htb-14 Search Results


u87  (ATCC)
99
ATCC u87
MDM2‐ and p53‐dependent activities of MDM2‐recruiting P‐TEFb PROTAC degraders. (A) Effects of siRNA‐mediated MDM2 knockdown on cellular sensitivity to dCDK9‐010. Data were presented as mean ± standard deviation (SD); n = 3. (B) Effects of MDM2 knockdown on dCDK9‐010‐mediated CDK9/Cyclin T degradation. TC‐32 cells were transfected with indicated siRNAs for 48 h, followed by treatment with 2 µM dCDK9‐010 for 8 h. (C) MDM2 mRNA levels in wild type versus TP53 ‐knockout <t>U87</t> cells, with or without compound treatment (2 µM, 8 h). Data were presented as mean ± SD ( n = 3); *** p < 0.001 based on one‐way analysis of variance (ANOVA); n.s., no significance. (D) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in wild‐type and TP53 ‐knockout isogenic U87 cells after compound treatment (2 µM, 8 h). (E) Viability of isogenic U87 cells treated with dCDK9‐010. Data were presented as mean ± SD ( n = 3). (F) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in NCI‐H226 and TC‐32 cells after siRNA‐mediated TP53 silencing and dCDK9‐010 treatment (2 µM, 8 h). (G) Effects of TP53 or MDM4 knockdown by siRNA relative to control on dCDK9‐010 sensitivity in NCI‐H226 and TC‐32 cells. Data were presented as mean ± SD ( n = 3).
U87, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human glioblastoma astrocytoma  (ATCC)
97
ATCC human glioblastoma astrocytoma
MDM2‐ and p53‐dependent activities of MDM2‐recruiting P‐TEFb PROTAC degraders. (A) Effects of siRNA‐mediated MDM2 knockdown on cellular sensitivity to dCDK9‐010. Data were presented as mean ± standard deviation (SD); n = 3. (B) Effects of MDM2 knockdown on dCDK9‐010‐mediated CDK9/Cyclin T degradation. TC‐32 cells were transfected with indicated siRNAs for 48 h, followed by treatment with 2 µM dCDK9‐010 for 8 h. (C) MDM2 mRNA levels in wild type versus TP53 ‐knockout <t>U87</t> cells, with or without compound treatment (2 µM, 8 h). Data were presented as mean ± SD ( n = 3); *** p < 0.001 based on one‐way analysis of variance (ANOVA); n.s., no significance. (D) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in wild‐type and TP53 ‐knockout isogenic U87 cells after compound treatment (2 µM, 8 h). (E) Viability of isogenic U87 cells treated with dCDK9‐010. Data were presented as mean ± SD ( n = 3). (F) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in NCI‐H226 and TC‐32 cells after siRNA‐mediated TP53 silencing and dCDK9‐010 treatment (2 µM, 8 h). (G) Effects of TP53 or MDM4 knockdown by siRNA relative to control on dCDK9‐010 sensitivity in NCI‐H226 and TC‐32 cells. Data were presented as mean ± SD ( n = 3).
Human Glioblastoma Astrocytoma, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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u87 fluc  (ATCC)
94
ATCC u87 fluc
MDM2‐ and p53‐dependent activities of MDM2‐recruiting P‐TEFb PROTAC degraders. (A) Effects of siRNA‐mediated MDM2 knockdown on cellular sensitivity to dCDK9‐010. Data were presented as mean ± standard deviation (SD); n = 3. (B) Effects of MDM2 knockdown on dCDK9‐010‐mediated CDK9/Cyclin T degradation. TC‐32 cells were transfected with indicated siRNAs for 48 h, followed by treatment with 2 µM dCDK9‐010 for 8 h. (C) MDM2 mRNA levels in wild type versus TP53 ‐knockout <t>U87</t> cells, with or without compound treatment (2 µM, 8 h). Data were presented as mean ± SD ( n = 3); *** p < 0.001 based on one‐way analysis of variance (ANOVA); n.s., no significance. (D) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in wild‐type and TP53 ‐knockout isogenic U87 cells after compound treatment (2 µM, 8 h). (E) Viability of isogenic U87 cells treated with dCDK9‐010. Data were presented as mean ± SD ( n = 3). (F) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in NCI‐H226 and TC‐32 cells after siRNA‐mediated TP53 silencing and dCDK9‐010 treatment (2 µM, 8 h). (G) Effects of TP53 or MDM4 knockdown by siRNA relative to control on dCDK9‐010 sensitivity in NCI‐H226 and TC‐32 cells. Data were presented as mean ± SD ( n = 3).
U87 Fluc, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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panc-1 cell line  (ScienCell)
90
ScienCell panc-1 cell line
MDM2‐ and p53‐dependent activities of MDM2‐recruiting P‐TEFb PROTAC degraders. (A) Effects of siRNA‐mediated MDM2 knockdown on cellular sensitivity to dCDK9‐010. Data were presented as mean ± standard deviation (SD); n = 3. (B) Effects of MDM2 knockdown on dCDK9‐010‐mediated CDK9/Cyclin T degradation. TC‐32 cells were transfected with indicated siRNAs for 48 h, followed by treatment with 2 µM dCDK9‐010 for 8 h. (C) MDM2 mRNA levels in wild type versus TP53 ‐knockout <t>U87</t> cells, with or without compound treatment (2 µM, 8 h). Data were presented as mean ± SD ( n = 3); *** p < 0.001 based on one‐way analysis of variance (ANOVA); n.s., no significance. (D) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in wild‐type and TP53 ‐knockout isogenic U87 cells after compound treatment (2 µM, 8 h). (E) Viability of isogenic U87 cells treated with dCDK9‐010. Data were presented as mean ± SD ( n = 3). (F) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in NCI‐H226 and TC‐32 cells after siRNA‐mediated TP53 silencing and dCDK9‐010 treatment (2 µM, 8 h). (G) Effects of TP53 or MDM4 knockdown by siRNA relative to control on dCDK9‐010 sensitivity in NCI‐H226 and TC‐32 cells. Data were presented as mean ± SD ( n = 3).
Panc 1 Cell Line, supplied by ScienCell, 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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htb-14  (LGC Standards)
99
LGC Standards htb-14
MDM2‐ and p53‐dependent activities of MDM2‐recruiting P‐TEFb PROTAC degraders. (A) Effects of siRNA‐mediated MDM2 knockdown on cellular sensitivity to dCDK9‐010. Data were presented as mean ± standard deviation (SD); n = 3. (B) Effects of MDM2 knockdown on dCDK9‐010‐mediated CDK9/Cyclin T degradation. TC‐32 cells were transfected with indicated siRNAs for 48 h, followed by treatment with 2 µM dCDK9‐010 for 8 h. (C) MDM2 mRNA levels in wild type versus TP53 ‐knockout <t>U87</t> cells, with or without compound treatment (2 µM, 8 h). Data were presented as mean ± SD ( n = 3); *** p < 0.001 based on one‐way analysis of variance (ANOVA); n.s., no significance. (D) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in wild‐type and TP53 ‐knockout isogenic U87 cells after compound treatment (2 µM, 8 h). (E) Viability of isogenic U87 cells treated with dCDK9‐010. Data were presented as mean ± SD ( n = 3). (F) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in NCI‐H226 and TC‐32 cells after siRNA‐mediated TP53 silencing and dCDK9‐010 treatment (2 µM, 8 h). (G) Effects of TP53 or MDM4 knockdown by siRNA relative to control on dCDK9‐010 sensitivity in NCI‐H226 and TC‐32 cells. Data were presented as mean ± SD ( n = 3).
Htb 14, supplied by LGC Standards, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


MDM2‐ and p53‐dependent activities of MDM2‐recruiting P‐TEFb PROTAC degraders. (A) Effects of siRNA‐mediated MDM2 knockdown on cellular sensitivity to dCDK9‐010. Data were presented as mean ± standard deviation (SD); n = 3. (B) Effects of MDM2 knockdown on dCDK9‐010‐mediated CDK9/Cyclin T degradation. TC‐32 cells were transfected with indicated siRNAs for 48 h, followed by treatment with 2 µM dCDK9‐010 for 8 h. (C) MDM2 mRNA levels in wild type versus TP53 ‐knockout U87 cells, with or without compound treatment (2 µM, 8 h). Data were presented as mean ± SD ( n = 3); *** p < 0.001 based on one‐way analysis of variance (ANOVA); n.s., no significance. (D) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in wild‐type and TP53 ‐knockout isogenic U87 cells after compound treatment (2 µM, 8 h). (E) Viability of isogenic U87 cells treated with dCDK9‐010. Data were presented as mean ± SD ( n = 3). (F) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in NCI‐H226 and TC‐32 cells after siRNA‐mediated TP53 silencing and dCDK9‐010 treatment (2 µM, 8 h). (G) Effects of TP53 or MDM4 knockdown by siRNA relative to control on dCDK9‐010 sensitivity in NCI‐H226 and TC‐32 cells. Data were presented as mean ± SD ( n = 3).

Journal: MedComm

Article Title: Discovery of a First‐in‐Class Murine Double Minute 2‐Recruiting Positive Transcription Elongation Factor B PROTAC Degrader With Selective Antitumor Activity

doi: 10.1002/mco2.70723

Figure Lengend Snippet: MDM2‐ and p53‐dependent activities of MDM2‐recruiting P‐TEFb PROTAC degraders. (A) Effects of siRNA‐mediated MDM2 knockdown on cellular sensitivity to dCDK9‐010. Data were presented as mean ± standard deviation (SD); n = 3. (B) Effects of MDM2 knockdown on dCDK9‐010‐mediated CDK9/Cyclin T degradation. TC‐32 cells were transfected with indicated siRNAs for 48 h, followed by treatment with 2 µM dCDK9‐010 for 8 h. (C) MDM2 mRNA levels in wild type versus TP53 ‐knockout U87 cells, with or without compound treatment (2 µM, 8 h). Data were presented as mean ± SD ( n = 3); *** p < 0.001 based on one‐way analysis of variance (ANOVA); n.s., no significance. (D) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in wild‐type and TP53 ‐knockout isogenic U87 cells after compound treatment (2 µM, 8 h). (E) Viability of isogenic U87 cells treated with dCDK9‐010. Data were presented as mean ± SD ( n = 3). (F) Immunoblot analysis of P‐TEFb components, p53, and MDM2 in NCI‐H226 and TC‐32 cells after siRNA‐mediated TP53 silencing and dCDK9‐010 treatment (2 µM, 8 h). (G) Effects of TP53 or MDM4 knockdown by siRNA relative to control on dCDK9‐010 sensitivity in NCI‐H226 and TC‐32 cells. Data were presented as mean ± SD ( n = 3).

Article Snippet: HEK293T (ATCC), TC‐32 (COG Repository, USA), HCT116 (ATCC), A549 (ATCC), HEPG2 (ATCC), HT1080 (ATCC), MDA‐MB‐231 (ATCC), U87 (U‐87MG, ATCC), U251 (U251MG, ATCC), and MKN45 (ATCC) cells lines were maintained in Dulbecco's modified Eagle medium (DMEM; Sigma‐Aldrich, Taufkirchen, Germany).

Techniques: Knockdown, Standard Deviation, Transfection, Knock-Out, Western Blot, Control

Selective activities of compounds 12 (dCDK9‐009) and 13 (dCDK9‐010) against TP53 wild‐type cancer cells. (A and B) Examination of dose‐dependent impacts of dCDK9‐009 and dCDK9‐010 in TP53 wild‐type HCT116, HT1080, NCI‐H460, and U87. Cells were treated with increasing concentrations of indicated compounds for 24 h. (C and D) Examination of impacts of dCDK9‐009 and dCDK9‐010 in non‐malignant HEK293T and mesenchymal stem cell line ASC52telo. Cells were treated with increasing concentrations of indicated compounds for 24 h. (E and F) Effect of dCDK9‐009 and dCDK9‐010 treatment on cellular viabilities of indicated cancer cell lines, as well as ASC52telo. IC 50 was presented as mean ± SD with three independent replicates. (G) Heatmap summarizing the IC 50 values of dCDK9‐009 and dCDK9‐010 across human cell lines tested in this study (related to E and F, Figures S3, S4, and S8).

Journal: MedComm

Article Title: Discovery of a First‐in‐Class Murine Double Minute 2‐Recruiting Positive Transcription Elongation Factor B PROTAC Degrader With Selective Antitumor Activity

doi: 10.1002/mco2.70723

Figure Lengend Snippet: Selective activities of compounds 12 (dCDK9‐009) and 13 (dCDK9‐010) against TP53 wild‐type cancer cells. (A and B) Examination of dose‐dependent impacts of dCDK9‐009 and dCDK9‐010 in TP53 wild‐type HCT116, HT1080, NCI‐H460, and U87. Cells were treated with increasing concentrations of indicated compounds for 24 h. (C and D) Examination of impacts of dCDK9‐009 and dCDK9‐010 in non‐malignant HEK293T and mesenchymal stem cell line ASC52telo. Cells were treated with increasing concentrations of indicated compounds for 24 h. (E and F) Effect of dCDK9‐009 and dCDK9‐010 treatment on cellular viabilities of indicated cancer cell lines, as well as ASC52telo. IC 50 was presented as mean ± SD with three independent replicates. (G) Heatmap summarizing the IC 50 values of dCDK9‐009 and dCDK9‐010 across human cell lines tested in this study (related to E and F, Figures S3, S4, and S8).

Article Snippet: HEK293T (ATCC), TC‐32 (COG Repository, USA), HCT116 (ATCC), A549 (ATCC), HEPG2 (ATCC), HT1080 (ATCC), MDA‐MB‐231 (ATCC), U87 (U‐87MG, ATCC), U251 (U251MG, ATCC), and MKN45 (ATCC) cells lines were maintained in Dulbecco's modified Eagle medium (DMEM; Sigma‐Aldrich, Taufkirchen, Germany).

Techniques: