Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: The hypothetical pathway of this study. All the important molecular and pathways were indicated. Briefly, AMPK is a preferential substrate of Compound C than Akt in normal conditions. When TiO₂ NZs were added to cells, they inhibited the expression of AMPK and mTOR proteins, then with extra addition of Compound C or phenformin turned to inhibit the candidate target of Akt, and exerted contrary effects on regulating autophagy

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Expressing

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Contrasted effects of Compound C and phenformin on TiO₂ NZs–induced fetal growth impairment and placental cell energy/autophagy responses. ( A ) Representative fetal images and corresponding average fetal length and average fetal weight in the control, TiO₂ NZs, TiO₂ NZs + phenformin, and TiO₂ NZs + Compound C groups. ( B ) Immunofluorescence analysis of autophagy levels in HTR cells following exposure to 100 µg/mL TiO₂ NZs or 100 µg/mL bulk-TiO₂. ( C ) Corresponding cellular ATP levels measured after exposure to TiO₂ NZs and bulk-TiO₂. ( D - E ) Immunofluorescence analysis of autophagy levels following exposure to 100 µg/mL TiO₂ NZs or 100 µg/mL b-TiO₂, either alone or in combination with Compound C/phenformin. Cell nuclei were stained blue with DAPI, and autophagosomes were labeled red using CY3-conjugated secondary antibodies.Scale bar = 20 μm. ( F ) Uptake and location of TiO₂ NZs in HTR-8/Svneo (HTR) cells observed by TEM after cells were treated with 100 µg/mL of TiO₂ NZs. The TiO₂ NZs were indicated by red arrows. ( G ) The morphology of mitochondria observed by TEM after cells were exposed to 100 µg/mL of TiO₂ NZs. Normal or swollen mitochondria were indicated by red arrows, respectively. Data are expressed as mean ± SD. A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for ( A ). One-way ANOVA was used for ( C ). ** P < 0.01, *** P < 0.001 vs. control group; $ P < 0.05 TiO₂ NZs + phenformin vs. TiO₂ NZs group; # P < 0.05 TiO₂ NZs + Compound C vs. TiO₂ NZs group

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Control, Immunofluorescence, Staining, Labeling, Comparison

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Autophagosome accumulation and its modulation by Compound C and phenformin in placental cells. ( A - C ) Cell autophagy levels were assessed by immunofluorescence and observed using a confocal microscope after cells received corresponding treatments. ( D , E ) Cell autophagy levels were assessed by immunofluorescence after HTR cells were treated with Compound C and phenformin in the absence of TiO₂ NZs. ( F ) Autophagy levels were examined after Compound C was added to the starvation-induced autophagy group. Cell nuclei were stained with DAPI (blue), and autophagosomes were labeled with CY3-conjugated secondary antibodies (red). Scale bar = 100 μm

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Immunofluorescence, Microscopy, Staining, Labeling

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Compound C and phenformin differentially regulate AMPK/mTOR signaling and exhibit distinct binding modes to AKT1.( A ) Western blot analysis of AMPK, p-AMPK, mTOR, and p-mTOR expression levels in cells treated with 100 µg/mL TiO₂ NZs. ( B ) Western blot analysis of AMPK and p-AMPK expression levels in cells treated with TiO₂ NZs, either alone or in combination with Compound C or phenformin. ( C , D ) Western blot analysis of AMPK and p-AMPK expression levels in cells treated with Compound C ( C ) and phenformin ( D ). GAPDH served as a loading control. Molecular weights (kDa) are indicated beside the bands.Quantitative densitometric analysis corresponding to the western blots in ( A – D ) was performed using ImageJ software. All bands were normalized to GAPDH expression, and the tests were repeated three times. ( E ) Chemical structures of ATP-competitive AKT1 inhibitors. ( F ) Chemical structures of allosteric (auto-inhibitory) AKT1 inhibitors. ( G ) Docking conformation of Compound C at the interface of the AKT1 dimer, with AKT1a and AKT1b colored red and blue, respectively. ( H ) Docking conformation of the AKT inhibitor (4EJN) in AKT1. ( I ) Docking conformation of phenformin within the AKT1 binding site. ( J ) Superimposed binding modes of Compound C and phenformin in the AKT1 dimer. ( K, L ) Molecular docking results showing the overlapping binding region (blue frame) of Compound C and phenformin, with the upper interaction site specific to Compound C. ( M ) Docking scores (kcal/mol) of phenformin and Compound C bound to AKT1, where more negative values indicate stronger binding affinity.The data are presented as mean ± SD. An unpaired two-tailed t -test was used for ( A , C and D ). A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for (B). ** P < 0.01, *** P < 0.001 vs. control group; ### P < 0.001 vs. TiO₂ NZs group

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Binding Assay, Western Blot, Expressing, Control, Software, Two Tailed Test, Comparison

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Akt-targeted autophagy modulation emerges as AMPK declines in TiO₂ NZs-treated cells. ( A ) Western blot analysis of Akt and p-Akt protein levels in cells treated with 100 µg/mL TiO₂ NZs for 24 h. ( B, C ) Protein levels of Akt and p-Akt after treatment with Compound C or phenformin. ( D, E )Western blot analysis of Akt, p-Akt, mTOR, and p-mTOR in cells treated with TiO₂ NZs alone or in combination with Compound C or phenformin for 24 h. GAPDH served as a loading control. Molecular weights (kDa) are indicated beside the bands.Quantitative densitometric analysis corresponding to the western blots in ( A – E ) was performed using ImageJ software. All bands were normalized to GAPDH expression, and the tests were repeated three times. ( F ) AMPK mRNA and protein expression levels in cells transfected with AMPK siRNA or negative control. ( G ) Immunofluorescence analysis of autophagy levels in cells transfected with AMPK siRNA alone or in combination with Compound C or phenformin. ( H ) AMPK mRNA and protein expression levels in cells transfected with AMPK overexpression vector (pcDNA3.1-AMPK) or negative control vector (pcDNA3.1). All data are presented as the mean ± SD from three independent experiments. An unpaired two-tailed t-test was used for ( A - C ). A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for ( D , E , F , H ). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. control group; ## P < 0.01, ### P < 0.001 vs. TiO₂ NZs group

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Western Blot, Control, Software, Expressing, Transfection, Negative Control, Immunofluorescence, Over Expression, Plasmid Preparation, Two Tailed Test, Comparison

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Autophagy reversal via AMPK overexpression and Akt knockdown highlights dual-target mechanism. ( A , B ) Immunofluorescence analysis of autophagy levels in HTR cells exposed to the following treatments: ( A ) Control cells, TiO₂ NZs, TiO₂ NZs + AMPK overexpression vector (pcDNA3.1-AMPK), TiO₂ NZs + AMPK overexpression vector + Compound C, or TiO₂ NZs + Compound C; ( B ) Control cells, TiO₂ NZs, TiO₂ NZs + AMPK overexpression vector, TiO₂ NZs + AMPK overexpression vector + phenformin, or TiO₂ NZs + phenformin. Cell nuclei were stained blue with DAPI, and autophagosomes were labeled red using CY3-conjugated secondary antibodies. Scale bar = 100 μm. ( C ) AKT mRNA and protein levels examined by RT-PCR and western blotting after cells were transfected with the Akt siRNA and the negative control. ( D ) Immunofluorescence analysis of autophagy levels in HTR cells exposed to the following treatments: TiO₂ NZs, TiO₂ NZs + Akt siRNA, TiO₂ NZs + Akt siRNA + Compound C, TiO₂ NZs + Compound C, TiO₂ NZs + Akt siRNA + phenformin, or TiO₂ NZs + phenformin for 24 h. Cell nuclei were stained blue with DAPI, and autophagosomes were labeled red using CY3-conjugated secondary antibodies. All data are presented as the mean ± SD. A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for ( C ). **** P < 0.0001 vs. NC siRNA group

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Over Expression, Knockdown, Immunofluorescence, Control, Plasmid Preparation, Staining, Labeling, Reverse Transcription Polymerase Chain Reaction, Western Blot, Transfection, Negative Control, Comparison

Journal: Journal of Nanobiotechnology

Article Title: Nanozymes subvert pharmacological conventions: insights from counteracting the placental side effects of TiO₂ nanozymes

doi: 10.1186/s12951-026-04132-8

Figure Lengend Snippet: Phenformin and Compound C rewire AMPK/mTOR pathway in HTR cells post-TiO₂ exposure. ( A, B ) Western blot analysis of Akt, AMPK, mTOR, and their phosphorylated forms after cells were treated with 100 µg/mL TiO₂ NZs, TiO₂ NZs + AMPK overexpression vector (pcDNA3.1-AMPK), or TiO₂ NZs + AMPK overexpression vector + Compound C/phenformin for 24 h. ( C ) Protein levels of AKT, p-AKT, AMPK, p-AMPK, mTOR, p-mTOR, and LC3 in the control group, TiO₂ NZs exposure group, TiO₂ NZs + phenformin and TiO₂ NZs + Compound C groups, as determined by western blotting. GAPDH served as a loading control. Molecular weights (kDa) are indicated beside the bands. Quantitative densitometric analysis corresponding to the western blots in ( A – C ) was performed using ImageJ software. All bands were normalized to GAPDH expression, and the tests were repeated three times.Data were collected from three independent experiments and presented as mean ± SD. An unpaired two-tailed t -test was used for (C left panel). A one-way ANOVA was conducted, followed by a post-hoc Tukey’s multiple comparison test for ( A , B , C right panel). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. control group; # P < 0.05, ## P < 0.01, ### P < 0.001 TiO₂ NZs + AMPK-vector + Compound C vs. TiO₂ NZs group; $ P < 0.05, $$ P < 0.01, $$$ P < 0.001 TiO₂ NZs + AMPK-vector vs. TiO₂ NZs group; † P < 0.05, †† P < 0.01, ††† P < 0.001 TiO₂ NZs + AMPK-vector + Compound C vs. TiO₂ NZs + AMPK-vector group (A-B). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. control group; # P < 0.05, ### P < 0.001 TiO₂ NZs + Compound C vs. TiO₂ NZs group; $ P < 0.05, $$ P < 0.01, $$$ P < 0.001 TiO₂ NZs + phenformin vs. TiO₂ NZs group ( C )

Article Snippet: Compound C (an AMPK inhibitor, HY-13418 A) and phenformin (an AMPK activator, HY-16397) were bought from MedChemExpress (Monmouth Junction, NJ, USA).Bafilomycin A1 (B1793) and chloroquine (C6628) were gained from Sigma-Aldrich (St. Louis, MO, USA).Primary antibodies of AMPK (ab32047), p-AMPK (ab23875), Akt (ab8805),andp-Akt (ab38449)were supplied by Abcam (Cambridge, UK).The secondary antibody produced by CY3-conjugated goat anti-rabbit (ab6939) is a product of Abcam (Cambridge, UK).Primary antibodies against mTOR (2972), p-mTOR (5536), and LC3A/B (4108) were obtained from Cell Signaling Technology (Danvers, MA, USA).And the primary antibody of GAPDH (AF1186),BCA protein assay kit (P0010S), ATP assay kit (S0026), Trizol reagent (R0016), and cDNA synthesis kit (D7168M) were obtained from Beyotime Biotechnology (Shanghai, China).

Techniques: Western Blot, Over Expression, Plasmid Preparation, Control, Software, Expressing, Two Tailed Test, Comparison

Journal: Nature Communications

Article Title: Inhibitory role of Annexin A1 in pathological bone resorption and therapeutic implications in periprosthetic osteolysis

doi: 10.1038/s41467-022-31646-0

Figure Lengend Snippet: Debris was implanted and the calvarial bone of mice were then treated with BML111 (1 mg/kg), WRW4 (2.5 mg/kg) and Ac2–26 (1 mg/kg). a Quantification of the lytic area in calvarial bone tissues analyzed by micro-CT. Results represent the mean ± SEM of 7 mice. b , c Quantification of TRAP-stained areas and inflammatory infiltrate in calvarial bone tissues. Significant difference among the groups was determined by one-way ANOVA, followed by Tukey’s multiple-comparison procedure. * p < 0.05, ** p < 0.001, *** p < 0.0001, **** p < 0.00001. ns indicates no significant difference. d Representative images for micro-CT and histological observations of bone sections stained by TRAP and H&E. Scale bar 100 µm. Source data are provided as a Source Data file.

Article Snippet: For examining the therapeutic effects of AnxA1, eight-week-old male C57/BL6 mice was treated by N-terminal AnxA1 (Ac2–26) or BML111 (R&D Systems) was injected 5 times at a concentration of 1 mg/kg.

Techniques: Micro-CT, Staining, Comparison

Journal: Cell Death & Disease

Article Title: Oncogene PRR14 promotes breast cancer through activation of PI3K signal pathway and inhibition of CHEK2 pathway

doi: 10.1038/s41419-020-2640-8

Figure Lengend Snippet: CHEK2 mRNA expression ( a ), CHEK2 protein expression ( b ) and p-CHEK2 (T68) protein expression ( c ) in PRR14 genetically unaltered and altered (amplified and mutated) breast cancer cases in TCGA database are statistically analyzed by two-tailed Student’s t -test. CHEK2 protein expression is detected by immunostaining in xenografts in nude mice from established MCF7 cell lines and MDA-MB-231 cell lines ( d ), as well as human breast cancer ( e ). CHEK2 transcription in human breast cancer is also detected by qRT-PCR ( f ). The data are quantified and two-tailed Student’s t -test is employed to determine the significance of the difference. Established MCF7 and MDA-MB-231 ( g ) PRR14-overexpressing and control cell lines are treated with various of genotoxic chemicals including Bleo, Eto, 5-FU, H2O2 and HU at indicated concentrations for indicated time. Key components of the ATM/CHEK2/P53 signaling pathway are detected by immunostaining. And CHEK2 protein expression ( h ) and mRNA expression ( i ) are detected by immunostaining and qRT-PCR, respectively. The data are analyzed by two-tailed Student’s t -test. Established MCF7 and MDA-MB-231 ( j ) PRR14-overexpressing and control cell lines are treated with Eto at indicated concentration for indicated time to induce p-CHEK2 (T68), which is detected by immunostaining and quantified and normalized by CHEK2 total protein ( k ). The data are analyzed by two-tailed Student’s t -test.

Article Snippet: Chemicals including selective CHEK2 inhibitor BML-277 (BML, HY-13946, MCE) , and genotoxic chemicals, including bleomycin (Bleo, HY-17565, MCE), etoposide (Eto, HY-13629, MCE), 5-fluorouracil (5-FU, HY-90006, MCE), H 2 O 2 (88597, Millipore) and hydroxyurea (HU, HY-B0313, MCE), were used to treat cells.

Techniques: Expressing, Amplification, Two Tailed Test, Immunostaining, Quantitative RT-PCR, Control, Concentration Assay

Journal: Cell Death & Disease

Article Title: Oncogene PRR14 promotes breast cancer through activation of PI3K signal pathway and inhibition of CHEK2 pathway

doi: 10.1038/s41419-020-2640-8

Figure Lengend Snippet: MCF7 cells transfected with indicated siRNA sequences for 48 h are treated w/wo 5 μg/ml Eto for 6 h, then cells are harvested for immunostaining ( a ). PRR14 in cells is depleted by RNAi transfection for 48 h, and CHEK2 mRNA level are quantified by qRT-PCR in both MCF7 and MDA-MB-231 cell lines ( b ). MCF7, 10AKRAS, 7E6 and MDA-MB-231 cell lines are treated with increasing concentration of CHEK2 inhibitor BML for 24 h and followed with a 24 h treatment of Eto at 5 μg/ml. Cells are harvested to stain with PI followed with FACS analysis ( c ). The percentage of the 4N fraction is analyzed by one-way ANOVA analysis ( n = 3) ( d ).

Article Snippet: Chemicals including selective CHEK2 inhibitor BML-277 (BML, HY-13946, MCE) , and genotoxic chemicals, including bleomycin (Bleo, HY-17565, MCE), etoposide (Eto, HY-13629, MCE), 5-fluorouracil (5-FU, HY-90006, MCE), H 2 O 2 (88597, Millipore) and hydroxyurea (HU, HY-B0313, MCE), were used to treat cells.

Techniques: Transfection, Immunostaining, Quantitative RT-PCR, Concentration Assay, Staining

Journal: Cell Death & Disease

Article Title: Oncogene PRR14 promotes breast cancer through activation of PI3K signal pathway and inhibition of CHEK2 pathway

doi: 10.1038/s41419-020-2640-8

Figure Lengend Snippet: KM survival curves of breast cancer patients receiving chemotherapy are stratified by their expression levels of either CHEK2 ( a ) or PRR14 ( b ). For comparison, KM survival curves of breast cancer patients receiving endocrine therapy and stratified by PRR14 expression is also analyzed ( c ). KM survival curves of breast cancer patients receiving chemotherapy with mutant P53 ( d ) or wild-type P53 ( e ) are stratified by their expression level of PRR14.

Article Snippet: Chemicals including selective CHEK2 inhibitor BML-277 (BML, HY-13946, MCE) , and genotoxic chemicals, including bleomycin (Bleo, HY-17565, MCE), etoposide (Eto, HY-13629, MCE), 5-fluorouracil (5-FU, HY-90006, MCE), H 2 O 2 (88597, Millipore) and hydroxyurea (HU, HY-B0313, MCE), were used to treat cells.

Techniques: Expressing, Comparison, Mutagenesis