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MedChemExpress 15230 radicicol medchemexpress cat
15230 Radicicol Medchemexpress Cat, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 51 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/geldanamycin/Geldanamycin/pm42406593-233-36-38
Average 95 stars, based on 51 article reviews

15230 radicicol medchemexpress cat - by Bioz Stars, 2026-10

95/100 stars

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In Vitro:

Article Title: HER2-Driven Breast Cancer: Role of the Chaperonin HSP90 in Modulating Response to Trastuzumab-Based Therapeutic Combinations.
Article Snippet: .. For in vitro experiments, trastuzumab, pertuzumab, trastuzumab–emtansine (T-DM1), and docetaxel were provided by IFO Hospital pharmacy; tamoxifen and geldanamycin were acquired by MedChemExpress (Monmouth Junction, NJ, USA). ..

other:

Article Title: Insights into SARS-CoV-2 replication control via targeting the host hijacking function of NSP12
Article Snippet: Cycloheximide, Pronase E, Bafilomycin A1, Chloroquine, MG132, AR7, VER-155008, Geldanamycin, and Remdesivir (MedChemExpress, Shanghai, China) were dissolved in dimethylsulfoxide (DMSO) as stock solutions, followed by storage at − 20 ◦ C. The antibodies used were as follows: Hsc70 primary antibody (Abcam, Cambridge, UK); ß-actin, GAPDH, SARSCoV-2 NSP12 primary antibody (Cell Signaling Technology, Danvers, USA); HA, Flag, GFP primary antibody (TransGen Biotech, Beijing, China); Strep and SARS-CoV-2 Nucleocapsid Protein primary antibody, HRP-conjugated mouse anti-DDDDKTag, HRP-conjugated goat anti-Mouse, HRP-conjugated goat anti-Rabbit (ABclonal Technology, Wuhan, China); and ß-tubulin, LC3B, p62/SQSTM1, ATG5, LAMP2a, HSP90 primary antibody (Abmart, Shanghai, China).

Image Search Results

( A ) Heatmap of responses to HSP90 inhibitors (17-AAG, geldanamycin, and alvespimycin). Colors represent z -scores derived from the median inhibitory concentration (IC 50 ) values (scale shown). The bottom annotation indicates specimen subgroup [-3/del(3p) or control AML]. Columns are ordered by unsupervised hierarchical clustering of IC 50 values. ( B ) Correlation between responses to 17-AAG and alvespimycin (Pearson’s r = 0.79). The dashed line indicates least-squares regression. ( C ) Average response to HSP90 inhibitors [avg(HSP90i); mean of rescaled IC 50 values from −1 to 1] according to subgroup [-3/del(3p) versus control AML], TP53 status, and ribosomal eigengene expression (tier 1, low; and tier 3, high). ( D ) Representative Western blots of RPS14, RPL14, RPL29, and α-tubulin (TUBA; loading control) in U937 cells treated for 24 hours with DMSO or HSP90 inhibitors. ( E ) Representative Western blots of RPL29 and TUBA in primary AML cells [(A) to (D): control AML; (E) to (H): -3/del(3p)] treated for 24 hours with DMSO or HSP90 inhibitors. ( F ) Correlations between RPL29 protein levels (normalized to TUBA) and IC 50 values for each HSP90 inhibitor. Pearson’s r values are indicated; dashed lines represent least-squares regression. ( G ) Ex vivo proliferation of primary -3/del(3p) (gray) and control AML (white) following exposure to DMSO, geldanamycin, or alvespimycin. Cell counts were normalized to Fresh (D0) input and expressed as fold change at days 1 and 4 (NS, not significant). ( H ) Ex vivo viability of primary -3/del(3p) (gray) and control AML (white) after treatment, normalized to Fresh (D0), assessed at days 1 and 4.

Journal: Science Advances

Article Title: TP53 -mutant AML with ribosomal gene loss exhibits impaired protein translation and sensitivity to HSP90 inhibition

doi: 10.1126/sciadv.aed7122

Figure Lengend Snippet: ( A ) Heatmap of responses to HSP90 inhibitors (17-AAG, geldanamycin, and alvespimycin). Colors represent z -scores derived from the median inhibitory concentration (IC 50 ) values (scale shown). The bottom annotation indicates specimen subgroup [-3/del(3p) or control AML]. Columns are ordered by unsupervised hierarchical clustering of IC 50 values. ( B ) Correlation between responses to 17-AAG and alvespimycin (Pearson’s r = 0.79). The dashed line indicates least-squares regression. ( C ) Average response to HSP90 inhibitors [avg(HSP90i); mean of rescaled IC 50 values from −1 to 1] according to subgroup [-3/del(3p) versus control AML], TP53 status, and ribosomal eigengene expression (tier 1, low; and tier 3, high). ( D ) Representative Western blots of RPS14, RPL14, RPL29, and α-tubulin (TUBA; loading control) in U937 cells treated for 24 hours with DMSO or HSP90 inhibitors. ( E ) Representative Western blots of RPL29 and TUBA in primary AML cells [(A) to (D): control AML; (E) to (H): -3/del(3p)] treated for 24 hours with DMSO or HSP90 inhibitors. ( F ) Correlations between RPL29 protein levels (normalized to TUBA) and IC 50 values for each HSP90 inhibitor. Pearson’s r values are indicated; dashed lines represent least-squares regression. ( G ) Ex vivo proliferation of primary -3/del(3p) (gray) and control AML (white) following exposure to DMSO, geldanamycin, or alvespimycin. Cell counts were normalized to Fresh (D0) input and expressed as fold change at days 1 and 4 (NS, not significant). ( H ) Ex vivo viability of primary -3/del(3p) (gray) and control AML (white) after treatment, normalized to Fresh (D0), assessed at days 1 and 4.

Article Snippet: Alvespimicin (Selleckchem), geldanamycin (MedChemExpress), and 17-AAG (MedChemExpress) were used at 1 M for U937 cells (RRID:CVCL_0007) and 500 nM for primary specimens.

Techniques: Derivative Assay, Concentration Assay, Control, Expressing, Western Blot, Ex Vivo

a, Representative WB and quantification showing effect of VDAC, Hsp70, and Hsp90 inhibitor treatment on tau entry into mitochondria in the in vitro import assay. Mitochondrial p-tau level is normalized with the C-II protein SDHA. b , RET-ROS measurements after p-tau import into control or inhibitor-treated mitochondria. c , Representative WB and quantification showing total PHF-1 tau level in the in vitro import assay mixture. Total p-tau level is normalized with actin, which is known to be associated with mitochondria. d , RET-ROS measurements in control or inhibitor-treated mitochondria without p-tau import. e , WBs and quantification showing knockdown efficiency by VDAC1, Hsp70, and Hsp90 siRNAs. f , Representative WBs and quantification showing the effect of VDAC1, Hsp70, and Hsp90 siRNAs on tau entry into mitochondria in the in vitro import assay and total PHF-1 tau level in the in vitro import assay. g , h , RET-ROS measurements in mitochondria from control or siRNA treated cells with ( g ) or without ( h ) p-tau import into mitochondria. All data are means ± SEM; statistical significance was determined by one-way ANOVA with Dunnett’s multiple test ( a, b, c, d, f, g, h ), or two-tailed unpaired Student’s t test ( e ). *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001. Each data point in a - h represents an independent experimental repeat.

Journal: bioRxiv

Article Title: Tau-induced mitochondrial reverse electron transport drives neurodegeneration

doi: 10.64898/2026.04.04.716514

Figure Lengend Snippet: a, Representative WB and quantification showing effect of VDAC, Hsp70, and Hsp90 inhibitor treatment on tau entry into mitochondria in the in vitro import assay. Mitochondrial p-tau level is normalized with the C-II protein SDHA. b , RET-ROS measurements after p-tau import into control or inhibitor-treated mitochondria. c , Representative WB and quantification showing total PHF-1 tau level in the in vitro import assay mixture. Total p-tau level is normalized with actin, which is known to be associated with mitochondria. d , RET-ROS measurements in control or inhibitor-treated mitochondria without p-tau import. e , WBs and quantification showing knockdown efficiency by VDAC1, Hsp70, and Hsp90 siRNAs. f , Representative WBs and quantification showing the effect of VDAC1, Hsp70, and Hsp90 siRNAs on tau entry into mitochondria in the in vitro import assay and total PHF-1 tau level in the in vitro import assay. g , h , RET-ROS measurements in mitochondria from control or siRNA treated cells with ( g ) or without ( h ) p-tau import into mitochondria. All data are means ± SEM; statistical significance was determined by one-way ANOVA with Dunnett’s multiple test ( a, b, c, d, f, g, h ), or two-tailed unpaired Student’s t test ( e ). *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001. Each data point in a - h represents an independent experimental repeat.

Article Snippet: Newly emerged flies were treated with VDAC inhibitor DIDS (MedChemExpress #HY-D0086, 100 μM), Hsp70 inhibitor PES-CI (Sigma-Aldrich #5310670001, 60 μM), or Hsp90 inhibitor Geldanamycin (MedChemExpress #HY-15230, 10 μM) for 2-3 weeks.

Techniques: In Vitro, Control, Knockdown, Two Tailed Test

$a, Representative WBs and quantification showing effect of VDAC, Hsp70, and Hsp90 inhibitors on the mitochondrial level of PHF-1 tau and total PHF-1 tau in the elav-GS>tau-R406W flies. In this GeneSwitch inducible model, tau-R406W expression is tightly controlled by the addition of RU486 to the fly food. Mitochondrial fractions or total cell lysates were used for WB, and mitochondrial or total PHF-1 p-tau was normalized by SDHA or actin. b , RET-ROS measurements in the mitochondria from control or inhibitor treated elav-GS>tau-R406W flies after tau induction by RU486. c - e , aversive taste memory assays in VDACi ( c ), Hsp70i ( d ), and Hsp90i ( e ) treated elav-GS>tau-R406W flies after tau induction by RU486. f , Climbing activity assay in VDACi, Hsp70i, and Hsp90i treated elav-GS>tau-R406W flies after tau induction by RU486. g , h , RET ( g ) and aversive taste memory ( h ) assays of control flies without tau transgene expression. All data are means ± SEM; statistical significance was determined by one-way ANOVA with Dunnett’s multiple test ( a, b, f, g ), or group analysis using multiple t test with Sidak-Bonferroni multiple comparison ( c , d , e , h ). *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. Each data point represents independent experimental repeat. Three sets of flies with 10-12 flies in each set were used for the behavioral assays.$

Journal: bioRxiv

Article Title: Tau-induced mitochondrial reverse electron transport drives neurodegeneration

doi: 10.64898/2026.04.04.716514

Figure Lengend Snippet: a, Representative WBs and quantification showing effect of VDAC, Hsp70, and Hsp90 inhibitors on the mitochondrial level of PHF-1 tau and total PHF-1 tau in the elav-GS>tau-R406W flies. In this GeneSwitch inducible model, tau-R406W expression is tightly controlled by the addition of RU486 to the fly food. Mitochondrial fractions or total cell lysates were used for WB, and mitochondrial or total PHF-1 p-tau was normalized by SDHA or actin. b , RET-ROS measurements in the mitochondria from control or inhibitor treated elav-GS>tau-R406W flies after tau induction by RU486. c - e , aversive taste memory assays in VDACi ( c ), Hsp70i ( d ), and Hsp90i ( e ) treated elav-GS>tau-R406W flies after tau induction by RU486. f , Climbing activity assay in VDACi, Hsp70i, and Hsp90i treated elav-GS>tau-R406W flies after tau induction by RU486. g , h , RET ( g ) and aversive taste memory ( h ) assays of control flies without tau transgene expression. All data are means ± SEM; statistical significance was determined by one-way ANOVA with Dunnett’s multiple test ( a, b, f, g ), or group analysis using multiple t test with Sidak-Bonferroni multiple comparison ( c , d , e , h ). *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. Each data point represents independent experimental repeat. Three sets of flies with 10-12 flies in each set were used for the behavioral assays.

Techniques: Expressing, Control, Activity Assay, Comparison

a , Effect of H 2 O 2 and FK866 on the viability of tau-P301L hiPSC neurons and isogenic wildtype controls after 24h treatment, and the rescuing effect of CPT. b , Effect of H 2 O 2 and FK866 co-treatment on the viability of control and tau KD hiPSC neurons and the rescuing effect of CPT. c, d , Effect of DES treatment on the viability of control and tau KD hiPSC neurons ( c ) and the rescuing effect of CPT in DES (20 mM) treated control hiPSC neurons ( d ). e - g , WB and quantification showing the effect of inhibiting VDAC, Hsp70, or Hsp90 on PHF-1 tau entry into mitochondria without affecting total PHF-1 tau levels ( e ), and quantification of the effect of inhibitor treatment on RET activity ( f ) and stress sensitivity ( g ) of APP hiPSC neurons. h , Measurement of RET ROS and NAD + /NADH in purified mitochondria from control and tau-WT-EGFP or tau-S2A-EGFP-transfected normal hiPSC neurons. i , Representative images and quantification of p-S262 tau in tau-WT-EGFP or tau-S2A-EGFP transfected control hiPSC neurons with or without DES treatment. j , Measurement of RET ROS and NAD + /NADH in purified mitochondria from EGFP or MKI-EGFP transduced APP hiPSC neurons. k , Representative images and quantification of p-S262 tau in EGFP or MKI-EGFP transfected APP hiPSC neurons. l, m , Immunoblots ( l ) and quantification ( m ) showing effects of the various treatments on normalized levels of p-tau species in APP hiPSC neurons. n, o , Immunoblots ( n ) and quantification ( o ) showing effect of DES or DES/CPT co-treatment on normalized levels of p-tau species in control hiPSC neurons. All data are means ± SEM; statistical significance was determined by one-way ANOVA with Tukey’s post hoc test ( a, b, d, g, h, i, o ), two-way ANOVA with Tukey’s post hoc test ( c ), two-tailed unpaired Student’s t test ( j, k ), or one-way ANOVA with Dunnett’s multiple test ( e, f , m ). *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 ( a, b, c, d, g : n=6/group from 3 biological replicates and 2 wells/experiment; e, f, h, j, m, o : n=3 biological replicates; i, k : n=3 biological replicates, and each data point represents an average of 6 cells/experiment).

Journal: bioRxiv

Article Title: Tau-induced mitochondrial reverse electron transport drives neurodegeneration

doi: 10.64898/2026.04.04.716514

Figure Lengend Snippet: a , Effect of H 2 O 2 and FK866 on the viability of tau-P301L hiPSC neurons and isogenic wildtype controls after 24h treatment, and the rescuing effect of CPT. b , Effect of H 2 O 2 and FK866 co-treatment on the viability of control and tau KD hiPSC neurons and the rescuing effect of CPT. c, d , Effect of DES treatment on the viability of control and tau KD hiPSC neurons ( c ) and the rescuing effect of CPT in DES (20 mM) treated control hiPSC neurons ( d ). e - g , WB and quantification showing the effect of inhibiting VDAC, Hsp70, or Hsp90 on PHF-1 tau entry into mitochondria without affecting total PHF-1 tau levels ( e ), and quantification of the effect of inhibitor treatment on RET activity ( f ) and stress sensitivity ( g ) of APP hiPSC neurons. h , Measurement of RET ROS and NAD + /NADH in purified mitochondria from control and tau-WT-EGFP or tau-S2A-EGFP-transfected normal hiPSC neurons. i , Representative images and quantification of p-S262 tau in tau-WT-EGFP or tau-S2A-EGFP transfected control hiPSC neurons with or without DES treatment. j , Measurement of RET ROS and NAD + /NADH in purified mitochondria from EGFP or MKI-EGFP transduced APP hiPSC neurons. k , Representative images and quantification of p-S262 tau in EGFP or MKI-EGFP transfected APP hiPSC neurons. l, m , Immunoblots ( l ) and quantification ( m ) showing effects of the various treatments on normalized levels of p-tau species in APP hiPSC neurons. n, o , Immunoblots ( n ) and quantification ( o ) showing effect of DES or DES/CPT co-treatment on normalized levels of p-tau species in control hiPSC neurons. All data are means ± SEM; statistical significance was determined by one-way ANOVA with Tukey’s post hoc test ( a, b, d, g, h, i, o ), two-way ANOVA with Tukey’s post hoc test ( c ), two-tailed unpaired Student’s t test ( j, k ), or one-way ANOVA with Dunnett’s multiple test ( e, f , m ). *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 ( a, b, c, d, g : n=6/group from 3 biological replicates and 2 wells/experiment; e, f, h, j, m, o : n=3 biological replicates; i, k : n=3 biological replicates, and each data point represents an average of 6 cells/experiment).

Techniques: Control, Activity Assay, Purification, Transfection, Western Blot, Two Tailed Test

$a, Representative WBs and quantification showing effect of VDAC1, Hsp70, and Hsp90 lenti-shRNAs on the expression of the target proteins. b , Representative WBs and quantification showing effect of VDAC1, Hsp70, and Hsp90 lenti-shRNAs on the levels of mitochondrially localized PHF-1 tau and total PHF-1 tau in APP hiPSC neurons. Mitochondrial fractions or total cell lysates were used for WB, and mitochondrial or total PHF-1 p-tau was normalized by SDHA or actin. c , RET-ROS measurements in mitochondria from control or VDAC1, Hsp70, and Hsp90 lenti-shRNA treated APP hiPSC neurons. d , e , RET ( d ) and stress sensitivity ( e ) assays of control iPSC neurons treated with VDAC1, Hsp70, and Hsp90 inhibitors. All data are means ± SEM; statistical significance was determined by two-tailed unpaired Student’s t test ( a ) or one-way ANOVA with Dunnett’s multiple test ( b-e ). *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 ( e : n=6/group from 3 biological replicates and 2 wells/experiment).$

Journal: bioRxiv

Article Title: Tau-induced mitochondrial reverse electron transport drives neurodegeneration

doi: 10.64898/2026.04.04.716514

Figure Lengend Snippet: a, Representative WBs and quantification showing effect of VDAC1, Hsp70, and Hsp90 lenti-shRNAs on the expression of the target proteins. b , Representative WBs and quantification showing effect of VDAC1, Hsp70, and Hsp90 lenti-shRNAs on the levels of mitochondrially localized PHF-1 tau and total PHF-1 tau in APP hiPSC neurons. Mitochondrial fractions or total cell lysates were used for WB, and mitochondrial or total PHF-1 p-tau was normalized by SDHA or actin. c , RET-ROS measurements in mitochondria from control or VDAC1, Hsp70, and Hsp90 lenti-shRNA treated APP hiPSC neurons. d , e , RET ( d ) and stress sensitivity ( e ) assays of control iPSC neurons treated with VDAC1, Hsp70, and Hsp90 inhibitors. All data are means ± SEM; statistical significance was determined by two-tailed unpaired Student’s t test ( a ) or one-way ANOVA with Dunnett’s multiple test ( b-e ). *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 ( e : n=6/group from 3 biological replicates and 2 wells/experiment).

Techniques: Expressing, Control, shRNA, Two Tailed Test

A. Representative immunoblots and replicate quantitation of processed-Keima levels in the indicated HCT116 Ribo-Keima cell lines treated for 24 hours with Mps1i, DMSO (control) or Hsp90i Geldanamycin (1μM); vinculin was used as loading control. Mean ± SEM, n =4 for HCT116 RPS3-Keima, n =3 for HCT116 RPL28-Keima; Kruskal-Wallis test, followed by Dunn’s multiple comparison test: ** indicates p =0.0042. B. Representative immunoblots and replicate quantitation of processed-Keima levels in the indicated HCT116 Ribo-Keima cell lines treated for 24 hours with Mps1i, DMSO (control) or Hsp70i VER-155008 (50μM); vinculin was used as loading control. Mean ± SEM, n =3; Kruskal-Wallis test, followed by Dunn’s multiple comparison test: * indicates p =0.0459. C. Representative immunoblots and replicate quantitation of processed-Keima levels in the indicated HCT116 Ribo-Keima cell lines upon HSF1ca (or empty backbone) expression and treated for 24 hours with Mps1i or DMSO (control); HSF1 as overexpression control, Hsp90, Hsp70 and Hsp27 were blotted and GAPDH was used as loading control. Mean ± SEM, n =4; one sample and Wilcoxon test (Mps1i vs respective control=1): * indicates p =0.0335 (HCT116 RPS3-Keima Ctrl vs Mps1i) or p =0.0475 (HCT116 RPS3-Keima HSF1ca Ctrl vs Mps1i) or p =0.0128 (HCT116 RPL28-Keima Ctrl vs Mps1i); unpaired Student’s t-test: * indicates p =0.0486 (HCT116 RPS3-Keima Mps1i vs HSF1ca Mps1i), ** indicates p =0.0065 (HCT116 RPL28-Keima Mps1 vs HSF1ca Mps1i). D. Representative immunoblots and replicate quantitation of processed-Keima levels in the indicated HCT116 Ribo-Keima cell lines upon HA-Hsp90 (or mock) overexpression and treated for 24 hours with Mps1i or DMSO (control); HA was blotted as overexpression control and tubulin was used as loading control. Mean ± SEM, n =4; one sample and Wilcoxon test (Mps1i vs respective control=1): * indicates p =0.0267 (HCT116 RPS3-Keima Ctrl vs Mps1) or p =0.0479 (HCT116 RPS3-Keima HA-HSP90 Ctrl vs Mps1); unpaired Student’s t-test: * indicates p =0.0485 (HCT116 RPS3-Keima Mps1 vs HA-Hsp90 Mps1). E. Representative adult eyes in which CIN was induced with an eye-specific Gal4 driving bub3-RNAi (ey>bub3-i) or control wild-type eyes (ey>), where the indicated transgenes for either the depletion of Hsp70 (Hsp70A-i / Hsp70B-i) or its overexpression (Hsp70A) were expressed. F. Quantification of the analysed eye phenotypes, obtained as in (e) and expressed as the percentage of each phenotype across the samples. Number of replicates is shown on each histogram bar; Fisher’s exact test: * indicates p =0.0277 (Hsp70A-i) or p =0.0133 (Hsp70A-i), **** indicates p <0.0001. G. Representative images of larval wing discs in which CIN was induced with an apterous-specific Gal4 driving bub3-RNAi fused with a MyrT fluorescent protein (ap>myrT, bub3-i) or control wild-type tissues (ap>myrT), where the indicated transgenes for either the depletion of Hsp70 (Hsp70A-i / Hsp70B-i) or its overexpression (Hsp70A) were expressed. Tissues have been stained with cleaved-Dcp1 (cDcp1) and DAPI (to stain DNA); MyrT signal marks the aneuploid region; scale bars 50mm. H. Quantification of the area positive for cDcp1 signal, obtained as in (g) and normalised to the area of the dorsal region (D) (where ap>myrT, bub3-i is expressed) in the indicated samples. Number of replicates is shown on graph; one-way ANOVA, followed by Dunnett’s multiple comparison test (GFP-i vs each other sample): **** indicates p <0.0001. I. mRNA expression levels (log2(TPM+1)) of the reported genes, comparing the top and bottom aneuploidy quartiles of human cancer cell lines from the CCLE. Upper quartile, lower quartile and median of each violin plot are shown; two-tailed Student’s t-test: * indicates p =0.0185, *** indicates p =0.0007, **** indicates p <0.0001. J. CRISPR screens data of the reported genes, comparing the top and bottom aneuploidy quartiles of human cancer cell lines from the CCLE. Upper quartile, lower quartile and median of each violin plot are shown; two-tailed Student’s t-test: * indicates p =0.0292, **** indicates p <0.0001. K. RNAi dependency data of the reported genes, comparing the top and bottom aneuploidy quartiles of human cancer cell lines from the CCLE. Upper quartile, lower quartile and median of each violin plot are shown; two-tailed Student’s t-test: ** indicates p =0.0061 (HSF1) or p =0.0062 (HSPA1B), *** indicates p =0.0001.

Journal: bioRxiv

Article Title: Ribosome Quality Control Mitigates Proteotoxic Stress in Aneuploid Cells

doi: 10.64898/2026.01.19.700285

Figure Lengend Snippet: A. Representative immunoblots and replicate quantitation of processed-Keima levels in the indicated HCT116 Ribo-Keima cell lines treated for 24 hours with Mps1i, DMSO (control) or Hsp90i Geldanamycin (1μM); vinculin was used as loading control. Mean ± SEM, n =4 for HCT116 RPS3-Keima, n =3 for HCT116 RPL28-Keima; Kruskal-Wallis test, followed by Dunn’s multiple comparison test: ** indicates p =0.0042. B. Representative immunoblots and replicate quantitation of processed-Keima levels in the indicated HCT116 Ribo-Keima cell lines treated for 24 hours with Mps1i, DMSO (control) or Hsp70i VER-155008 (50μM); vinculin was used as loading control. Mean ± SEM, n =3; Kruskal-Wallis test, followed by Dunn’s multiple comparison test: * indicates p =0.0459. C. Representative immunoblots and replicate quantitation of processed-Keima levels in the indicated HCT116 Ribo-Keima cell lines upon HSF1ca (or empty backbone) expression and treated for 24 hours with Mps1i or DMSO (control); HSF1 as overexpression control, Hsp90, Hsp70 and Hsp27 were blotted and GAPDH was used as loading control. Mean ± SEM, n =4; one sample and Wilcoxon test (Mps1i vs respective control=1): * indicates p =0.0335 (HCT116 RPS3-Keima Ctrl vs Mps1i) or p =0.0475 (HCT116 RPS3-Keima HSF1ca Ctrl vs Mps1i) or p =0.0128 (HCT116 RPL28-Keima Ctrl vs Mps1i); unpaired Student’s t-test: * indicates p =0.0486 (HCT116 RPS3-Keima Mps1i vs HSF1ca Mps1i), ** indicates p =0.0065 (HCT116 RPL28-Keima Mps1 vs HSF1ca Mps1i). D. Representative immunoblots and replicate quantitation of processed-Keima levels in the indicated HCT116 Ribo-Keima cell lines upon HA-Hsp90 (or mock) overexpression and treated for 24 hours with Mps1i or DMSO (control); HA was blotted as overexpression control and tubulin was used as loading control. Mean ± SEM, n =4; one sample and Wilcoxon test (Mps1i vs respective control=1): * indicates p =0.0267 (HCT116 RPS3-Keima Ctrl vs Mps1) or p =0.0479 (HCT116 RPS3-Keima HA-HSP90 Ctrl vs Mps1); unpaired Student’s t-test: * indicates p =0.0485 (HCT116 RPS3-Keima Mps1 vs HA-Hsp90 Mps1). E. Representative adult eyes in which CIN was induced with an eye-specific Gal4 driving bub3-RNAi (ey>bub3-i) or control wild-type eyes (ey>), where the indicated transgenes for either the depletion of Hsp70 (Hsp70A-i / Hsp70B-i) or its overexpression (Hsp70A) were expressed. F. Quantification of the analysed eye phenotypes, obtained as in (e) and expressed as the percentage of each phenotype across the samples. Number of replicates is shown on each histogram bar; Fisher’s exact test: * indicates p =0.0277 (Hsp70A-i) or p =0.0133 (Hsp70A-i), **** indicates p <0.0001. G. Representative images of larval wing discs in which CIN was induced with an apterous-specific Gal4 driving bub3-RNAi fused with a MyrT fluorescent protein (ap>myrT, bub3-i) or control wild-type tissues (ap>myrT), where the indicated transgenes for either the depletion of Hsp70 (Hsp70A-i / Hsp70B-i) or its overexpression (Hsp70A) were expressed. Tissues have been stained with cleaved-Dcp1 (cDcp1) and DAPI (to stain DNA); MyrT signal marks the aneuploid region; scale bars 50mm. H. Quantification of the area positive for cDcp1 signal, obtained as in (g) and normalised to the area of the dorsal region (D) (where ap>myrT, bub3-i is expressed) in the indicated samples. Number of replicates is shown on graph; one-way ANOVA, followed by Dunnett’s multiple comparison test (GFP-i vs each other sample): **** indicates p <0.0001. I. mRNA expression levels (log2(TPM+1)) of the reported genes, comparing the top and bottom aneuploidy quartiles of human cancer cell lines from the CCLE. Upper quartile, lower quartile and median of each violin plot are shown; two-tailed Student’s t-test: * indicates p =0.0185, *** indicates p =0.0007, **** indicates p <0.0001. J. CRISPR screens data of the reported genes, comparing the top and bottom aneuploidy quartiles of human cancer cell lines from the CCLE. Upper quartile, lower quartile and median of each violin plot are shown; two-tailed Student’s t-test: * indicates p =0.0292, **** indicates p <0.0001. K. RNAi dependency data of the reported genes, comparing the top and bottom aneuploidy quartiles of human cancer cell lines from the CCLE. Upper quartile, lower quartile and median of each violin plot are shown; two-tailed Student’s t-test: ** indicates p =0.0061 (HSF1) or p =0.0062 (HSPA1B), *** indicates p =0.0001.

Article Snippet: To inhibit Hsp90 chaperone family, cells were treated either with Geldanamycin (Geld, 1μM, Tocris) or 17-allylamino-17-demethoxy-geldanamycin (17-AAG, 1μM, Tocris), as indicated in figure legends.

Techniques: Western Blot, Quantitation Assay, Control, Comparison, Expressing, Over Expression, Staining, Two Tailed Test, CRISPR

$A. Representative immunoblots and replicate quantitation of puromycin incorporation (10μg/mL over 30 minutes) into the indicated cell lines, treated with Mps1i pulse or DMSO (control) and collected at 24 hours (HCT116) or 72 hours (RPE1); treatment with cycloheximide (CHX) (10μg/mL, 6h) was used as a negative control; vinculin was used as loading control for puromycin smear quantitation. Mean ± SEM, n =3 for HCT116, n =4 for RPE1; one sample and Wilcoxon test (Mps1i vs respective control=1): * indicates p =0.0382 (HCT116) or p =0.0170 (RPE1). B. Representative immunoblots and replicate quantitation of puromycin incorporation (10μg/mL over 30 minutes) into the indicated cell lines treated for 24 hours with Mps1i, DMSO (control) or Hsp90i Geldanamycin (1μM); vinculin was used as loading control for puromycin smear quantitation. Mean ± SEM, n =3 for HCT116, n =4 for RPE1; Kruskal-Wallis test, followed by Dunn’s multiple comparison test: * indicates p =0.0190 (HCT116) or p =0.0156 (RPE1). C. Representative immunoblots and replicate quantitation of puromycin incorporation (10μg/mL over 30 minutes) into the indicated HCT116 cell line, upon HSF1ca (or empty backbone) expression and treated for 24 hours with Mps1i or DMSO (control); vinculin and GAPDH were used as loading control. Mean ± SEM, n =6; one sample and Wilcoxon test. ** indicates p =0.0063. D. Schematic showing polysome profiling (left) and representative sucrose gradient absorbance at 254nm profiles (right) obtained from the cytoplasmic lysates of RPE1 cells treated with Mps1i pulse or DMSO (Ctrl) and analysed at 72 hours. E. Representative immunoblots for the co-sedimentation profiles of two ribosomal subunit markers (RPL26 and RPS6) in the sucrose gradient fractions obtained as in (D) . F. Quantitation of the relative absorbance (at 254nm) distribution of each component in Mps1i-and DMSO (Ctrl)-treated samples, calculated from the profiles obtained as in (D) . Mean ± SD; n =4; unpaired Student’s t-test: ** indicates p =0.0081. G. Comparison between the fraction of ribosomes in polysomes (FRP%) in Mps1i- and DMSO (Ctrl)-treated samples, calculated from the profiles obtained as in (D) . Mean ± SD; n =4; unpaired Student’s t-test: * indicates p =0.0201.$

Journal: bioRxiv

Article Title: Ribosome Quality Control Mitigates Proteotoxic Stress in Aneuploid Cells

doi: 10.64898/2026.01.19.700285

Figure Lengend Snippet: A. Representative immunoblots and replicate quantitation of puromycin incorporation (10μg/mL over 30 minutes) into the indicated cell lines, treated with Mps1i pulse or DMSO (control) and collected at 24 hours (HCT116) or 72 hours (RPE1); treatment with cycloheximide (CHX) (10μg/mL, 6h) was used as a negative control; vinculin was used as loading control for puromycin smear quantitation. Mean ± SEM, n =3 for HCT116, n =4 for RPE1; one sample and Wilcoxon test (Mps1i vs respective control=1): * indicates p =0.0382 (HCT116) or p =0.0170 (RPE1). B. Representative immunoblots and replicate quantitation of puromycin incorporation (10μg/mL over 30 minutes) into the indicated cell lines treated for 24 hours with Mps1i, DMSO (control) or Hsp90i Geldanamycin (1μM); vinculin was used as loading control for puromycin smear quantitation. Mean ± SEM, n =3 for HCT116, n =4 for RPE1; Kruskal-Wallis test, followed by Dunn’s multiple comparison test: * indicates p =0.0190 (HCT116) or p =0.0156 (RPE1). C. Representative immunoblots and replicate quantitation of puromycin incorporation (10μg/mL over 30 minutes) into the indicated HCT116 cell line, upon HSF1ca (or empty backbone) expression and treated for 24 hours with Mps1i or DMSO (control); vinculin and GAPDH were used as loading control. Mean ± SEM, n =6; one sample and Wilcoxon test. ** indicates p =0.0063. D. Schematic showing polysome profiling (left) and representative sucrose gradient absorbance at 254nm profiles (right) obtained from the cytoplasmic lysates of RPE1 cells treated with Mps1i pulse or DMSO (Ctrl) and analysed at 72 hours. E. Representative immunoblots for the co-sedimentation profiles of two ribosomal subunit markers (RPL26 and RPS6) in the sucrose gradient fractions obtained as in (D) . F. Quantitation of the relative absorbance (at 254nm) distribution of each component in Mps1i-and DMSO (Ctrl)-treated samples, calculated from the profiles obtained as in (D) . Mean ± SD; n =4; unpaired Student’s t-test: ** indicates p =0.0081. G. Comparison between the fraction of ribosomes in polysomes (FRP%) in Mps1i- and DMSO (Ctrl)-treated samples, calculated from the profiles obtained as in (D) . Mean ± SD; n =4; unpaired Student’s t-test: * indicates p =0.0201.

Techniques: Western Blot, Quantitation Assay, Control, Negative Control, Comparison, Expressing, Sedimentation

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