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MedChemExpress hsp90 inhibitor geldanamycin

a, Representative WB and quantification showing effect of VDAC, Hsp70, and <t>Hsp90</t> 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.

Hsp90 Inhibitor Geldanamycin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Tau-induced mitochondrial reverse electron transport drives neurodegeneration"

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

Journal: bioRxiv

doi: 10.64898/2026.04.04.716514

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.

Figure Legend 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.

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

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

Figure Legend 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 Used: Control, Activity Assay, Purification, Transfection, Western Blot, Two Tailed Test

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

Image Search Results

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

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

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

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

CD93 interacts with HSP90 to maintain its proangiogenic ability. A Peak map of MS detection in the CD93 IgG and CD93 IP groups. B Gene Ontology (GO) analysis of the MS results. BP, biological process; CC, cellular component; MF, molecular function. C Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of the MS results. D Predicted schematic diagram of the interaction between HSP90 and CD93 via the AutoDock website. The black line indicates the boundary: the left represents CD93, and the right represents HSP90. E Local schematic representation of the interaction between HSP90 and CD93. Cyan represents CD93 (left), purple represents HSP90 (right), and yellow represents the hydrogen bonds between HSP90 and CD93. F Co-IP experiments were performed to identify the interaction between HSP90 and CD93. G Co-IP experiments were performed to identify the interaction between HSP27 and CD93. H CD93 protein expression after treatment with 50 nM 17-AAG with or without ad.CD93. G-CD93, glycosylated CD93; NG-CD93, nonglycosylated CD93. I Relative expression levels of glycosylated and nonglycosylated CD93 protein in ( H ) after normalization to β-actin. J Cell spheroid sprouting assay after treatment with 50 nM 17-AAG with or without ad.CD93; the lower column shows the local map of the top right quarter of the cell spheroids. Scale bar = 200 μm. K Length of the sprouts in ( J ). L Migration of ECs after treatment with 50 nM 17-AAG with or without ad.CD93. Scale bar = 200 μm. M The number of migrated ECs in ( L ). * P < 0.05; ** P < 0.01; *** P < 0.001, ns: not significant. Data represent three independent experiments and are shown as means (SDs)

Journal: Cellular & Molecular Biology Letters

Article Title: Heat shock protein 90 stabilizes CD93 glycosylation to influence angiogenesis during diabetic wound healing

doi: 10.1186/s11658-025-00847-y

Figure Lengend Snippet: CD93 interacts with HSP90 to maintain its proangiogenic ability. A Peak map of MS detection in the CD93 IgG and CD93 IP groups. B Gene Ontology (GO) analysis of the MS results. BP, biological process; CC, cellular component; MF, molecular function. C Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of the MS results. D Predicted schematic diagram of the interaction between HSP90 and CD93 via the AutoDock website. The black line indicates the boundary: the left represents CD93, and the right represents HSP90. E Local schematic representation of the interaction between HSP90 and CD93. Cyan represents CD93 (left), purple represents HSP90 (right), and yellow represents the hydrogen bonds between HSP90 and CD93. F Co-IP experiments were performed to identify the interaction between HSP90 and CD93. G Co-IP experiments were performed to identify the interaction between HSP27 and CD93. H CD93 protein expression after treatment with 50 nM 17-AAG with or without ad.CD93. G-CD93, glycosylated CD93; NG-CD93, nonglycosylated CD93. I Relative expression levels of glycosylated and nonglycosylated CD93 protein in ( H ) after normalization to β-actin. J Cell spheroid sprouting assay after treatment with 50 nM 17-AAG with or without ad.CD93; the lower column shows the local map of the top right quarter of the cell spheroids. Scale bar = 200 μm. K Length of the sprouts in ( J ). L Migration of ECs after treatment with 50 nM 17-AAG with or without ad.CD93. Scale bar = 200 μm. M The number of migrated ECs in ( L ). * P < 0.05; ** P < 0.01; *** P < 0.001, ns: not significant. Data represent three independent experiments and are shown as means (SDs)

Article Snippet: In addition, the HSP90 inhibitor 17-AAG (MCE) was delivered via intraperitoneal injection at a dosage of 100 mg/kg 2 weeks prior to skin wound construction, and recombinant CD93 (rCD93, R&D) was administered via local injections at the periphery of the wound for three consecutive days at a dosage of 80 ng.

Techniques: Co-Immunoprecipitation Assay, Expressing, Migration

HSP90 protects CD93 from ubiquitin‒proteasome-mediated degradation and facilitates FAK signaling pathway activation. ( A ) HSP90α mRNA expression after treatment with siHSP90α. ( B ) HSP90α protein expression after treatment with siHSP90α. ( C ) Relative HSP90α protein expression levels in ( B ) after normalization to that of β-actin. ( D ) Cell spheroid sprouting assay after treatment with siHSP90α-3 with or without ad.CD93. Scale bar = 200 μm. ( E ) Local magnification of the top right quadrant of the cell spheroids. ( F ) Statistical analysis of the length of the sprouts in ( D ). ( G ) CD93 protein expression after treatment with bortezomib with or without 17-AAG. ( H ) Relative protein expression of glycosylated and nonglycosylated CD93 in ( G ) after normalization to that of β-actin. G-CD93, glycosylated CD93; NG-CD93, non-glycosylated CD93. ( I , J ) Co-IP experiment testing the ubiquitination of CD93 after treatment with 17-AAG with or without bortezomib. ( K ) Schematic diagrams of the full-length CD93 plasmid and a truncated CD93 plasmid lacking the intracellular domain (CD93△), both of which are tagged with red fluorescent protein (RFP). CTLD, Sushi, epidermal growth factor-like, and mucin are extracellular domains of CD93. TM is a transmembrane domain. Cy is a cytosolic domain. ( L ) CoIP experiment to detect the interaction between HSP90 and CD93 or CD93△. ( M ) The expression of p-FAK and FAK after ad.CD93 treatment. ( N ) Relative expression of p-FAK and FAK in ( M ) after normalization to that of β-actin. ( O ) The expression of p-FAK and FAK after siCD93 treatment. ( P ) Relative expression of p-FAK and FAK in ( O ) after normalization to that of β-actin. ( Q ) The expression of p-FAK and FAK after treatment with 17-AAG with or without ad.CD93. * P < 0.05; ** P < 0.01; *** P < 0.001, ns = not significant. Data represent three independent experiments and are shown as means (SDs)

Journal: Cellular & Molecular Biology Letters

Article Title: Heat shock protein 90 stabilizes CD93 glycosylation to influence angiogenesis during diabetic wound healing

doi: 10.1186/s11658-025-00847-y

Figure Lengend Snippet: HSP90 protects CD93 from ubiquitin‒proteasome-mediated degradation and facilitates FAK signaling pathway activation. ( A ) HSP90α mRNA expression after treatment with siHSP90α. ( B ) HSP90α protein expression after treatment with siHSP90α. ( C ) Relative HSP90α protein expression levels in ( B ) after normalization to that of β-actin. ( D ) Cell spheroid sprouting assay after treatment with siHSP90α-3 with or without ad.CD93. Scale bar = 200 μm. ( E ) Local magnification of the top right quadrant of the cell spheroids. ( F ) Statistical analysis of the length of the sprouts in ( D ). ( G ) CD93 protein expression after treatment with bortezomib with or without 17-AAG. ( H ) Relative protein expression of glycosylated and nonglycosylated CD93 in ( G ) after normalization to that of β-actin. G-CD93, glycosylated CD93; NG-CD93, non-glycosylated CD93. ( I , J ) Co-IP experiment testing the ubiquitination of CD93 after treatment with 17-AAG with or without bortezomib. ( K ) Schematic diagrams of the full-length CD93 plasmid and a truncated CD93 plasmid lacking the intracellular domain (CD93△), both of which are tagged with red fluorescent protein (RFP). CTLD, Sushi, epidermal growth factor-like, and mucin are extracellular domains of CD93. TM is a transmembrane domain. Cy is a cytosolic domain. ( L ) CoIP experiment to detect the interaction between HSP90 and CD93 or CD93△. ( M ) The expression of p-FAK and FAK after ad.CD93 treatment. ( N ) Relative expression of p-FAK and FAK in ( M ) after normalization to that of β-actin. ( O ) The expression of p-FAK and FAK after siCD93 treatment. ( P ) Relative expression of p-FAK and FAK in ( O ) after normalization to that of β-actin. ( Q ) The expression of p-FAK and FAK after treatment with 17-AAG with or without ad.CD93. * P < 0.05; ** P < 0.01; *** P < 0.001, ns = not significant. Data represent three independent experiments and are shown as means (SDs)

Techniques: Activation Assay, Expressing, Co-Immunoprecipitation Assay, Ubiquitin Proteomics, Plasmid Preparation

$The role of the HSP90–CD93 interaction in wound healing angiogenesis in vivo. A Wound healing in the control group, 17-AAG group, rCD93 group, and 17-AAG + rCD93 group at D0, D2, D4, and D6, respectively. Ruler = 5 mm. B Schematic diagram of overlapping wound healing at different times drawn via ImageJ. C Statistical analysis of the wound area in the four groups of mice at D0. D Statistical analysis of the wound area in the four groups of mice at D2. E Statistical analysis of the wound area in the four groups of mice at D4. F Statistical analysis of the wound area in the four groups at D6. G HE staining of wounds in the four groups at D0, D2, D4, and D6. The dotted lines delineate the boundary between the epidermal and dermal layers, and the length of the wound is marked by arrows. Scale bar = 1 mm. H Statistical analysis of the wound length at D7 in ( G ). I Masson staining of wounds in the four groups at D0, D2, D4, and D6. Blue represents collagen. Scale bar = 1 mm. J Statistical analysis of the collagen volume fraction in the four groups; the collagen volume fraction = collagen volume/total area. K Merged IF image of new vessels at D7. Red represents CD31 (a marker of new vessels), green represents CD93, and blue represents DAPI. Scale bar = 20 μm. See Supplementary Fig. S6A for fluorescence images of each individual channel. L Statistical analysis of the CD31-positive area at D7. M Merged IF image of new vessels and pericytes at D7; red represents CD31, green represents NG2 (a marker of pericytes), and blue represents DAPI. Scale bar = 20 μm. See Supplementary Fig. S6B for fluorescence images of each individual channel. ( N ) Statistical analysis of the NG2-positive area at D7. * P < 0.05; ** P < 0.01; *** P < 0.001, ns: not significant. Data are shown as means (SDs)$

Journal: Cellular & Molecular Biology Letters

Article Title: Heat shock protein 90 stabilizes CD93 glycosylation to influence angiogenesis during diabetic wound healing

doi: 10.1186/s11658-025-00847-y

Figure Lengend Snippet: The role of the HSP90–CD93 interaction in wound healing angiogenesis in vivo. A Wound healing in the control group, 17-AAG group, rCD93 group, and 17-AAG + rCD93 group at D0, D2, D4, and D6, respectively. Ruler = 5 mm. B Schematic diagram of overlapping wound healing at different times drawn via ImageJ. C Statistical analysis of the wound area in the four groups of mice at D0. D Statistical analysis of the wound area in the four groups of mice at D2. E Statistical analysis of the wound area in the four groups of mice at D4. F Statistical analysis of the wound area in the four groups at D6. G HE staining of wounds in the four groups at D0, D2, D4, and D6. The dotted lines delineate the boundary between the epidermal and dermal layers, and the length of the wound is marked by arrows. Scale bar = 1 mm. H Statistical analysis of the wound length at D7 in ( G ). I Masson staining of wounds in the four groups at D0, D2, D4, and D6. Blue represents collagen. Scale bar = 1 mm. J Statistical analysis of the collagen volume fraction in the four groups; the collagen volume fraction = collagen volume/total area. K Merged IF image of new vessels at D7. Red represents CD31 (a marker of new vessels), green represents CD93, and blue represents DAPI. Scale bar = 20 μm. See Supplementary Fig. S6A for fluorescence images of each individual channel. L Statistical analysis of the CD31-positive area at D7. M Merged IF image of new vessels and pericytes at D7; red represents CD31, green represents NG2 (a marker of pericytes), and blue represents DAPI. Scale bar = 20 μm. See Supplementary Fig. S6B for fluorescence images of each individual channel. ( N ) Statistical analysis of the NG2-positive area at D7. * P < 0.05; ** P < 0.01; *** P < 0.001, ns: not significant. Data are shown as means (SDs)

Techniques: In Vivo, Control, Staining, Marker, Fluorescence

Cytotoxicity and inhibitory effects on RV replication of different HSP90 inhibitors. ( A ) Plots for cell viability of MA104, Caco-2, and HT-29 cells after treatment with NVP-HSP990, GA, or 17-AAG at indicated concentrations for 24 h. Cell viability was tested using the CCK-8 assay. ( B ) Plots for RV (Wa and SA11 strains) inhibition in MA104, Caco-2, and HT-29 cells after treatment with NVP-HSP990, GA, or 17-AAG at indicated concentrations for 24 h. RV replication was tested by PFA, and IC 50 values are indicated at the top of each plot. The experiments were performed in triplicate, and the data are presented as mean ± SEM and are representative of four ( A ) and two ( B ) independent experiments. ns, not significant; * P < 0.05, ** P < 0.01, **** P < 0.0001 (two-way ANOVA).

Journal: Journal of Virology

Article Title: A small-molecule HSP90 inhibitor, NVP-HSP990, alleviates rotavirus infection

doi: 10.1128/jvi.01883-25

Figure Lengend Snippet: Cytotoxicity and inhibitory effects on RV replication of different HSP90 inhibitors. ( A ) Plots for cell viability of MA104, Caco-2, and HT-29 cells after treatment with NVP-HSP990, GA, or 17-AAG at indicated concentrations for 24 h. Cell viability was tested using the CCK-8 assay. ( B ) Plots for RV (Wa and SA11 strains) inhibition in MA104, Caco-2, and HT-29 cells after treatment with NVP-HSP990, GA, or 17-AAG at indicated concentrations for 24 h. RV replication was tested by PFA, and IC 50 values are indicated at the top of each plot. The experiments were performed in triplicate, and the data are presented as mean ± SEM and are representative of four ( A ) and two ( B ) independent experiments. ns, not significant; * P < 0.05, ** P < 0.01, **** P < 0.0001 (two-way ANOVA).

Article Snippet: HSP90 inhibitors (NVP-HSP990, GA, and 17-AAG) and Ribavirin (Selleck, USA) were dissolved in DMSO (Sigma, USA).

Techniques: CCK-8 Assay, Inhibition

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