Journal: Cells

Article Title: Estetrol Enhances Mitochondrial Bioenergetics and Neurite Outgrowth in Cellular Models of Alzheimer’s Disease

doi: 10.3390/cells15050452

Figure Lengend Snippet: Impact of estrogen receptor antagonists on the E2- and E4-mediated increase in ATP levels in Control, APP and P301L cells. Cells were first pre-treated with 0.1 μM MPP (ERα antagonist), 0.1 μM PHTPP (ERβ antagonist), 0.1 μM fulvestrant (ER antagonist), or 0.1 μM G-15 (GPER1 antagonist) for 1 h and then treated with vehicle alone (Veh = DMSO), E2 0.1 μM, and E4 1 μM for 48 h. Data represent the ATP levels as mean ±SEM of three independent experiments, expressed as a percentage of the vehicle (Veh) condition. In addition, the mean of each independent experiment (biological replicates) is presented as circles (for Control cells), squares (for APP cells), or diamonds (for P301L cells). Total number of technical replicates per condition: n = 11–36 ( A ); n = 11–36 ( B ); and n = 12–32 ( C ). All the data were normalized on the CellTracker Blue fluorescence intensity, which corresponds to the area of living cells. * p < 0.05, ** p < 0.01, two-way ANOVA versus Veh/DMSO. MPP: Methyl-piperidino-pyrazole, E2: estradiol, E4: estetrol.

Article Snippet: MPP (#HY-103454), PHTPP (#HY-103456), Fulvestrant (#HY-103636) and G-15 (#HY-103449) were obtained from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Control, Fluorescence

Journal: Nature Communications

Article Title: A degron-mimicking molecular glue drives CRBN homo-dimerization and degradation

doi: 10.1038/s41467-025-65094-3

Figure Lengend Snippet: a Chemical structure of MRT-31619, OUN20985 (CRBN homo-PROTAC) and Lenalidomide. b , c Global quantitative proteomics in Jurkat cells. Volcano plots show compound/DMSO protein abundance upon treatment with 1 μM of MRT-31619 or CRBN homo-PROTAC for 1 h, 3 h and 24 h, and with 10 μM of MRT-31619 or CRBN homo-PROTAC for 24 h. d HEK293T_HiBiT-CRBN cells were treated with MRT-31619 for 1 h. Bortezomib at 2 μM, MLN4924 at 2 μM, and lenalidomide at 20 μM were added 1 h prior to MRT-31619 treatment. Values were normalized to DMSO treatment. Four biological replicates were plotted as mean ± Standard Deviation (SD). e HEK293T_HiBiT-CRBN cells were treated with CRBN homo-PROTAC for 1 h. Bortezomib at 2 μM, MLN4924 at 2 μM, and lenalidomide at 20 μM were added 1 h prior to CRBN homo-PROTAC treatment. Values were normalized to DMSO treatment. Four biological replicates were plotted as mean ± SD. f NanoBRET assay for HaloTag-CRBN and CRBN-NanoLuc constructs upon MRT-31619 or lenalidomide treatment. In the double treatment condition, lenalidomide was added at 20 μM, 1 h prior to MRT-31619 treatment. Values were normalized to DMSO treatment. Three biological replicates were plotted as mean ± Standard Error of Measurement (SEM). g NanoBRET assay for HaloTag-CRBN and CRBN-NanoLuc (CRBN-Nluc) wild-type (WT) and W386A constructs upon MRT-31619 treatment. Values were normalized to DMSO treatment. Three biological replicates were plotted as mean ± SEM. Source data are provided as a Source Data file.

Article Snippet: Cells were treated for 1 h with DMSO (Sigma Cat#41639) at 0.1% final concentration and MRT compounds or homo-PROTAC CRBN degrader (Selleckchem Cat#S2881) at serial dilution using a Tecan D300e Digital Dispenser.

Techniques: Quantitative Proteomics, Standard Deviation, Construct

Journal: Nature Communications

Article Title: A degron-mimicking molecular glue drives CRBN homo-dimerization and degradation

doi: 10.1038/s41467-025-65094-3

Figure Lengend Snippet: a Cryo-EM density of conformation 1 at 2.9 Å, overall resolution (EMD-52330). b Model of DDB1 and the two CRBN protomers (CULT and LON domains) in cartoon representation. Overview and zoom-in at the tri-tryptophan CRBN pockets, illustrating how two molecules of MRT-31619 bridge the two CRBN subunits. c Zoom-in at the tri-tryptophan CRBN pockets, showing the MGD1–MGD2 interactions. d Footprints for CRBN-MRT-31619, protomer 1 and protomer 2: MRT-31619 footprints in blue and footprints of PPI in yellow. e NanoBRET assay for mouse CRBN mutants upon MRT-31619 treatment. Six biological replicates were plotted as mean ± SD. Human and mouse CRBN are indicated as hCRBN and mCRBN, respectively. Wild type (WT) and mutant HaloTag-CRBN constructs are indicated. For this experiment, hCRBN-NanoLuc constructs with a 191-248 aa deletion (Trunc) that do not bind DDB1 were used. f NanoBRET assay for hCRBN mutants upon MRT-31619 treatment. Three biological replicates were plotted as mean ± SEM. Wild type (WT) and mutant HaloTag-hCRBN and hCRBN-NanoLuc constructs are indicated. For this experiment, hCRBN-NanoLuc constructs with a 191-248 aa deletion (Trunc) that do not bind DDB1 were used. g Zoom-in at the tri-tryptophan CRBN pockets, showing key aminoacid interactions. Source data are provided as a Source Data file.

Article Snippet: Cells were treated for 1 h with DMSO (Sigma Cat#41639) at 0.1% final concentration and MRT compounds or homo-PROTAC CRBN degrader (Selleckchem Cat#S2881) at serial dilution using a Tecan D300e Digital Dispenser.

Techniques: Cryo-EM Sample Prep, Mutagenesis, Construct

Journal: Nature Communications

Article Title: A degron-mimicking molecular glue drives CRBN homo-dimerization and degradation

doi: 10.1038/s41467-025-65094-3

Figure Lengend Snippet: a The cis CRBN (CRBN 1 ) binds one MRT-31619 molecule (MGD 1 ) at the tri-tryptophan pocket and interacts with the trans MRT-31619 molecule (MGD 2 ) via a hydrogen bond to W400. b CRBN W400 interacts with the CK1α G-loop via a hydrogen bond in the presence of lenalidomide. c Superposition of panels a and b indicates that MGD 2 is a structural mimic of the CK1α G-loop and employs the same hydrogen bond. d – f Chemical structures of MRT-31619, MRT-31015, or MRT-30568 and their corresponding global quantitative proteomics data in Jurkat cells. Volcano plots show compound/DMSO protein abundance upon treatment with 10 μM of MRT-31619, MRT-31015, or MRT-30568 for 24 h. g HEK293T_HiBiT-CRBN degradation upon MRT-31619, MRT-31015, or MRT-30568 treatment for 1 h. Four biological replicates were plotted as mean ± SD. h NanoBRET assay for HaloTag-CRBN and CRBN-NanoLuc constructs upon MRT-31619, MRT-31015, or MRT-30568 treatment. Three biological replicates were plotted as mean ± SEM. i Flow-induced dispersion analysis (FIDA) for MRT-31619, MRT-31015, or MRT-30568 and the corresponding EC 50 and Max R h values. The predicted value of R h calculated from the cryo-EM structure of the ternary complex is 7.47 nm. Three biological replicates were plotted as mean ± SD. Source data are provided as a Source Data file.

Article Snippet: Cells were treated for 1 h with DMSO (Sigma Cat#41639) at 0.1% final concentration and MRT compounds or homo-PROTAC CRBN degrader (Selleckchem Cat#S2881) at serial dilution using a Tecan D300e Digital Dispenser.

Techniques: Quantitative Proteomics, Construct, Dispersion, Cryo-EM Sample Prep

Journal: Nature Communications

Article Title: A degron-mimicking molecular glue drives CRBN homo-dimerization and degradation

doi: 10.1038/s41467-025-65094-3

Figure Lengend Snippet: a Global ubiquitinomics in Jurkat cells at 10 μM of MRT-31619 for 30 min. b Model for MRT-31619-driven CRBN ubiquitination at the CRL4CRBN complex.

Article Snippet: Cells were treated for 1 h with DMSO (Sigma Cat#41639) at 0.1% final concentration and MRT compounds or homo-PROTAC CRBN degrader (Selleckchem Cat#S2881) at serial dilution using a Tecan D300e Digital Dispenser.

Techniques: Ubiquitin Proteomics

Journal: Scientific reports

Article Title: Orthogonal validation of PROTAC mediated degradation of the integral membrane proteins EGFR and c-MET.

doi: 10.1038/s41598-024-84217-2

Figure Lengend Snippet: Fig. 4. Degradation profile of wildtype EGFR in A549 cells. Cells were pre-treated as described in (Fig. 1) with EGF as RTK ligand and either PROTAC3 (A,C,E,G,I) or Gefitinib (B,D,F,H,J) was added for 24 h. Cells were then analysed by immunoblotting (A,B) with quantification (C,D), immunofluorescence for the whole cell (E,F) or plasma membrane only (G,H) or flow cytometry (I,J). Graphs show the mean SEM of at least 3 biological replicates. The dotted line indicates a value of 0.8. All details regarding statistical analyses and p-values are provided in the (Supplementary Table 3).

Article Snippet: For starvation experiments, cells were washed twice in PBS and grown in respective growth media without FBS for 6–8 h. Subsequently media were exchanged for full growth media and cells were treated with SJF8240 (Tocris, 7266), Foretinib (Stratech, ORB322222), PROTAC3 (Tocris, 7258) or Gefitinib (AstraZeneca).

Techniques: Western Blot, Immunofluorescence, Clinical Proteomics, Membrane, Flow Cytometry

Journal: Scientific reports

Article Title: Orthogonal validation of PROTAC mediated degradation of the integral membrane proteins EGFR and c-MET.

doi: 10.1038/s41598-024-84217-2

Figure Lengend Snippet: Fig. 5. Degradation profile of ex19del EGFR in HCC827 cells. Cells were pre-treated as described in (Fig. 1) with EGF as RTK ligand and either PROTAC3 (A,C,E,G,I) or Gefitinib (B,D,F,H,J) was added for 24 h. Cells were then analysed by immunoblotting (A,B) with quantification (C,D), immunofluorescence for the whole cell (E,F) or plasma membrane only (G,H) or flow cytometry (I,J). Graphs show the mean SEM of at least 3 biological replicates. The dotted line indicates a value of 0.8. All details regarding statistical analyses and p-values are provided in the (Supplementary Table 4).

Article Snippet: For starvation experiments, cells were washed twice in PBS and grown in respective growth media without FBS for 6–8 h. Subsequently media were exchanged for full growth media and cells were treated with SJF8240 (Tocris, 7266), Foretinib (Stratech, ORB322222), PROTAC3 (Tocris, 7258) or Gefitinib (AstraZeneca).

Techniques: Western Blot, Immunofluorescence, Clinical Proteomics, Membrane, Flow Cytometry

Journal: Nature

Article Title: Androgen activity in the male embryonic hindbrain drives lethal PFA ependymoma

doi: 10.1038/s41586-026-10264-6

Figure Lengend Snippet: a , b , Western blots showing AR expression in PFA9 ( a ) and PFA4 ( b ) cells using whole-cell lysate. T, testosterone; Veh, vehicle. c , d , Western blots showing AR expression in PFA9 ( c ) and PFA4 ( d ) cells using subcellular protein fractionation extract. Cyt, cytoplasmic fraction; LMNB1, lamin B1; Nuc, nuclear fraction; WC, whole cell. a – d , Western blots shown are representative of n = 4 biological replicates with similar results. e , PFA-EPN cells were treated with 50 nM testosterone, oestradiol or progesterone for in vitro LDA to assess the frequency of colony-forming stem cells. n = 8 technical replicates per condition. f , PFA-EPN cell lines were cultured with testosterone for seven days. g , PFA-EPN cells were treated with 5 µM enzalutamide or MTX-23 for LDA. n = 6 technical replicates per condition. h , PFA-EPN cells were treated with 5 µM enzalutamide or MTX-23 for LDA. Cells were pre-treated with 50 nM testosterone before drug exposure. n = 8 technical replicates (control); n = 6 technical replicates (drug). e , g , h , Statistical comparisons were performed using a two-sided extreme limiting dilution analysis (ELDA) Chi-squared test. Solid lines represent maximum-likelihood estimates of clonogenic frequency from ELDA; dashed lines indicate 95% confidence intervals. i , j , PFA-EPN cell lines were pre-treated with 50 nM testosterone for seven days, followed by treatment with enzalutamide ( i ) or MTX-23 ( j ) for seven days. f , i , j , Cell counts are normalized to the vehicle control for each line. n = 2 biological replicates, each with 3 technical replicates. Data are mean ± s.d. Statistical comparisons were performed using a one-way ANOVA on replicates followed by a Tukey’s post-hoc test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; NS, not significant. Exact P values are provided in the .

Article Snippet: The PROTAC-based AR inhibitor MTX-23 (MedChemExpress, HY-148771) and enzalutamide (MedChemExpress, HY-70002) were dissolved in dimethyl sulfoxide (DMSO; Sigma-Aldrich, D8418), and DMSO was used as a vehicle control.

Techniques: Western Blot, Expressing, Fractionation, In Vitro, Cell Culture, Control

Journal: Nature

Article Title: Androgen activity in the male embryonic hindbrain drives lethal PFA ependymoma

doi: 10.1038/s41586-026-10264-6

Figure Lengend Snippet: a , b , Quantified western blots of the female (F) PFA4 ( a ) and male (M) PFA9 ( b ) cell lines showing AR expression normalized to vehicle in whole-cell lysates. c , d , Quantified western blots of the female (F) PFA4 ( c ) and male (M) PFA9 ( d ) cell lines showing AR expression normalized to vehicle in subcellular protein fractionation extracts. e , f , Box plot showing normalized AR expression relative to vehicle in the female (F) PFA4 ( e ) and male (M) PFA9 ( f ) cell lines, measured in cytoplasmic and nuclear fractions across four biological replicates. n = 4 per group. Data are presented as mean ± s.e.m. P values were calculated using a two-sided Wilcoxon test. * P < 0.05; NS, not significant. Exact P values are provided in the . g , Images of cell culture confluency of (F) PFA4, (M) PFA5, and (M) PFA9 after being cultured with vehicle control or testosterone at different concentrations for 7 days. Scale bars, 100 μm. h , i , PFA male cell lines (PFA5 ( h ) and PFA9 ( i )) were cultured with 50 nM or 100 nM of sex hormones (testosterone, DHT, progesterone or oestradiol) for 7 days. Cell counts were normalized to vehicle control for each line. n = 2 biological replicates, each with 2 technical replicates. j , k , Male PFA cell lines (PFA5, PFA7, PFA9, and PFA15) and female PFA cell lines (PFA4, PFA6) were cultured with oestradiol ( j ) or progesterone ( k ) for 7 days at concentrations ranging from 10 nM to 1 uM. Cell counts were normalized to vehicle control for each line. l , Box plot of expression levels of AR in ST ZFTA fusion-EPN or PFA-EPN bulk RNA-seq patient samples. ST ZFTA-EPN (n = 4), PFA-EPN (n = 14). In box plots, the centre line denotes the median, box hinges indicate the 25th and 75th percentiles, and whiskers mark 1.5× the IQR. P values were calculated using a two-sided Student’s t -test. m , n , Male PFA cell lines (PFA5, PFA7, PFA9, and PFA15) and female PFA cell lines (PFA4, PFA6) were cultured with the AR inhibitor enzalutamide ( m ) or MTX-23 ( n ) at concentrations ranging from 2.5 µM to 20 µM for 7 days. Cell counts were normalized to the vehicle control for each line. j , k , m , n , n = 2 biological replicates, each with 3 technical replicates. h–n , Data are displayed as mean ± s.d. Statistical comparisons were performed using a one-way ANOVA on replicates followed by a Tukey’s post-hoc test; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; NS, not significant. Exact P values are provided in the .

Article Snippet: The PROTAC-based AR inhibitor MTX-23 (MedChemExpress, HY-148771) and enzalutamide (MedChemExpress, HY-70002) were dissolved in dimethyl sulfoxide (DMSO; Sigma-Aldrich, D8418), and DMSO was used as a vehicle control.

Techniques: Western Blot, Expressing, Fractionation, Cell Culture, Control, RNA Sequencing

Journal: Nature

Article Title: Androgen activity in the male embryonic hindbrain drives lethal PFA ependymoma

doi: 10.1038/s41586-026-10264-6

Figure Lengend Snippet: a – c , ST-EPN cell lines (ST1 and ST4) and DIPG cell lines (DIPG004 and DIPG007) were cultured with testosterone ( a ), oestradiol ( b ) or progesterone ( c ) for 7 days at concentrations ranging from 10 nM to 1 uM. Cell counts were normalized to vehicle control for each line. d , e , ST-EPN cell lines (ST1 and ST4) and DIPG cell lines (DIPG004 and DIPG007) were cultured with the AR inhibitor enzalutamide ( d ) or MTX-23 ( e ) at concentrations ranging from 2.5 µM to 20 µM for 7 days. Cell counts were normalized to the vehicle control for each line. f , g , ST-EPN cell lines (ST1 and ST4) and DIPG cell lines (DIPG004 and DIPG007) were pre-treated with 50 nM testosterone for 7 days, followed by treatment with the AR inhibitor enzalutamide ( f ) or MTX-23 ( g ) at concentrations ranging from 2.5 µM to 20 µM for 7 days. Cell counts were normalized to the vehicle control for each line. a – g , n = 2 biological replicates, each with 3 technical replicates. Data are displayed as mean ± s.d. Statistical comparisons were performed using a one-way ANOVA on replicates followed by a Tukey’s post-hoc test; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; NS, not significant. Exact P values are provided in the . h , Schematic of proposed cellular hierarchy for PFA-EPNs. Created in BioRender; Pomada Villalbi, A. https://BioRender.com/y8qtbvf (2025).

Article Snippet: The PROTAC-based AR inhibitor MTX-23 (MedChemExpress, HY-148771) and enzalutamide (MedChemExpress, HY-70002) were dissolved in dimethyl sulfoxide (DMSO; Sigma-Aldrich, D8418), and DMSO was used as a vehicle control.

Techniques: Cell Culture, Control

Journal: Scientific Reports

Article Title: Metabotropic glutamate receptor-1 regulates inflammation in triple negative breast cancer

doi: 10.1038/s41598-018-34502-8

Figure Lengend Snippet: Riluzole and BAY36-7620 increase cytokine protein expression in TNBC cells. Effect of riluzole and BAY36-7620 on CXCL1 ( A ) and IL-8 ( B ) secretion from SUM159, BT549 and MDA-MB-231 cells treated for 24 or 48 hours. Results represent the mean ± SEM of n = 2 experiments, performed in triplicate, where *is P < 0.05 compared to vehicle treated cells.

Article Snippet: The specific mGluR1 inhibitor, BAY36-7260, and riluzole were purchased from Tocris Bioscience (Minneapolis, MN).

Techniques: Expressing

Journal: bioRxiv

Article Title: EGFR/TBK1-dependent mitochondrial quality control contributes to acquired resistance to temozolomide

doi: 10.64898/2025.12.19.695123

Figure Lengend Snippet: A. U251 cells were treated by TMZ. Cells were harvested, fixed and stained by pTBK1 antibody coupled to fluorescent secondary antibody. pTBK1 specific fluorescence was detected by flow cytometry and expressed as a ratio to D0 fluorescence (*: p<0.05 vs D0). B. EGFR phosphorylation was measured by flow cytometry by the use of phospho-specific antibodies (pEGFR Y845 or pEGFR Y1068) on U251 or U251 Rho0 cells. Fluorescence was normalized to the fluorescence measured at D0 (*: p<0.05, **: p<0.01). C. EGFR Y845 as measured as in B. in the presence or absence of NAC 5mM (*: p<0.05, **: p<0.01). D. Phosphorylation of EGFR (Y845 and Y1068) and TBK1 was measured as in B in the presence or absence of PP1 (Src inhibitor). E. Src and TBK1 phosphorylation was measured as in B in U251 and U251 EGFR-cells treated by TMZ for the time indicated on the graph (*: p<0.05, **: p<0.01, ***: p<0.001). F. U251 and U251 EGFR-cells were treated by TMZ 50µM twice a week and cells were counted by flow cytometry at each time point. Cell number was normalized by the cell count at D0. G. The sensitivity of U251 cells to erlotinib was evaluated by MTT during TMZ treatment and the IC50 was calculated by AAT Bioquest “IC50 Calculator” tool ( https://www.aatbio.com/tools/ic50-calculator ).

Article Snippet: MitoSOX Red #M36008, Invitrogen (Thermo Fisher Scientific, Waltham, MA, USA); Rhod2-AM #R1244, Invitrogen; Prolong Gold with DAPI #836941, Invitrogen; PROTAC TBK1 and negative control TBK1 PROTAC 3i (#7259) and TBK1 control PROTAC 4 (#7260), Tocris Bioscience (BioTechne SAS, Noyal Chatillon sur Seiche, France).

Techniques: Staining, Fluorescence, Flow Cytometry, Phospho-proteomics, Cell Counting

Journal: bioRxiv

Article Title: EGFR/TBK1-dependent mitochondrial quality control contributes to acquired resistance to temozolomide

doi: 10.64898/2025.12.19.695123

Figure Lengend Snippet: A. mRNA analyses from the TCGA_GBM (HG-UG133A) database to stratify patients according to EGFR expression (cutoff = median). The survival of both groups is shown by the Kaplan-Meier curve obtained from data extracted from GlioVis (orange: EGFR-high; cyan: EGFR-low). The same analysis was performed with Src mRNA expression (B) and TBK1 (C). D. GBM patients from the TCGA_GBM dataset were stratified according to their combined EGFR/Src/TBK1 expression. The Kaplan-Meier curve of the Src-low subgroups patients is shown. E. Data from D were analyzed by comparing the EGFR-low/Src-low/TBK1-low patients to other Src-low patients.

Article Snippet: MitoSOX Red #M36008, Invitrogen (Thermo Fisher Scientific, Waltham, MA, USA); Rhod2-AM #R1244, Invitrogen; Prolong Gold with DAPI #836941, Invitrogen; PROTAC TBK1 and negative control TBK1 PROTAC 3i (#7259) and TBK1 control PROTAC 4 (#7260), Tocris Bioscience (BioTechne SAS, Noyal Chatillon sur Seiche, France).

Techniques: Expressing

Journal: Frontiers in Immunology

Article Title: Thrombospondin-1 mitigates osteoarthritis progression by inhibiting mechanical stress-induced chondrocyte ferroptosis via the integrin/YAP pathway

doi: 10.3389/fimmu.2025.1577234

Figure Lengend Snippet: THBS1 inhibits chondrocyte ferroptosis through the integrinαVβ1/YAP pathway. THBS1 knockout chondrocytes and normal chondrocytes were subjected to 1 MPa mechanical stress for 2 hours, with or without the addition of YAP1 inhibitor PROTAC YAP d1 (20μM) and rhTHBS1(100ng/ml). Immediately following stimulation, IF detection was performed. Additional analyses were conducted after chondrocytes were further incubated with or without YAP1 inhibitor PROTAC YAP d1 (20μM) and rhTHBS1(100ng/ml) for 24 hours post-stimulation. (A) Representative image of chondrocytes undergoing IF detection immediately after mechanical stress stimulation. YAP (red) and DAPI (blue) are also shown. Scale bar = 20 μm. (B) Quantification of YAP localization. In each experiment 150 to 200 cells were evaluated (n = 3). YAP localization in the nucleus (green) or cytoplasm (red) is shown. (C) Western blot (WB) analysis of YAP1. (D) Quantification of WB analysis (n=3 for each group). (E) Representative image of chondrocytes undergoing IF detection immediately after mechanical stress stimulation. YAP (red) and DAPI (blue) are also shown. Scale bar = 20 μm. (F) Quantification of YAP localization. In each experiment 150 to 200 cells were evaluated (n = 3). (G) Western blot (WB) analysis of YAP1. (H) Quantification of WB analysis (n=3 for each group). (I) Mitochondrial membrane potential was detected by JC-1 assay. Scale bar = 10 μm. (J) The relative IOD ratio of red fluorescence to green fluorescence was used for quantitative analysis (n=3 for each group). (K) Representative TEM images of chondrocytes of indicated groups. (n=3 for each group). Green arrows show the normal mitochondria. Red arrows show the shrunken mitochondria. Scale bars, 5.0 μm (low field), 500 nm (high field). (L) Representative fluorescence images of mitochondria in chondrocytes. Scale bar = 50 μm. (M) Quantitative analysis of fluorescence intensity (n=3 for each group). (N) The expression of GSH in chondrocytes of indicated groups was detected by ELISA (n=3 for each group). Data were presented as the mean ± SD. NS P>0.05 *P<0.05, **P<0.01.

Article Snippet: YAP1 inhibitor PROTAC YAP d1 was obtained from MCE (HY-168016).

Techniques: Knock-Out, Incubation, Western Blot, Membrane, Fluorescence, Expressing, Enzyme-linked Immunosorbent Assay