma cell lines. (B) PCA plot of before and after puromycin selection, also see S1 for heatmap. (C) S curve plot displaying the depletion of genes essential for Myc-MB cell line viability. Genes essential to Myc-MB growth previously identified by shRNA screen identified in black, new genes in red. (D) The expression of CDK7 before puromycin selection and 18 days after. (E) CDK7 expression in medulloblastoma by subtype. (F) Patient overall survival in Group 3 medulloblastoma in relation to CDK7 expression. (G) Immunoblot of CDK7 protein levels in three group 3 MB cell lines and two SHH MB cell lines. Quantification (S1) (H) Immunohistochemistry staining of CDK7 in normal cerebellum and 4 patient group 3 MB tumors and two group 4 tumors. Images shown at 20x.

Article Snippet: Primary antibodies α-RNA Pol II CTD S2 #13499, α-RNA Pol II CTD S5 #13523, α-CDK7 #2916, α-CDK9 #2316, α-PARP #9542, and α-cMYC #5605 (Cell Signaling Technology) were exposed overnight at 4°C.

Techniques: Expressing, CRISPR, Selection, shRNA, Western Blot, Immunohistochemistry, Staining

Journal: bioRxiv

Article Title: Transcriptional control of DNA repair networks by CDK7 regulates sensitivity to radiation in Myc-driven Medulloblastoma

doi: 10.1101/2020.04.30.069237

Figure Lengend Snippet: Genetic depletion of CDK7 decreases proliferation and tumor growth. (A) Immunoblot for indicated proteins of lysates transduced with three shRNAs against CDK7 or shNull. (B,C) Neurosphere assay growth in CDK7 depleted D458 or D425 MB cell lines. D458 or D425 cells expressing a NucRed™ marker were plated at 10 cells/well and monitored for growth using the Incucyte S3 over 10 days, representative images at 10 days are shown (above). Total average growth of neurospheres over 10 day period as determined by NucRed™ fluorescence (below). Experiment performed in triplicate, data shown as mean ± SD. (D) Methylcellulose assay of CDK7 knockdown cell lines (D458,D425; shown left). Colony count for D425 (middle) and D458 (right). Experiment performed in triplicate. Shown is a scatter plot with mean and ±SD. Statistical analysis, two-way Anova. ****,p<0.0001; ***,p<0.001. (E) Annexin V (+) staining assay. D458 (top) and D425 (bottom) knockdown cells were stained for Annexin V and measured by guava flow cytometry. Box and whisker plot of the % (+) Annexin V stained cells (y-axis) is shown. Experiments performed in triplicate. Statistical analysis, two-way nova. ***,p<0.001; **,p<0.005; *,p<0.05. (F) Representative bioluminescence images of xenograft D458 CDK7 knockdown or shNull (top) and D425 shCDK7 or shNull (bottom). Days post injection indicated on the left. Color scales indicate bioluminescence radiance in photons/sec/cm 2 /steradian shown right. (G) Kaplan-Meier survival curve of D458 CDK7 knockdown (n=6) and shNull (n=5), (top). D425 shNull (n=6) or shCDK7 (n=5) (bottom). Statistical analysis log-rank (Mantel-Cox) test; ***,p<0.001.

Article Snippet: Primary antibodies α-RNA Pol II CTD S2 #13499, α-RNA Pol II CTD S5 #13523, α-CDK7 #2916, α-CDK9 #2316, α-PARP #9542, and α-cMYC #5605 (Cell Signaling Technology) were exposed overnight at 4°C.

Techniques: Western Blot, Transduction, Neurosphere Assay, Expressing, Marker, Fluorescence, Methylcellulose Assay, Knockdown, Annexin V Staining Assay, Staining, Flow Cytometry, Whisker Assay, Injection

Journal: bioRxiv

Article Title: Transcriptional control of DNA repair networks by CDK7 regulates sensitivity to radiation in Myc-driven Medulloblastoma

doi: 10.1101/2020.04.30.069237

Figure Lengend Snippet: In vivo efficacy of CDK7 inhibition. (A) Nude mice xenografts injected with D458 cells were treated with vehicle (n=6) or THZ2 (n=6) 15mg/kg daily. Representative images of bioluminescence imaging conducted at 12, 18, and 28 days post-injection is shown. Color scales indicate bioluminescence radiance in photons/sec/cm 2 /steradian shown right. (B) Violin plot of mean total radiance in photons/sec/cm 2 /steradian. Statistical analysis two-way Anova, ****, p<0.0001. (C) D425 nude mice xenografts treated with vehicle (n=9) and THZ2 (n=9) 15mg/kg daily. Representative images show bioluminescence imaging at days 8, 15, and 22 post-injection. Color scales indicate bioluminescence radiance in photons/sec/cm 2 /steradian shown right. X indicates mouse death. (D) Violin plot of mean total radiance in photons/sec/cm 2 /steradian. (E) Representative MRI of vehicle and THZ2 treated D458 and D425 xenografts (top). White arrows indicate tumor edge. (Bottom) Tumor volume in mm 3 (y-axis) in vehicle and THZ2 treated mice for D458 (left) and D425 (right). (F) Kaplan-Meier survival curve of D458, D425, and PDX411 xenograft mice treated with vehicle or THZ2. Treatment period for 25 days indicated in shaded box. Statistical analysis log-rank (Mantel-Cox) test, **,p<0.005; *,p<0.05. (G) PDX411 MRI and corresponding tumor volume in mm 3 (y-axis) at 28, 42, and 49 days post-injection. Statistical analysis two-way Anova, *,p<0.05. (H) Representative immunohistochemistry staining for P-H2AX, Ki67, and caspase 3 of D458, D425, and PDX411 tumors from vehicle and THZ2 treated mice. Images taken at 40x. Statistical analysis one-way Anova. ****,p<0.0001; **,p<0.01; *p<0.05.

Article Snippet: Primary antibodies α-RNA Pol II CTD S2 #13499, α-RNA Pol II CTD S5 #13523, α-CDK7 #2916, α-CDK9 #2316, α-PARP #9542, and α-cMYC #5605 (Cell Signaling Technology) were exposed overnight at 4°C.

Techniques: In Vivo, Inhibition, Injection, Imaging, Immunohistochemistry, Staining

Journal: bioRxiv

Article Title: Transcriptional control of DNA repair networks by CDK7 regulates sensitivity to radiation in Myc-driven Medulloblastoma

doi: 10.1101/2020.04.30.069237

Figure Lengend Snippet: CDK7 Inhibition abrogates RNA Pol II and Myc promoter occupancy. (A) ChIP sequencing with RNA Pol II antibody performed on D458 cells treated with DMSO vs THZ1 10nM. Heatmap of normalized RNA Pol II occupancy at the TSS and, GO functional categories for cluster 1 genes effected by THZ1 treatment using metascape. Enrichment scores shown as −Log10(Pval). (B) Average read density of RNA Pol II ChIP-sequencing at the TSS. DMSO (blue) or 10nM THZ1 (orange). (C) ChIP sequencing with Myc antibody performed on D458 cells treated with DMSO vs THZ1 10nM. Heatmap of normalized Myc occupancy at the TSS and, GO functional categories for cluster 1 genes effected by THZ1 treatment using metascape. Enrichment scores shown as −Log10(Pval). (D) Average read density of Myc ChIP-sequencing at the TSS. DMSO (blue) or 10nM THZ1 (orange). (E) Venn diagram of gene overlap between cluster 1 of RNA Pol II ChIP, cluster 1 of Myc Chip, and genes downregulated by THZ1 treatment. (F) Box and whisker plots of the total number of reads within 200bp of the TSS for the top genes within the DNA Repair ontology of cluster 1 for RNA Pol II ChIP and Myc ChIP (top). Myc ChIP read numbers for top DNA repair genes, shown right. Color scale indicates high (red) to low (white) reads. Top genes within the mRNA processing ontology of cluster 2 for RNA Pol II and Myc ChIPs (bottom). Statistical analysis, two-tailed, unpaired t-test. ****, p<0.0001; **,p<0.01.

Article Snippet: Primary antibodies α-RNA Pol II CTD S2 #13499, α-RNA Pol II CTD S5 #13523, α-CDK7 #2916, α-CDK9 #2316, α-PARP #9542, and α-cMYC #5605 (Cell Signaling Technology) were exposed overnight at 4°C.

Techniques: Inhibition, ChIP-sequencing, Functional Assay, Whisker Assay, Two Tailed Test

Journal: bioRxiv

Article Title: Transcriptional control of DNA repair networks by CDK7 regulates sensitivity to radiation in Myc-driven Medulloblastoma

doi: 10.1101/2020.04.30.069237

Figure Lengend Snippet: CDK7 inhibition minimizes DNA damage response enhancing susceptibility to ionizing radiation (A) GSEA from THZ1 D458 treatment RNA-seq. Kauffman DNA repair, KEGG Homologous Recombination. FDR q-Value=0.0. (B) Volcano plot of Kauffman DNA repair (green), KEGG homologous recombination (yellow), and MYC targets (blue). (C) Individual ChIP gene tracks of RNA Pol II, MYC signals, and RNA transcript profile for DMSO and THZ1 10nM D458 treatments. Y-axis signal density (rpm/bp) of BRCA2 promoter and RAD51C promoter. (D) Immunofluorescence of P-H2AX (green) shown at 100X and Dapi. D425 (left) and D458 (right) cells treated with THZ1 IC20 and exposed to 0 Gy or 6 Gy were fixed at 4hrs and 24hrs. Quantification of P-H2AX foci/nuclei (below). Statistical analysis, one-way Anova, ****,p<0.0001; **,p<0.001. (E) Annexin V (+) staining assay. D458 cells treated with DMSO or THZ1 200pM and ionizing radiation at 0, 2, and 6Gy were stained for Annexin V and measured by guava flow cytometery. Violin plot of the % (+) Annexin V stained cells (y-axis) is shown. Experiments performed in triplicate. Statistical analysis, two-way Anova. **,p<0.005. (F) Survival fraction plots of D458 (left) and D425 (right) from cells treated with DMSO or THZ1 200pM or THZ2 200pM and increasing ionizing radiation 0,2,4,6,8,10 Gy. Cells were grown in methylcellulose and colonies counted after 10 days. Survival fraction (y-axis) is plotted versus ionizing radiation (x-axis). Survival enhancement ratio is shown for THZ1 and THZ2.

Article Snippet: Primary antibodies α-RNA Pol II CTD S2 #13499, α-RNA Pol II CTD S5 #13523, α-CDK7 #2916, α-CDK9 #2316, α-PARP #9542, and α-cMYC #5605 (Cell Signaling Technology) were exposed overnight at 4°C.

Techniques: Inhibition, RNA Sequencing, Homologous Recombination, Immunofluorescence, Annexin V Staining Assay, Staining

Journal: bioRxiv

Article Title: Transcriptional control of DNA repair networks by CDK7 regulates sensitivity to radiation in Myc-driven Medulloblastoma

doi: 10.1101/2020.04.30.069237

Figure Lengend Snippet: In vivo ionizing radiation with CDK7 inhibition. (A) Representative bioluminescence images of xenograft D458 vehicle (left) or THZ2 15mg/kg (right) treated with 1.5Gy over five days starting at day 15 post-injection. Color scales indicate bioluminescence radiance in photons/sec/cm 2 /steradian shown right. (B) Representative MRI of vehicle and THZ2 plus ionizing radiation treated D458 xenograft mice at 23 days and 49 days. White arrows indicate tumor. (C) Violin plot of mean total radiance in photons/sec/cm 2 /steradian. Statistical analysis, two-way Anova, ***,p<0.001. (D) Kaplan-Meier survival curve of D458 xenograft mice treated with vehicle or THZ2 and 1.5Gy for 5 days (violet box). THZ2 treatment period for 25 days indicated in shaded box. Statistical analysis log-rank (Mantel-Cox) test, p=0.16.

Article Snippet: Primary antibodies α-RNA Pol II CTD S2 #13499, α-RNA Pol II CTD S5 #13523, α-CDK7 #2916, α-CDK9 #2316, α-PARP #9542, and α-cMYC #5605 (Cell Signaling Technology) were exposed overnight at 4°C.

Techniques: In Vivo, Inhibition, Injection

Journal: Molecular carcinogenesis

Article Title: EEF1E1 promotes glioma proliferation by regulating cell cycle through PTEN/AKT signaling pathway.

doi: 10.1002/mc.23611

Figure Lengend Snippet: FIGURE 3 EEF1E1 interacts with the downstream PTEN/AKT pathway. (A) Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology analysis of EEF1E1‐related genes obtained from the STRING database reveals a relationship between EEF1E1 and the cell cycle. (B) Single gene expression heatmaps suggest a relationship between EEF1E1 and AKT3, PTEN, p53, CDK2, CDK4, and CDK7. (C, D) Pathway correlation analysis using theThe Cancer Genome Atlas database demonstrates that EEF1E1 is correlated with the phosphatidylinositol‐3‐kinase (PI3K)/AKT signaling pathway and the cell cycle pathway (p < 0.01). (E) Western blot analysis verification of cell cycle‐related proteins. (F) Immunofluorescence double staining confirms the colocalization of EEF1E1 and PTEN in cells. (G) Colocalization of EEF1E1 and PTEN in glioma tissue using immunofluorescence double staining. (H) Co‐ immunoprecipitation (IP) experiment verifies the protein interaction between EEF1E1 and PTEN. CDK, cyclin‐dependent kinase; DAPI, 4′,6‐diamidino‐2‐ phenylindole; TPM, transcripts per million.

Article Snippet: Proteins were then separated by 10% sodium dodecyl‐sulfate polyacrylamide gel electrophoresis, transferred onto polyvinylidene fluoride membranes, and blocked for 1 h. Membranes were incubated with primary antibodies EEF1E1 (Abcam), PTEN, CDK2, CDK4 (Servicebio), CDK7 (Protein), AKT, P‐AKT (Cell Signaling), and P‐PTEN (Abclonal), and β‐Tubulin (Protein) was selected as the internal control at 4°C overnight.

Techniques: Gene Expression, Western Blot, Immunofluorescence, Double Staining, Immunoprecipitation

Journal: Molecular carcinogenesis

Article Title: EEF1E1 promotes glioma proliferation by regulating cell cycle through PTEN/AKT signaling pathway.

doi: 10.1002/mc.23611

Figure Lengend Snippet: FIGURE 6 EEF1E1 promotes the expression of cell cycle proteins cyclin‐dependent kinases (CDK2, CDK4, and CDK7) through interaction with the PTEN/AKT pathway, thereby affecting the G1 and S phases of the cell cycle and promoting glioma cell proliferation. PI3K, phosphatidylinositol‐3‐kinase.

Article Snippet: Proteins were then separated by 10% sodium dodecyl‐sulfate polyacrylamide gel electrophoresis, transferred onto polyvinylidene fluoride membranes, and blocked for 1 h. Membranes were incubated with primary antibodies EEF1E1 (Abcam), PTEN, CDK2, CDK4 (Servicebio), CDK7 (Protein), AKT, P‐AKT (Cell Signaling), and P‐PTEN (Abclonal), and β‐Tubulin (Protein) was selected as the internal control at 4°C overnight.

Techniques: Expressing

Journal: Journal of experimental & clinical cancer research : CR

Article Title: Novel covalent CDK7 inhibitor potently induces apoptosis in acute myeloid leukemia and synergizes with Venetoclax.

doi: 10.1186/s13046-023-02750-w

Figure Lengend Snippet: Fig. 1 Efficacy of XL102 and its effects on downstream targets of CDK7. A Kinase activity of CDK7 in the presence of XL102 was measured using the LANCE TR-FRET in vitro kinase assay by incubating both CDK7 and XL102 followed by addition of ATP and U-light-MBP peptide substrate. Time-resolved fluorescence (excitation, 320 nm; emission donor, 615 nm; emission acceptor, 665 nm) was monitored by using 2030 multilabel reader Victor5 (PerkinElmer). The IC50 values were derived by fitting a sigmoidal dose–response curve to a plot of assay readout over inhibitor concentration, computed with the Graph Pad Prism. B The pull-down assay using bio-THZ1 show a dose dependent target engagement in AML cells harvested after 3 h of XL102 treatment followed by washing to remove any unbound XL102 (time point-0 h). C XL102 inhibited CTD phosphorylation of conserved residues of RPII in AML cells in dose dependent manner at 6 h and 24 h along with quantification of Western blot data. Results are the mean ± SD of three independent experiments

Article Snippet: Antibodies used against various proteins were CDK7 (Bethyl Laboratories, Massachusetts, US) and Beta actin (Santa Cruz Biotechnology, Texas, US).

Techniques: Activity Assay, In Vitro, Kinase Assay, Fluorescence, Derivative Assay, Concentration Assay, Pull Down Assay, Drug discovery, Phospho-proteomics, Western Blot

Journal: International Journal of Oral Science

Article Title: Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression

doi: 10.1038/s41368-025-00363-x

Figure Lengend Snippet: Proteomics analysis showing LSD1 inhibition impairs STAT3 protein and phospho-protein network: a Global proteomics of tongue tumor protein lysate from 4MOSC1 syngeneic mouse model showing SP2509 treatment reduces LSD1 and STAT3, whereas increased NFATc1 and IRF3. b Phosphoproteomics analysis of 4MOSC1 tumors treated with SP2509 reversed phosphorylated oncoproteins expression shown in the heat map, including phospho-CDK7 (Tyr170). c Kinase-substrate enrichment analysis (KSEA) in Phosphomatics tool reveals the kinase activity-based z-score (activation/deactivation) on the reduced activity for phosphorylated CDK7

Article Snippet: For genetic knockout, we used plasmids CDK7 sgRNA (BRDN0001162216) (Addgene #76077), EF.STAT3C.Ubc.GFP (Addgene #24983), KDM1A sgRNA CRISPR/Cas9 All-in-one Lentivector (abm #K2776607).

Techniques: Inhibition, Phospho-proteomics, Expressing, Activity Assay, Activation Assay

Journal: International Journal of Oral Science

Article Title: Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression

doi: 10.1038/s41368-025-00363-x

Figure Lengend Snippet: Phosphoproteomics analysis showing LSD1 inhibition impairs CDK7 and EGFR-STAT3 network: a Kinase substrate interaction analysis in SP2509 treated groups shows inhibition of CDK7 phosphorylation, which has various substrates, including other CDKs and eukaryotic translation initiation factors. b IPA analysis generated by global proteomics data shows that SP2509 reduces the EGFR-STAT3 network, whereas upregulation of NFATc1 results in accumulation of inflammatory leukocyte network

Article Snippet: For genetic knockout, we used plasmids CDK7 sgRNA (BRDN0001162216) (Addgene #76077), EF.STAT3C.Ubc.GFP (Addgene #24983), KDM1A sgRNA CRISPR/Cas9 All-in-one Lentivector (abm #K2776607).

Techniques: Phospho-proteomics, Inhibition, Generated

Journal: International Journal of Oral Science

Article Title: Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression

doi: 10.1038/s41368-025-00363-x

Figure Lengend Snippet: CDK7 is a key mediator of LSD1-induced STAT3 expression: RT-qPCR analysis to evaluate the effect of LSD1, STAT3, or CDK7 inhibitors on expression KDM1A, STAT3 , and CDK7 expression in; a HSC3 cells, and b CAL27 cells. RT-qPCR analysis to evaluate the effect of genetic knockout of KDM1A, STAT3 , or CDK7 on expression of KDM1A, STAT3 , and CDK7 in; c HSC3 cells, and d CAL27 cells. “ns” P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.000 1

Article Snippet: For genetic knockout, we used plasmids CDK7 sgRNA (BRDN0001162216) (Addgene #76077), EF.STAT3C.Ubc.GFP (Addgene #24983), KDM1A sgRNA CRISPR/Cas9 All-in-one Lentivector (abm #K2776607).

Techniques: Expressing, Quantitative RT-PCR, Knock-Out

Journal: International Journal of Oral Science

Article Title: Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression

doi: 10.1038/s41368-025-00363-x

Figure Lengend Snippet: Impact on phosphorylation of CDK7 and methylation of H3K4 and H3K9 after LSD1 inhibition: a Effect on phospho-CDK7 (T170) after LSD1, STAT3 and CDK7 inhibition. b Status of H3K4 and H3K9 methylation on STAT3 and CDK7. Statistical analysis was performed by t -test and one-way ANOVA. “ns” P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.000 1

Article Snippet: For genetic knockout, we used plasmids CDK7 sgRNA (BRDN0001162216) (Addgene #76077), EF.STAT3C.Ubc.GFP (Addgene #24983), KDM1A sgRNA CRISPR/Cas9 All-in-one Lentivector (abm #K2776607).

Techniques: Phospho-proteomics, Methylation, Inhibition

Journal: International Journal of Oral Science

Article Title: Lysine-specific demethylase 1 controls key OSCC preneoplasia inducer STAT3 through CDK7 phosphorylation during oncogenic progression and immunosuppression

doi: 10.1038/s41368-025-00363-x

Figure Lengend Snippet: Graphical Abstract. The potential mechanism after blocking LSD1 inhibits novel CDK7 phospho-protein networks and STAT3 signaling ultimately promotes CD8+ T cell infiltration and activation by relieving CTLA4-mediated immunosuppression

Article Snippet: For genetic knockout, we used plasmids CDK7 sgRNA (BRDN0001162216) (Addgene #76077), EF.STAT3C.Ubc.GFP (Addgene #24983), KDM1A sgRNA CRISPR/Cas9 All-in-one Lentivector (abm #K2776607).

Techniques: Blocking Assay, Activation Assay