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

Vdac Inhibitor Dids, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/vdac+inhibitor+dids/bio_rxiv__64898__2026__04__04__716514-378-6-9?v=MedChemExpress
Average 94 stars, based on 27 article reviews

vdac inhibitor dids - by Bioz Stars, 2026-07

94/100 stars

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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

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

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