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geldanamycin
Geldanamycin, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/geldanamycin/Geldanamycin/bio_rxiv__64898__2026__01__19__700285-185-10-13
Average 93 stars, based on 31 article reviews
Geldanamycin, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/geldanamycin/Geldanamycin/bio_rxiv__64898__2026__01__19__700285-185-10-13
Average 93 stars, based on 31 article reviews
geldanamycin - by Bioz Stars,
2026-09
93/100 stars
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1) Product Images from "Ribosome Quality Control Mitigates Proteotoxic Stress in Aneuploid Cells"
Article Title: Ribosome Quality Control Mitigates Proteotoxic Stress in Aneuploid Cells
Journal: bioRxiv
doi: 10.64898/2026.01.19.700285
Figure Legend 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.
Techniques Used: Western Blot, Quantitation Assay, Control, Comparison, Expressing, Over Expression, Staining, Two Tailed Test, CRISPR
Figure Legend 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 Used: Western Blot, Quantitation Assay, Control, Negative Control, Comparison, Expressing, Sedimentation
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![( A ) Heatmap of responses to HSP90 inhibitors (17-AAG, <t>geldanamycin,</t> 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.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_8563/pmc13178563/pmc13178563__sciadv.aed7122-f7.jpg)
