crm Search Results


99
ATCC hela cells
PlasDIC microscopy images (40× magnification) of <t>HeLa</t> <t>cells</t> after 72 hr incubation with ( A ) medium control, ( B ) solvent control (1% ethanol), ( C ) 10 µM 25(OH)D 3 , or ( D ) 250 µM calcipotriol.
Hela Cells, 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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95
ATCC human breast cancer cell line mda mb 231
PlasDIC microscopy images (40× magnification) of <t>HeLa</t> <t>cells</t> after 72 hr incubation with ( A ) medium control, ( B ) solvent control (1% ethanol), ( C ) 10 µM 25(OH)D 3 , or ( D ) 250 µM calcipotriol.
Human Breast Cancer Cell Line Mda Mb 231, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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97
ATCC miapaca 2 cells
(A) Dose-dependent effect of MRTX849 on the proliferation <t>of</t> <t>MiaPaCa-2</t> and H358 cells based on live cell imaging. AsPC-1 cells were treated with different concentrations of MRTX1133, and the cell growth was monitored. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (B) Effect of the mutant-specific KRAS inhibitors, MRTX849 and MRTX1133 on the proliferation of MiaPaCa-2-MR, H358-MR and AsPC-1-MR cells that have developed acquired resistance following long-term selection. Mean and SD were determined from triplicates, and the experiments were carried out 3 independent times. (C) Live cell imaging to examine the effect of MRTX849 on the proliferation of UM53 and RS4774 cell lines. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (D) Western blot analysis on MiaPaCa-2-MR, UM53 and RS4774 cells to evaluate the effect of MRTX849 on ERK phosphorylation following 48-hour exposure at the indicated concentration. (E) Differential effects of KRAS knockdown on the proliferation of MiaPaCa-2-WT, AsPC-1-WT, MiaPaCa-2-MR, AsPC-1-MR and UM53 cells. Error bars indicate mean and SD from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. Experiments were done at three independent times. (F) In vivo efficacy of MRTX849 on xenografts derived from MiaPaCa-2-WT and MiaPaCa-2-MR cells and on the tumor growth of RS4774 PDX. Error bars represent mean and SEM. *** represents p<0.0001 as determined by 2-way ANOVA. (G) Representative images of immunohistochemical staining on the vehicle- and MRTX849-treated tissues to determine the phosphorylation status of ERK. Scale bar represents 50 microns.
Miapaca 2 Cells, 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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99
ATCC human lung carcinoma a549
(A) Dose-dependent effect of MRTX849 on the proliferation <t>of</t> <t>MiaPaCa-2</t> and H358 cells based on live cell imaging. AsPC-1 cells were treated with different concentrations of MRTX1133, and the cell growth was monitored. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (B) Effect of the mutant-specific KRAS inhibitors, MRTX849 and MRTX1133 on the proliferation of MiaPaCa-2-MR, H358-MR and AsPC-1-MR cells that have developed acquired resistance following long-term selection. Mean and SD were determined from triplicates, and the experiments were carried out 3 independent times. (C) Live cell imaging to examine the effect of MRTX849 on the proliferation of UM53 and RS4774 cell lines. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (D) Western blot analysis on MiaPaCa-2-MR, UM53 and RS4774 cells to evaluate the effect of MRTX849 on ERK phosphorylation following 48-hour exposure at the indicated concentration. (E) Differential effects of KRAS knockdown on the proliferation of MiaPaCa-2-WT, AsPC-1-WT, MiaPaCa-2-MR, AsPC-1-MR and UM53 cells. Error bars indicate mean and SD from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. Experiments were done at three independent times. (F) In vivo efficacy of MRTX849 on xenografts derived from MiaPaCa-2-WT and MiaPaCa-2-MR cells and on the tumor growth of RS4774 PDX. Error bars represent mean and SEM. *** represents p<0.0001 as determined by 2-way ANOVA. (G) Representative images of immunohistochemical staining on the vehicle- and MRTX849-treated tissues to determine the phosphorylation status of ERK. Scale bar represents 50 microns.
Human Lung Carcinoma A549, 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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96
ATCC rpmi8226 ffluc cells
(A) Dose-dependent effect of MRTX849 on the proliferation <t>of</t> <t>MiaPaCa-2</t> and H358 cells based on live cell imaging. AsPC-1 cells were treated with different concentrations of MRTX1133, and the cell growth was monitored. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (B) Effect of the mutant-specific KRAS inhibitors, MRTX849 and MRTX1133 on the proliferation of MiaPaCa-2-MR, H358-MR and AsPC-1-MR cells that have developed acquired resistance following long-term selection. Mean and SD were determined from triplicates, and the experiments were carried out 3 independent times. (C) Live cell imaging to examine the effect of MRTX849 on the proliferation of UM53 and RS4774 cell lines. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (D) Western blot analysis on MiaPaCa-2-MR, UM53 and RS4774 cells to evaluate the effect of MRTX849 on ERK phosphorylation following 48-hour exposure at the indicated concentration. (E) Differential effects of KRAS knockdown on the proliferation of MiaPaCa-2-WT, AsPC-1-WT, MiaPaCa-2-MR, AsPC-1-MR and UM53 cells. Error bars indicate mean and SD from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. Experiments were done at three independent times. (F) In vivo efficacy of MRTX849 on xenografts derived from MiaPaCa-2-WT and MiaPaCa-2-MR cells and on the tumor growth of RS4774 PDX. Error bars represent mean and SEM. *** represents p<0.0001 as determined by 2-way ANOVA. (G) Representative images of immunohistochemical staining on the vehicle- and MRTX849-treated tissues to determine the phosphorylation status of ERK. Scale bar represents 50 microns.
Rpmi8226 Ffluc Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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95
ATCC clostridium
(A) Dose-dependent effect of MRTX849 on the proliferation <t>of</t> <t>MiaPaCa-2</t> and H358 cells based on live cell imaging. AsPC-1 cells were treated with different concentrations of MRTX1133, and the cell growth was monitored. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (B) Effect of the mutant-specific KRAS inhibitors, MRTX849 and MRTX1133 on the proliferation of MiaPaCa-2-MR, H358-MR and AsPC-1-MR cells that have developed acquired resistance following long-term selection. Mean and SD were determined from triplicates, and the experiments were carried out 3 independent times. (C) Live cell imaging to examine the effect of MRTX849 on the proliferation of UM53 and RS4774 cell lines. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (D) Western blot analysis on MiaPaCa-2-MR, UM53 and RS4774 cells to evaluate the effect of MRTX849 on ERK phosphorylation following 48-hour exposure at the indicated concentration. (E) Differential effects of KRAS knockdown on the proliferation of MiaPaCa-2-WT, AsPC-1-WT, MiaPaCa-2-MR, AsPC-1-MR and UM53 cells. Error bars indicate mean and SD from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. Experiments were done at three independent times. (F) In vivo efficacy of MRTX849 on xenografts derived from MiaPaCa-2-WT and MiaPaCa-2-MR cells and on the tumor growth of RS4774 PDX. Error bars represent mean and SEM. *** represents p<0.0001 as determined by 2-way ANOVA. (G) Representative images of immunohistochemical staining on the vehicle- and MRTX849-treated tissues to determine the phosphorylation status of ERK. Scale bar represents 50 microns.
Clostridium, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
ATCC mda mb 231 cells
The effect of SIRT1 knockdown in regulating the mRNA expression of CoQ10 biosynthetic enzymes levels and COQ6 protein <t>expression</t> <t>in</t> <t>MDA-MB-231</t> cells. (A) SIRT1 mRNA expression following SIRT1 knockdown for 4 days. MDA-MB-231 cells were seeded at a density of 2.5 × 10 5 cells/ml, and siRNA was transfected. After 48 ‍h of incubation, the medium and siRNA were replaced, followed by an additional 48 ‍h incubation. (B) SIRT1 and ACTB protein level following SIRT1 knockdown for 4 days. (C) SIRT1 mRNA expression following SIRT1 knockdown for 9 days. MDA-MB-231 cells were seeded at a density of 2.0 × 10 5 cells/ml and siRNA was transfected, followed by 72 ‍h of incubation. The cells were then passaged at a density of 1.5 × 10 5 cells/ml and incubated for another 72 ‍h. The medium and siRNA were replaced, and the cells were incubated for an additional 72 ‍h. (D) SIRT1 and ACTB protein level following SIRT1 knockdown for 9 days. (E, F) mRNA expression following SIRT1 knockdown for 4 days. (G, H) mRNA expression following SIRT1 knockdown for 9 days. Gene expression levels were corrected for ACTB . (I) COQ6 protein level following SIRT1 knockdown for 4 days. The ACTB used for normalization is the same as in (B). (J) COQ6 protein level following SIRT1 knockdown for 9 days. The ACTB used for normalization is the same as in (D). Statistical analysis was determined using Student’s t test. * p <0.05 and ** p <0.01 ( n = 3).
Mda Mb 231 Cells, 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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97
Macrocyclics Inc materials dota mono n hydroxysuccinimide ester
The effect of SIRT1 knockdown in regulating the mRNA expression of CoQ10 biosynthetic enzymes levels and COQ6 protein <t>expression</t> <t>in</t> <t>MDA-MB-231</t> cells. (A) SIRT1 mRNA expression following SIRT1 knockdown for 4 days. MDA-MB-231 cells were seeded at a density of 2.5 × 10 5 cells/ml, and siRNA was transfected. After 48 ‍h of incubation, the medium and siRNA were replaced, followed by an additional 48 ‍h incubation. (B) SIRT1 and ACTB protein level following SIRT1 knockdown for 4 days. (C) SIRT1 mRNA expression following SIRT1 knockdown for 9 days. MDA-MB-231 cells were seeded at a density of 2.0 × 10 5 cells/ml and siRNA was transfected, followed by 72 ‍h of incubation. The cells were then passaged at a density of 1.5 × 10 5 cells/ml and incubated for another 72 ‍h. The medium and siRNA were replaced, and the cells were incubated for an additional 72 ‍h. (D) SIRT1 and ACTB protein level following SIRT1 knockdown for 9 days. (E, F) mRNA expression following SIRT1 knockdown for 4 days. (G, H) mRNA expression following SIRT1 knockdown for 9 days. Gene expression levels were corrected for ACTB . (I) COQ6 protein level following SIRT1 knockdown for 4 days. The ACTB used for normalization is the same as in (B). (J) COQ6 protein level following SIRT1 knockdown for 9 days. The ACTB used for normalization is the same as in (D). Statistical analysis was determined using Student’s t test. * p <0.05 and ** p <0.01 ( n = 3).
Materials Dota Mono N Hydroxysuccinimide Ester, supplied by Macrocyclics Inc, 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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95
ATCC human pancreatic adenocarcinoma cells psn 1
A) Uptake of [ 123 I]Italia_A in <t>PSN-1</t> cells at different time points. B) Efflux of [ 123 I]Italia_A in PSN1 cells. C) Comparison of u ptake and blocking of [ 123 I]Italia_A, B and racemic mix. in PSN-1, cas1, KO cells after 1 hour exposure. D) Comparison of b locking of [ 123 I]Italia_A, B and racemic mix. uptake in PSN-1 cells by panel of PARP inhibitors.
Human Pancreatic Adenocarcinoma Cells Psn 1, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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97
ATCC human lung carcinoma epithelial cell line
Immunohistochemistry results (A) and Western blotting results and quantitative data (B, C) for TRIM72 expression in 7-day-old and 14-day-old rats in the normoxia and O 2 -enriched groups. TRIM72 immunoreactivity was observed in endothelial cells (black arrow), superior surface of bronchial <t>epithelial</t> cells (red arrow), and alveolar type I (short black arrow) and II cells (short red arrow). The normoxia group showed faint immunoreactivity in bronchial epithelial cells (red arrow) and alveolar type I (short black arrow) and II cells (short red arrow). The rats in the O 2 -enriched group exhibited significantly higher TRIM72 expression than those in the normoxia group on postnatal days 7 and 14. * p < 0.05.
Human Lung Carcinoma Epithelial Cell Line, 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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95
ATCC pseudomonas aeruginosa
Immunohistochemistry results (A) and Western blotting results and quantitative data (B, C) for TRIM72 expression in 7-day-old and 14-day-old rats in the normoxia and O 2 -enriched groups. TRIM72 immunoreactivity was observed in endothelial cells (black arrow), superior surface of bronchial <t>epithelial</t> cells (red arrow), and alveolar type I (short black arrow) and II cells (short red arrow). The normoxia group showed faint immunoreactivity in bronchial epithelial cells (red arrow) and alveolar type I (short black arrow) and II cells (short red arrow). The rats in the O 2 -enriched group exhibited significantly higher TRIM72 expression than those in the normoxia group on postnatal days 7 and 14. * p < 0.05.
Pseudomonas Aeruginosa, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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c33 a  (ATCC)
96
ATCC c33 a
Immunohistochemistry results (A) and Western blotting results and quantitative data (B, C) for TRIM72 expression in 7-day-old and 14-day-old rats in the normoxia and O 2 -enriched groups. TRIM72 immunoreactivity was observed in endothelial cells (black arrow), superior surface of bronchial <t>epithelial</t> cells (red arrow), and alveolar type I (short black arrow) and II cells (short red arrow). The normoxia group showed faint immunoreactivity in bronchial epithelial cells (red arrow) and alveolar type I (short black arrow) and II cells (short red arrow). The rats in the O 2 -enriched group exhibited significantly higher TRIM72 expression than those in the normoxia group on postnatal days 7 and 14. * p < 0.05.
C33 A, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


PlasDIC microscopy images (40× magnification) of HeLa cells after 72 hr incubation with ( A ) medium control, ( B ) solvent control (1% ethanol), ( C ) 10 µM 25(OH)D 3 , or ( D ) 250 µM calcipotriol.

Journal: Current Protocols

Article Title: Analysis of Reactive Oxygen Species–Induced Cellular Damage in Cervical Cancer

doi: 10.1002/cpz1.70328

Figure Lengend Snippet: PlasDIC microscopy images (40× magnification) of HeLa cells after 72 hr incubation with ( A ) medium control, ( B ) solvent control (1% ethanol), ( C ) 10 µM 25(OH)D 3 , or ( D ) 250 µM calcipotriol.

Article Snippet: HeLa cells (ATCC, cat. no. CCL‐2) Complete DMEM (see recipe) 1× PBS, pH 7.4 (see recipe) .25% trypsin‐EDTA (Sigma‐Aldrich, cat. no. T4049) .4% Cytiva‐LM‐trypan blue (Separations, cat. no. SV30084.01) 10 μM 25(OH)D 3 (see recipe) 25 mM calcipotriol (see recipe) Ethanol, ACS grade, 96%, without additive (Sigma‐Aldrich, cat. no. 02870) 1 mg/ml actinomycin D (Sigma‐Aldrich, cat. no. D8418) in DMSO T25 tissue culture flasks with vent screw caps (Separations, cat. no. TPP‐90025) Humidified 37°C, 5% CO 2 incubator (water jacket type; Astec Bio, model WCl‐165) Microscope (Zeiss Axiovert 5, Carl Zeiss Microscopy) Counting chambers Neubauer improved, bright‐lined (Separations, cat. no. 810_02_04) 6‐well clear, flat‐bottom, polystyrene tissue culture plates (Lasec, cat. no. P1PLA044C‐000006)

Techniques: Microscopy, Incubation, Control, Solvent

Transmission electron microscopy images of cellular and mitochondrial structure. HeLa cells were treated for 72 hr with ( A , E ) medium, ( B , F ) solvent (1% ethanol), ( C , G ) 10 µM 25(OH)D 3 , or ( D , H ) 250 µM calcipotriol. Scale bar: 2 µm ( A ‐ D ), 200 nm ( E , F , H ), 500 nm ( G ).

Journal: Current Protocols

Article Title: Analysis of Reactive Oxygen Species–Induced Cellular Damage in Cervical Cancer

doi: 10.1002/cpz1.70328

Figure Lengend Snippet: Transmission electron microscopy images of cellular and mitochondrial structure. HeLa cells were treated for 72 hr with ( A , E ) medium, ( B , F ) solvent (1% ethanol), ( C , G ) 10 µM 25(OH)D 3 , or ( D , H ) 250 µM calcipotriol. Scale bar: 2 µm ( A ‐ D ), 200 nm ( E , F , H ), 500 nm ( G ).

Article Snippet: HeLa cells (ATCC, cat. no. CCL‐2) Complete DMEM (see recipe) 1× PBS, pH 7.4 (see recipe) .25% trypsin‐EDTA (Sigma‐Aldrich, cat. no. T4049) .4% Cytiva‐LM‐trypan blue (Separations, cat. no. SV30084.01) 10 μM 25(OH)D 3 (see recipe) 25 mM calcipotriol (see recipe) Ethanol, ACS grade, 96%, without additive (Sigma‐Aldrich, cat. no. 02870) 1 mg/ml actinomycin D (Sigma‐Aldrich, cat. no. D8418) in DMSO T25 tissue culture flasks with vent screw caps (Separations, cat. no. TPP‐90025) Humidified 37°C, 5% CO 2 incubator (water jacket type; Astec Bio, model WCl‐165) Microscope (Zeiss Axiovert 5, Carl Zeiss Microscopy) Counting chambers Neubauer improved, bright‐lined (Separations, cat. no. 810_02_04) 6‐well clear, flat‐bottom, polystyrene tissue culture plates (Lasec, cat. no. P1PLA044C‐000006)

Techniques: Transmission Assay, Electron Microscopy, Solvent

Bar graph showing relative protein expression of AKT in HeLa cells. Protein levels were normalized to the loading control (β‐actin) and expressed relative to the solvent control. Corresponding immunoblots illustrate band patterns across treatment groups. Error bars represent the mean ± standard error of the mean across three passages of cells. p < .05 was considered significant. **** p < .0001.

Journal: Current Protocols

Article Title: Analysis of Reactive Oxygen Species–Induced Cellular Damage in Cervical Cancer

doi: 10.1002/cpz1.70328

Figure Lengend Snippet: Bar graph showing relative protein expression of AKT in HeLa cells. Protein levels were normalized to the loading control (β‐actin) and expressed relative to the solvent control. Corresponding immunoblots illustrate band patterns across treatment groups. Error bars represent the mean ± standard error of the mean across three passages of cells. p < .05 was considered significant. **** p < .0001.

Article Snippet: HeLa cells (ATCC, cat. no. CCL‐2) Complete DMEM (see recipe) 1× PBS, pH 7.4 (see recipe) .25% trypsin‐EDTA (Sigma‐Aldrich, cat. no. T4049) .4% Cytiva‐LM‐trypan blue (Separations, cat. no. SV30084.01) 10 μM 25(OH)D 3 (see recipe) 25 mM calcipotriol (see recipe) Ethanol, ACS grade, 96%, without additive (Sigma‐Aldrich, cat. no. 02870) 1 mg/ml actinomycin D (Sigma‐Aldrich, cat. no. D8418) in DMSO T25 tissue culture flasks with vent screw caps (Separations, cat. no. TPP‐90025) Humidified 37°C, 5% CO 2 incubator (water jacket type; Astec Bio, model WCl‐165) Microscope (Zeiss Axiovert 5, Carl Zeiss Microscopy) Counting chambers Neubauer improved, bright‐lined (Separations, cat. no. 810_02_04) 6‐well clear, flat‐bottom, polystyrene tissue culture plates (Lasec, cat. no. P1PLA044C‐000006)

Techniques: Expressing, Control, Solvent, Western Blot

(A) Dose-dependent effect of MRTX849 on the proliferation of MiaPaCa-2 and H358 cells based on live cell imaging. AsPC-1 cells were treated with different concentrations of MRTX1133, and the cell growth was monitored. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (B) Effect of the mutant-specific KRAS inhibitors, MRTX849 and MRTX1133 on the proliferation of MiaPaCa-2-MR, H358-MR and AsPC-1-MR cells that have developed acquired resistance following long-term selection. Mean and SD were determined from triplicates, and the experiments were carried out 3 independent times. (C) Live cell imaging to examine the effect of MRTX849 on the proliferation of UM53 and RS4774 cell lines. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (D) Western blot analysis on MiaPaCa-2-MR, UM53 and RS4774 cells to evaluate the effect of MRTX849 on ERK phosphorylation following 48-hour exposure at the indicated concentration. (E) Differential effects of KRAS knockdown on the proliferation of MiaPaCa-2-WT, AsPC-1-WT, MiaPaCa-2-MR, AsPC-1-MR and UM53 cells. Error bars indicate mean and SD from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. Experiments were done at three independent times. (F) In vivo efficacy of MRTX849 on xenografts derived from MiaPaCa-2-WT and MiaPaCa-2-MR cells and on the tumor growth of RS4774 PDX. Error bars represent mean and SEM. *** represents p<0.0001 as determined by 2-way ANOVA. (G) Representative images of immunohistochemical staining on the vehicle- and MRTX849-treated tissues to determine the phosphorylation status of ERK. Scale bar represents 50 microns.

Journal: bioRxiv

Article Title: Targeting Distinct Cell Cycle Nodes Overcomes KRAS/RAS Inhibitor Resistance

doi: 10.64898/2026.03.10.710937

Figure Lengend Snippet: (A) Dose-dependent effect of MRTX849 on the proliferation of MiaPaCa-2 and H358 cells based on live cell imaging. AsPC-1 cells were treated with different concentrations of MRTX1133, and the cell growth was monitored. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (B) Effect of the mutant-specific KRAS inhibitors, MRTX849 and MRTX1133 on the proliferation of MiaPaCa-2-MR, H358-MR and AsPC-1-MR cells that have developed acquired resistance following long-term selection. Mean and SD were determined from triplicates, and the experiments were carried out 3 independent times. (C) Live cell imaging to examine the effect of MRTX849 on the proliferation of UM53 and RS4774 cell lines. Error bars represent mean and SD from triplicates. Experiments were done at three independent times. (D) Western blot analysis on MiaPaCa-2-MR, UM53 and RS4774 cells to evaluate the effect of MRTX849 on ERK phosphorylation following 48-hour exposure at the indicated concentration. (E) Differential effects of KRAS knockdown on the proliferation of MiaPaCa-2-WT, AsPC-1-WT, MiaPaCa-2-MR, AsPC-1-MR and UM53 cells. Error bars indicate mean and SD from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. Experiments were done at three independent times. (F) In vivo efficacy of MRTX849 on xenografts derived from MiaPaCa-2-WT and MiaPaCa-2-MR cells and on the tumor growth of RS4774 PDX. Error bars represent mean and SEM. *** represents p<0.0001 as determined by 2-way ANOVA. (G) Representative images of immunohistochemical staining on the vehicle- and MRTX849-treated tissues to determine the phosphorylation status of ERK. Scale bar represents 50 microns.

Article Snippet: MiaPaCa-2 cells were purchased from the ATCC and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% FBS and 1% antibiotic–antimycotic.

Techniques: Live Cell Imaging, Mutagenesis, Selection, Western Blot, Phospho-proteomics, Concentration Assay, Knockdown, In Vivo, Derivative Assay, Immunohistochemical staining, Staining

(A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and cyclin A expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.

Journal: bioRxiv

Article Title: Targeting Distinct Cell Cycle Nodes Overcomes KRAS/RAS Inhibitor Resistance

doi: 10.64898/2026.03.10.710937

Figure Lengend Snippet: (A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and cyclin A expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.

Article Snippet: MiaPaCa-2 cells were purchased from the ATCC and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% FBS and 1% antibiotic–antimycotic.

Techniques: Phospho-proteomics, Expressing, Mutagenesis

(A) Comparison of the antiproliferative effects of mutant-selective KRAS inhibitors and RMC-6236 in the indicated cell lines. Error bars represent mean and SD from triplicates. Experiments were done 3 independent times. *** represents p<0.0001 as determined by 2-way ANOVA. (B) EC 50 values of mutant specific KRAS inhibitors and RMC-6236 in multiple cell lines. Error bar represents mean and SD from 2 independent experiments. *** represents p<0.0001 as determined by unpaired student t-test. (C) GSEA analysis highlighting the top pathways that were differentially impacted in AsPC-1-MR cells following the treatment with MRTX1133 (100 nM) and RMC-6236 (50 nM) for 48 hours. (D) Heatmap depicts the differential expression of the indicated genes associated with MEK, MTOR and cell cycle pathways following the treatment with MRTX1133 and RMC-6236 in AsPC-1-MR cells. (E) Immunoblot analysis comparing the effect of mutant-specific KRAS inhibitors and RMC-62366 on the indicated proteins after exposing the cells to different drug concentrations up to 48 hours. (F) Long term colony formation assay in AsPC-MR and MiaPaCa-2-MR cells following the treatment with RMC-6236. AsPC-1-MR cells were treated with 50 nM RMC-6236 for 19 days and MiaPaCa-2-MR cells were treated 100 nM of RMC-6236 for 9 days. (G) Differential effect of RMC-6236 on the proliferation of MiaPaCa-2-WT and MiaPaCa-2-RR cells following the treatment with different drug concentrations. Error bars represent mean and SD from triplicates. Experiment was done at 3 independent times. (H) Biochemical analysis to compare the effect of RMC-6236 on the indicated proteins between the MiaPaCa-2-WT and MiaPaCa-2-RR cells following 48-hour exposure.

Journal: bioRxiv

Article Title: Targeting Distinct Cell Cycle Nodes Overcomes KRAS/RAS Inhibitor Resistance

doi: 10.64898/2026.03.10.710937

Figure Lengend Snippet: (A) Comparison of the antiproliferative effects of mutant-selective KRAS inhibitors and RMC-6236 in the indicated cell lines. Error bars represent mean and SD from triplicates. Experiments were done 3 independent times. *** represents p<0.0001 as determined by 2-way ANOVA. (B) EC 50 values of mutant specific KRAS inhibitors and RMC-6236 in multiple cell lines. Error bar represents mean and SD from 2 independent experiments. *** represents p<0.0001 as determined by unpaired student t-test. (C) GSEA analysis highlighting the top pathways that were differentially impacted in AsPC-1-MR cells following the treatment with MRTX1133 (100 nM) and RMC-6236 (50 nM) for 48 hours. (D) Heatmap depicts the differential expression of the indicated genes associated with MEK, MTOR and cell cycle pathways following the treatment with MRTX1133 and RMC-6236 in AsPC-1-MR cells. (E) Immunoblot analysis comparing the effect of mutant-specific KRAS inhibitors and RMC-62366 on the indicated proteins after exposing the cells to different drug concentrations up to 48 hours. (F) Long term colony formation assay in AsPC-MR and MiaPaCa-2-MR cells following the treatment with RMC-6236. AsPC-1-MR cells were treated with 50 nM RMC-6236 for 19 days and MiaPaCa-2-MR cells were treated 100 nM of RMC-6236 for 9 days. (G) Differential effect of RMC-6236 on the proliferation of MiaPaCa-2-WT and MiaPaCa-2-RR cells following the treatment with different drug concentrations. Error bars represent mean and SD from triplicates. Experiment was done at 3 independent times. (H) Biochemical analysis to compare the effect of RMC-6236 on the indicated proteins between the MiaPaCa-2-WT and MiaPaCa-2-RR cells following 48-hour exposure.

Article Snippet: MiaPaCa-2 cells were purchased from the ATCC and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% FBS and 1% antibiotic–antimycotic.

Techniques: Comparison, Mutagenesis, Quantitative Proteomics, Western Blot, Colony Assay

Venn diagram showing drugs that enhanced the efficacy of mutant-selective KRAS inhibitors in MiaPaCa-2-MR, AsPC-1-MR, and UM53 cells, identified through combinatorial drug screening. Common hits included the CDK4/6 inhibitors palbociclib, abemaciclib, and G1T38. Correlation plot comparing the fold change in growth rate for individual drugs in combination with DMSO or mutant-selective KRAS inhibitors. (B) Synergistic interactions between palbociclib and KRAS or RAS inhibitors in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Isobolograms were generated based on normalized fold change in growth rate following treatment with increasing concentrations of palbociclib in combination with KRAS or RAS inhibitors. Bliss synergy scores were calculated using the SynergyFinder online platform. (C) Western blot analysis in MiaPaCa-2-MR, UM53 and RS4774 following the treatment with palbociclib (100 nM) in combination with MRTX849 (250 nM) up to 48 hours. AsPC-1-MR cells were treated with palbociclib (100 nM) in combination with MRTX1133 (250 nM). (D) Western blotting in UM53 cells to examine the effect of palbociclib (100 nM) in combination with the RAS inhibitor, RMC-6236 (25 nM) on the cell cycle proteins following 48-hour treatment. (E) Effect of Palbociclib in combination with MRTX849 on the growth of spheroids derived from MiaPaCa-2-MR and UM53 cells. Error bars represent mean and SEM from triplicates. *** represents p<0.0001 and ** represents p<0.001 as determined by 2-way ANOVA. Experiments were done at 3 independent times.

Journal: bioRxiv

Article Title: Targeting Distinct Cell Cycle Nodes Overcomes KRAS/RAS Inhibitor Resistance

doi: 10.64898/2026.03.10.710937

Figure Lengend Snippet: Venn diagram showing drugs that enhanced the efficacy of mutant-selective KRAS inhibitors in MiaPaCa-2-MR, AsPC-1-MR, and UM53 cells, identified through combinatorial drug screening. Common hits included the CDK4/6 inhibitors palbociclib, abemaciclib, and G1T38. Correlation plot comparing the fold change in growth rate for individual drugs in combination with DMSO or mutant-selective KRAS inhibitors. (B) Synergistic interactions between palbociclib and KRAS or RAS inhibitors in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Isobolograms were generated based on normalized fold change in growth rate following treatment with increasing concentrations of palbociclib in combination with KRAS or RAS inhibitors. Bliss synergy scores were calculated using the SynergyFinder online platform. (C) Western blot analysis in MiaPaCa-2-MR, UM53 and RS4774 following the treatment with palbociclib (100 nM) in combination with MRTX849 (250 nM) up to 48 hours. AsPC-1-MR cells were treated with palbociclib (100 nM) in combination with MRTX1133 (250 nM). (D) Western blotting in UM53 cells to examine the effect of palbociclib (100 nM) in combination with the RAS inhibitor, RMC-6236 (25 nM) on the cell cycle proteins following 48-hour treatment. (E) Effect of Palbociclib in combination with MRTX849 on the growth of spheroids derived from MiaPaCa-2-MR and UM53 cells. Error bars represent mean and SEM from triplicates. *** represents p<0.0001 and ** represents p<0.001 as determined by 2-way ANOVA. Experiments were done at 3 independent times.

Article Snippet: MiaPaCa-2 cells were purchased from the ATCC and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% FBS and 1% antibiotic–antimycotic.

Techniques: Mutagenesis, Drug discovery, Generated, Western Blot, Derivative Assay

(A) Live cell imaging to monitor the proliferation of MiaPaCa-2-MR, AsPC-1-MR and UM53 cells following the treatment with INX-315 in combination with mutant-specific KRAS inhibitors. The effect of INX-315 in combination with RMC-6236 on the proliferation of MiaPaCa-2-MR and UM53 cells. Error bars represent mean and SD from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. (B) The impact of INX-315 in combination with MRTX849 on the growth of spheroids derived from MiaPaCa-2-MR cells. Error bars were determined from mean and SEM from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. Experiment was done at 3 independent times. Representative images of the spheroids from MiaPaCa-2-MR cells. (C) Western blotting on the indicated proteins from MiaPaCa-2-MR, UM53 and RS4774 cells following the treatment with INX-315 in combination with MRTX849 up to 48 hours. (D) Stack plots illustrating the % of cell population at each phase of cell cycle based on PI profile following the treatment with MRTX849 in combination palbociclib or INX-315. (E) Bivariate flow cytometry analysis of UM53 cells showing the effects of palbociclib or INX-315 in combination with MRTX849 or RMC-6236 on BrdU incorporation. (F) Immunofluorescence analysis of phospho–histone H3 (S10) in UM53 cells pretreated with DMSO or INX-315 in combination with MRTX849 for 48 hours and subsequently treated with nocodazole (250 nM) for 24 hours. Scale bar represents 75 microns. (G) Comparison of cellular outgrowth in the indicated cell lines following removal of KRAS or RAS inhibitors in combination with palbociclib or INX-315 after 4 days of treatment. Error bars represent mean and SD from triplicates. *** represent p<0.0001 as determined by 2-way ANOVA.

Journal: bioRxiv

Article Title: Targeting Distinct Cell Cycle Nodes Overcomes KRAS/RAS Inhibitor Resistance

doi: 10.64898/2026.03.10.710937

Figure Lengend Snippet: (A) Live cell imaging to monitor the proliferation of MiaPaCa-2-MR, AsPC-1-MR and UM53 cells following the treatment with INX-315 in combination with mutant-specific KRAS inhibitors. The effect of INX-315 in combination with RMC-6236 on the proliferation of MiaPaCa-2-MR and UM53 cells. Error bars represent mean and SD from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. (B) The impact of INX-315 in combination with MRTX849 on the growth of spheroids derived from MiaPaCa-2-MR cells. Error bars were determined from mean and SEM from triplicates. *** represents p<0.0001 as determined by 2-way ANOVA. Experiment was done at 3 independent times. Representative images of the spheroids from MiaPaCa-2-MR cells. (C) Western blotting on the indicated proteins from MiaPaCa-2-MR, UM53 and RS4774 cells following the treatment with INX-315 in combination with MRTX849 up to 48 hours. (D) Stack plots illustrating the % of cell population at each phase of cell cycle based on PI profile following the treatment with MRTX849 in combination palbociclib or INX-315. (E) Bivariate flow cytometry analysis of UM53 cells showing the effects of palbociclib or INX-315 in combination with MRTX849 or RMC-6236 on BrdU incorporation. (F) Immunofluorescence analysis of phospho–histone H3 (S10) in UM53 cells pretreated with DMSO or INX-315 in combination with MRTX849 for 48 hours and subsequently treated with nocodazole (250 nM) for 24 hours. Scale bar represents 75 microns. (G) Comparison of cellular outgrowth in the indicated cell lines following removal of KRAS or RAS inhibitors in combination with palbociclib or INX-315 after 4 days of treatment. Error bars represent mean and SD from triplicates. *** represent p<0.0001 as determined by 2-way ANOVA.

Article Snippet: MiaPaCa-2 cells were purchased from the ATCC and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% FBS and 1% antibiotic–antimycotic.

Techniques: Live Cell Imaging, Mutagenesis, Derivative Assay, Western Blot, Flow Cytometry, BrdU Incorporation Assay, Immunofluorescence, Comparison

(A) In vivo effect of palbociclib in combination with MRTX849 on tumor growth in MiaPaCa-2-MR xenografts and RS4774 PDX. Error bars were determined based on mean and SEM. *** represents p value <0.0001 as determined by 2-way ANOVA. (B) Column graphs illustrate the tumor weights from MiaPaCa-2-MR xenografts and RS4774 PDX following the treatment with palbociclib in combination with MRTX849. *** p<0.0001, ** p<0.01 as determined by unpaired student t-test. (C) Effect of palbociclib in combination with MRTX849 on the mice body weights. Error bar represents mean and SEM. (D) Immunohistochemical analysis of RB phosphorylation in tumor tissues from MiaPaCa-2-MR xenografts and RS4774 PDX models following treatment with palbociclib in combination with MRTX849. Corresponding H&E-stained sections are shown. Scale bar represents 100 microns. (E) Effect of INX-315 in combination MRTX849 on tumor progression in mice bearing MiaPaCa-2-MR xenografts. The change in mice body weights following the combination treatment was monitored. (F) Immunohistochemical analysis of phospho-RB and phospho–histone H3 in tumor tissues following 5 days of treatment with palbociclib or INX-315 in combination with MRTX849. Scale bar represents 100 microns.

Journal: bioRxiv

Article Title: Targeting Distinct Cell Cycle Nodes Overcomes KRAS/RAS Inhibitor Resistance

doi: 10.64898/2026.03.10.710937

Figure Lengend Snippet: (A) In vivo effect of palbociclib in combination with MRTX849 on tumor growth in MiaPaCa-2-MR xenografts and RS4774 PDX. Error bars were determined based on mean and SEM. *** represents p value <0.0001 as determined by 2-way ANOVA. (B) Column graphs illustrate the tumor weights from MiaPaCa-2-MR xenografts and RS4774 PDX following the treatment with palbociclib in combination with MRTX849. *** p<0.0001, ** p<0.01 as determined by unpaired student t-test. (C) Effect of palbociclib in combination with MRTX849 on the mice body weights. Error bar represents mean and SEM. (D) Immunohistochemical analysis of RB phosphorylation in tumor tissues from MiaPaCa-2-MR xenografts and RS4774 PDX models following treatment with palbociclib in combination with MRTX849. Corresponding H&E-stained sections are shown. Scale bar represents 100 microns. (E) Effect of INX-315 in combination MRTX849 on tumor progression in mice bearing MiaPaCa-2-MR xenografts. The change in mice body weights following the combination treatment was monitored. (F) Immunohistochemical analysis of phospho-RB and phospho–histone H3 in tumor tissues following 5 days of treatment with palbociclib or INX-315 in combination with MRTX849. Scale bar represents 100 microns.

Article Snippet: MiaPaCa-2 cells were purchased from the ATCC and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% FBS and 1% antibiotic–antimycotic.

Techniques: In Vivo, Immunohistochemical staining, Phospho-proteomics, Staining

The effect of SIRT1 knockdown in regulating the mRNA expression of CoQ10 biosynthetic enzymes levels and COQ6 protein expression in MDA-MB-231 cells. (A) SIRT1 mRNA expression following SIRT1 knockdown for 4 days. MDA-MB-231 cells were seeded at a density of 2.5 × 10 5 cells/ml, and siRNA was transfected. After 48 ‍h of incubation, the medium and siRNA were replaced, followed by an additional 48 ‍h incubation. (B) SIRT1 and ACTB protein level following SIRT1 knockdown for 4 days. (C) SIRT1 mRNA expression following SIRT1 knockdown for 9 days. MDA-MB-231 cells were seeded at a density of 2.0 × 10 5 cells/ml and siRNA was transfected, followed by 72 ‍h of incubation. The cells were then passaged at a density of 1.5 × 10 5 cells/ml and incubated for another 72 ‍h. The medium and siRNA were replaced, and the cells were incubated for an additional 72 ‍h. (D) SIRT1 and ACTB protein level following SIRT1 knockdown for 9 days. (E, F) mRNA expression following SIRT1 knockdown for 4 days. (G, H) mRNA expression following SIRT1 knockdown for 9 days. Gene expression levels were corrected for ACTB . (I) COQ6 protein level following SIRT1 knockdown for 4 days. The ACTB used for normalization is the same as in (B). (J) COQ6 protein level following SIRT1 knockdown for 9 days. The ACTB used for normalization is the same as in (D). Statistical analysis was determined using Student’s t test. * p <0.05 and ** p <0.01 ( n = 3).

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: The effect of SIRT1 knockdown on the gene expression of CoQ10 biosynthetic enzymes

doi: 10.3164/jcbn.24-239

Figure Lengend Snippet: The effect of SIRT1 knockdown in regulating the mRNA expression of CoQ10 biosynthetic enzymes levels and COQ6 protein expression in MDA-MB-231 cells. (A) SIRT1 mRNA expression following SIRT1 knockdown for 4 days. MDA-MB-231 cells were seeded at a density of 2.5 × 10 5 cells/ml, and siRNA was transfected. After 48 ‍h of incubation, the medium and siRNA were replaced, followed by an additional 48 ‍h incubation. (B) SIRT1 and ACTB protein level following SIRT1 knockdown for 4 days. (C) SIRT1 mRNA expression following SIRT1 knockdown for 9 days. MDA-MB-231 cells were seeded at a density of 2.0 × 10 5 cells/ml and siRNA was transfected, followed by 72 ‍h of incubation. The cells were then passaged at a density of 1.5 × 10 5 cells/ml and incubated for another 72 ‍h. The medium and siRNA were replaced, and the cells were incubated for an additional 72 ‍h. (D) SIRT1 and ACTB protein level following SIRT1 knockdown for 9 days. (E, F) mRNA expression following SIRT1 knockdown for 4 days. (G, H) mRNA expression following SIRT1 knockdown for 9 days. Gene expression levels were corrected for ACTB . (I) COQ6 protein level following SIRT1 knockdown for 4 days. The ACTB used for normalization is the same as in (B). (J) COQ6 protein level following SIRT1 knockdown for 9 days. The ACTB used for normalization is the same as in (D). Statistical analysis was determined using Student’s t test. * p <0.05 and ** p <0.01 ( n = 3).

Article Snippet: MDA-MB-231 cells were purchased from ATCC (#HTB-26; ATCC, Manassas, VA) and cultured in Leibovitz’s L-15 medium supplemented with 15% FBS, 1% penicillin-streptomycin solution, and 0.075% NaHCO 3 .

Techniques: Knockdown, Expressing, Transfection, Incubation, Gene Expression

Long-term SIRT1 knockdown increased CoQ10 levels in MDA-MB-231 cells. (A–D) Effects of SIRT1 knockdown for 4 days. (A) Total protein level in the culture dish quantified using the BCA method. (B, C) Total CoQ10 levels normalized to total protein (B) or free cholesterol (FC) levels (C). The shaded lines represent oxidized CoQ10, and white bars represent reduced CoQ10. (D) FC level normalized to total protein. (E–H) Effects of SIRT1 knockdown for 9 days. (E) Total protein level in the culture dish. (F, G) Total CoQ10 levels normalized to total protein (F) or FC levels (G). The shaded lines represent oxidized CoQ10, and white bars represent reduced CoQ10. Statistical analysis was determined using Student’s t test. Values are represented as mean ± SD ( n = 3) of the data obtained from three independent experiments. * p <0.05 compared with control Total CoQ10 levels. # p <0.05 compared with negative control reduced CoQ10 levels.

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: The effect of SIRT1 knockdown on the gene expression of CoQ10 biosynthetic enzymes

doi: 10.3164/jcbn.24-239

Figure Lengend Snippet: Long-term SIRT1 knockdown increased CoQ10 levels in MDA-MB-231 cells. (A–D) Effects of SIRT1 knockdown for 4 days. (A) Total protein level in the culture dish quantified using the BCA method. (B, C) Total CoQ10 levels normalized to total protein (B) or free cholesterol (FC) levels (C). The shaded lines represent oxidized CoQ10, and white bars represent reduced CoQ10. (D) FC level normalized to total protein. (E–H) Effects of SIRT1 knockdown for 9 days. (E) Total protein level in the culture dish. (F, G) Total CoQ10 levels normalized to total protein (F) or FC levels (G). The shaded lines represent oxidized CoQ10, and white bars represent reduced CoQ10. Statistical analysis was determined using Student’s t test. Values are represented as mean ± SD ( n = 3) of the data obtained from three independent experiments. * p <0.05 compared with control Total CoQ10 levels. # p <0.05 compared with negative control reduced CoQ10 levels.

Article Snippet: MDA-MB-231 cells were purchased from ATCC (#HTB-26; ATCC, Manassas, VA) and cultured in Leibovitz’s L-15 medium supplemented with 15% FBS, 1% penicillin-streptomycin solution, and 0.075% NaHCO 3 .

Techniques: Knockdown, Control, Negative Control

The effect of PGC-1α and NRF1 knockdown in regulating the mRNA expression of CoQ10 biosynthetic enzymes and CoQ10 levels in MDA-MB-231 cells. (A, B) Relative mRNA expression due to PGC-1α knockdown. (C) Total protein level in the culture dish by BCA method of PGC-1α knockdown. (D, E) Total CoQ10 levels of PGC-1α knockdown normalized to total protein (D) or free cholesterol (FC) levels (E). The shaded lines represent oxidized CoQ10, and white bars represent reduced CoQ10. (F) FC level normalized to total protein. (G, H) Relative mRNA expression due to NRF1 knockdown. (I) Total protein level in the culture dish of NRF1 knockdown. (J, K) Total CoQ10 levels of NRF1 knockdown normalized to total protein (J) or FC levels (K). The shaded lines represent oxidized CoQ10, and white bars represent reduced CoQ10. (L) FC level normalized to total protein. MDA-MB-231 cells were seeded at a density of 1.0 × 10 5 cells/ml, and siRNA was transfected, followed by 96 ‍h of incubation. Statistical analysis was determined using Student’s t test. * p <0.05 and ** p <0.01 ( n = 3). # p <0.05 and ## p <0.01 compared with negative control reductive CoQ10 levels. † p <0.05 compared with negative control oxidized CoQ10 levels.

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: The effect of SIRT1 knockdown on the gene expression of CoQ10 biosynthetic enzymes

doi: 10.3164/jcbn.24-239

Figure Lengend Snippet: The effect of PGC-1α and NRF1 knockdown in regulating the mRNA expression of CoQ10 biosynthetic enzymes and CoQ10 levels in MDA-MB-231 cells. (A, B) Relative mRNA expression due to PGC-1α knockdown. (C) Total protein level in the culture dish by BCA method of PGC-1α knockdown. (D, E) Total CoQ10 levels of PGC-1α knockdown normalized to total protein (D) or free cholesterol (FC) levels (E). The shaded lines represent oxidized CoQ10, and white bars represent reduced CoQ10. (F) FC level normalized to total protein. (G, H) Relative mRNA expression due to NRF1 knockdown. (I) Total protein level in the culture dish of NRF1 knockdown. (J, K) Total CoQ10 levels of NRF1 knockdown normalized to total protein (J) or FC levels (K). The shaded lines represent oxidized CoQ10, and white bars represent reduced CoQ10. (L) FC level normalized to total protein. MDA-MB-231 cells were seeded at a density of 1.0 × 10 5 cells/ml, and siRNA was transfected, followed by 96 ‍h of incubation. Statistical analysis was determined using Student’s t test. * p <0.05 and ** p <0.01 ( n = 3). # p <0.05 and ## p <0.01 compared with negative control reductive CoQ10 levels. † p <0.05 compared with negative control oxidized CoQ10 levels.

Article Snippet: MDA-MB-231 cells were purchased from ATCC (#HTB-26; ATCC, Manassas, VA) and cultured in Leibovitz’s L-15 medium supplemented with 15% FBS, 1% penicillin-streptomycin solution, and 0.075% NaHCO 3 .

Techniques: Knockdown, Expressing, Transfection, Incubation, Negative Control

Proposed mechanism of increased CoQ10 content by SIRT1 knockdown in MDA-MB-231 cells.

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: The effect of SIRT1 knockdown on the gene expression of CoQ10 biosynthetic enzymes

doi: 10.3164/jcbn.24-239

Figure Lengend Snippet: Proposed mechanism of increased CoQ10 content by SIRT1 knockdown in MDA-MB-231 cells.

Article Snippet: MDA-MB-231 cells were purchased from ATCC (#HTB-26; ATCC, Manassas, VA) and cultured in Leibovitz’s L-15 medium supplemented with 15% FBS, 1% penicillin-streptomycin solution, and 0.075% NaHCO 3 .

Techniques: Knockdown

A) Uptake of [ 123 I]Italia_A in PSN-1 cells at different time points. B) Efflux of [ 123 I]Italia_A in PSN1 cells. C) Comparison of u ptake and blocking of [ 123 I]Italia_A, B and racemic mix. in PSN-1, cas1, KO cells after 1 hour exposure. D) Comparison of b locking of [ 123 I]Italia_A, B and racemic mix. uptake in PSN-1 cells by panel of PARP inhibitors.

Journal: bioRxiv

Article Title: [ 123 I]Italia: A PARP-Directed Auger Electron-Emitting Agent for Targeted Radionuclide Therapy of Cancer

doi: 10.64898/2026.03.13.711622

Figure Lengend Snippet: A) Uptake of [ 123 I]Italia_A in PSN-1 cells at different time points. B) Efflux of [ 123 I]Italia_A in PSN1 cells. C) Comparison of u ptake and blocking of [ 123 I]Italia_A, B and racemic mix. in PSN-1, cas1, KO cells after 1 hour exposure. D) Comparison of b locking of [ 123 I]Italia_A, B and racemic mix. uptake in PSN-1 cells by panel of PARP inhibitors.

Article Snippet: Human pancreatic adenocarcinoma cells (PSN-1), and human prostate cancer cells (PC-3) were purchased from ATCC; the murine breast cancer cell line 4T1 was a kind gift from prof. Nicola Sibson, Department of Oncology, University of Oxford.

Techniques: Comparison, Blocking Assay

A) IC 50 in PSN-1 cells (IC 50 : 2.85 nM, 95%CI: 1.98 nM-4.08 nM, R squared: 0.984 (of [ 123 I]Italia), IC 50 : 1.36 nM, 95%CI: 0.5 nM −3.67 nM, R squared: 0.899 of [ 123 I]Italia_B), IC50: 2.96 nM, 95%CI: 1.1 nM-7.9 nM, R 2 : 0.970 (of racemic mix.). B ) Cell fractionation of [ 123 I]Italia_A in PSN-1 cells: western blot. C) Cell fractionation of [ 123 I]Italia_A in different cell lines. In membrane bound fraction. D) Cytoplasm soluble fraction. E) Chromatin soluble fraction. F) Nuclear soluble fraction.

Journal: bioRxiv

Article Title: [ 123 I]Italia: A PARP-Directed Auger Electron-Emitting Agent for Targeted Radionuclide Therapy of Cancer

doi: 10.64898/2026.03.13.711622

Figure Lengend Snippet: A) IC 50 in PSN-1 cells (IC 50 : 2.85 nM, 95%CI: 1.98 nM-4.08 nM, R squared: 0.984 (of [ 123 I]Italia), IC 50 : 1.36 nM, 95%CI: 0.5 nM −3.67 nM, R squared: 0.899 of [ 123 I]Italia_B), IC50: 2.96 nM, 95%CI: 1.1 nM-7.9 nM, R 2 : 0.970 (of racemic mix.). B ) Cell fractionation of [ 123 I]Italia_A in PSN-1 cells: western blot. C) Cell fractionation of [ 123 I]Italia_A in different cell lines. In membrane bound fraction. D) Cytoplasm soluble fraction. E) Chromatin soluble fraction. F) Nuclear soluble fraction.

Article Snippet: Human pancreatic adenocarcinoma cells (PSN-1), and human prostate cancer cells (PC-3) were purchased from ATCC; the murine breast cancer cell line 4T1 was a kind gift from prof. Nicola Sibson, Department of Oncology, University of Oxford.

Techniques: Cell Fractionation, Western Blot, Membrane

A) Clonogenic survival of PSN-1 and PARP1 knock out cells (PSN-1 PARP1−/− ) after exposure of cells for 1h to [ 123 I]Italia_rac, and the separated enantiomers of [ 123 I]Italia_A or _B (0-500 kBq in 2 mL of growth medium). B) Clonogenic survival of various cell lines after exposure of cells for 1h to [ 123 I]Italia_A (0-500 kBq in 2mL of growth medium).

Journal: bioRxiv

Article Title: [ 123 I]Italia: A PARP-Directed Auger Electron-Emitting Agent for Targeted Radionuclide Therapy of Cancer

doi: 10.64898/2026.03.13.711622

Figure Lengend Snippet: A) Clonogenic survival of PSN-1 and PARP1 knock out cells (PSN-1 PARP1−/− ) after exposure of cells for 1h to [ 123 I]Italia_rac, and the separated enantiomers of [ 123 I]Italia_A or _B (0-500 kBq in 2 mL of growth medium). B) Clonogenic survival of various cell lines after exposure of cells for 1h to [ 123 I]Italia_A (0-500 kBq in 2mL of growth medium).

Article Snippet: Human pancreatic adenocarcinoma cells (PSN-1), and human prostate cancer cells (PC-3) were purchased from ATCC; the murine breast cancer cell line 4T1 was a kind gift from prof. Nicola Sibson, Department of Oncology, University of Oxford.

Techniques: Knock-Out

Immunohistochemistry results (A) and Western blotting results and quantitative data (B, C) for TRIM72 expression in 7-day-old and 14-day-old rats in the normoxia and O 2 -enriched groups. TRIM72 immunoreactivity was observed in endothelial cells (black arrow), superior surface of bronchial epithelial cells (red arrow), and alveolar type I (short black arrow) and II cells (short red arrow). The normoxia group showed faint immunoreactivity in bronchial epithelial cells (red arrow) and alveolar type I (short black arrow) and II cells (short red arrow). The rats in the O 2 -enriched group exhibited significantly higher TRIM72 expression than those in the normoxia group on postnatal days 7 and 14. * p < 0.05.

Journal: Journal of the Chinese Medical Association : JCMA

Article Title: TRIM72 mediates lung epithelial cell death upon hyperoxia exposure

doi: 10.1097/JCMA.0000000000000413

Figure Lengend Snippet: Immunohistochemistry results (A) and Western blotting results and quantitative data (B, C) for TRIM72 expression in 7-day-old and 14-day-old rats in the normoxia and O 2 -enriched groups. TRIM72 immunoreactivity was observed in endothelial cells (black arrow), superior surface of bronchial epithelial cells (red arrow), and alveolar type I (short black arrow) and II cells (short red arrow). The normoxia group showed faint immunoreactivity in bronchial epithelial cells (red arrow) and alveolar type I (short black arrow) and II cells (short red arrow). The rats in the O 2 -enriched group exhibited significantly higher TRIM72 expression than those in the normoxia group on postnatal days 7 and 14. * p < 0.05.

Article Snippet: RLE-6TN, a rat alveolar type II epithelial cell line, and A549, a human lung carcinoma epithelial cell line (ATCC, Manassas, VA, USA), were maintained in an F-12 medium in 75-cm 2 tissue culture flasks at 37.8°C in 5% CO 2 and 95% air.

Techniques: Immunohistochemistry, Western Blot, Expressing