HY-108438 Search Results


atf6 inhibitor  (MedChemExpress)
95
MedChemExpress atf6 inhibitor
IVA employed <t>ATF6</t> to induce the expression of FBXO24 to mediate RAD51 down-regulation. A IVA treatment and co-treatment of IVA and OLA reduced the expression of RAD51 only. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was performed. GAPDH was the loading control. B ATF6 inhibition abolished the effect of RAD51 down-regulation mediated by IVA. 5 μM of ATF6 inhibitor Ceapin-A7, 0.1 µM of IVA and 5 μM of OLA were used. The cells were treated for 72 h. Western blot was performed. HSP90 was the loading control. C IVA enhanced ATF6 binding to the promoter region of FBXO24 . The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. ChIP was performed with anti-ATF6. qPCR was employed to determine the enrichment of 3 different regions of FBXO24 promoter in the elute. Results were shown as mean ± SD from 4 independent experiments. One-way ANOVA was employed. D ATF6 inhibition abolished the effect of IVA on FBXO24 induction. 5 μM of ATF6 inhibitor Ceapin-A7 and 0.1 µM of IVA and/or 5 μM of OLA were used for treating the cells for 48 h. qPCR was performed. Results were shown as mean ± SD from 4 independent experiments. E IVA treatment enhanced FBXO24 protein expression. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was used. HSP90 was the loading control. F Knockdown of FBXO24 compromised the effect of IVA on RAD51 down-regulation. The cells were treated with 0.1 µM of IVA and 15 μM of siFBXO24 for 72 h. Western blot was used. HSP90 was the loading control. NT represents no treatment control. *** represent P < 0.001
Atf6 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a 485  (MedChemExpress)
93
MedChemExpress a 485
IVA employed <t>ATF6</t> to induce the expression of FBXO24 to mediate RAD51 down-regulation. A IVA treatment and co-treatment of IVA and OLA reduced the expression of RAD51 only. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was performed. GAPDH was the loading control. B ATF6 inhibition abolished the effect of RAD51 down-regulation mediated by IVA. 5 μM of ATF6 inhibitor Ceapin-A7, 0.1 µM of IVA and 5 μM of OLA were used. The cells were treated for 72 h. Western blot was performed. HSP90 was the loading control. C IVA enhanced ATF6 binding to the promoter region of FBXO24 . The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. ChIP was performed with anti-ATF6. qPCR was employed to determine the enrichment of 3 different regions of FBXO24 promoter in the elute. Results were shown as mean ± SD from 4 independent experiments. One-way ANOVA was employed. D ATF6 inhibition abolished the effect of IVA on FBXO24 induction. 5 μM of ATF6 inhibitor Ceapin-A7 and 0.1 µM of IVA and/or 5 μM of OLA were used for treating the cells for 48 h. qPCR was performed. Results were shown as mean ± SD from 4 independent experiments. E IVA treatment enhanced FBXO24 protein expression. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was used. HSP90 was the loading control. F Knockdown of FBXO24 compromised the effect of IVA on RAD51 down-regulation. The cells were treated with 0.1 µM of IVA and 15 μM of siFBXO24 for 72 h. Western blot was used. HSP90 was the loading control. NT represents no treatment control. *** represent P < 0.001
A 485, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
a 485 - by Bioz Stars, 2026-02
93/100 stars
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661w cells  (MedChemExpress)
93
MedChemExpress 661w cells
IVA employed <t>ATF6</t> to induce the expression of FBXO24 to mediate RAD51 down-regulation. A IVA treatment and co-treatment of IVA and OLA reduced the expression of RAD51 only. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was performed. GAPDH was the loading control. B ATF6 inhibition abolished the effect of RAD51 down-regulation mediated by IVA. 5 μM of ATF6 inhibitor Ceapin-A7, 0.1 µM of IVA and 5 μM of OLA were used. The cells were treated for 72 h. Western blot was performed. HSP90 was the loading control. C IVA enhanced ATF6 binding to the promoter region of FBXO24 . The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. ChIP was performed with anti-ATF6. qPCR was employed to determine the enrichment of 3 different regions of FBXO24 promoter in the elute. Results were shown as mean ± SD from 4 independent experiments. One-way ANOVA was employed. D ATF6 inhibition abolished the effect of IVA on FBXO24 induction. 5 μM of ATF6 inhibitor Ceapin-A7 and 0.1 µM of IVA and/or 5 μM of OLA were used for treating the cells for 48 h. qPCR was performed. Results were shown as mean ± SD from 4 independent experiments. E IVA treatment enhanced FBXO24 protein expression. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was used. HSP90 was the loading control. F Knockdown of FBXO24 compromised the effect of IVA on RAD51 down-regulation. The cells were treated with 0.1 µM of IVA and 15 μM of siFBXO24 for 72 h. Western blot was used. HSP90 was the loading control. NT represents no treatment control. *** represent P < 0.001
661w Cells, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/661w cells/product/MedChemExpress
Average 93 stars, based on 1 article reviews
661w cells - by Bioz Stars, 2026-02
93/100 stars
  Buy from Supplier

Image Search Results


IVA employed ATF6 to induce the expression of FBXO24 to mediate RAD51 down-regulation. A IVA treatment and co-treatment of IVA and OLA reduced the expression of RAD51 only. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was performed. GAPDH was the loading control. B ATF6 inhibition abolished the effect of RAD51 down-regulation mediated by IVA. 5 μM of ATF6 inhibitor Ceapin-A7, 0.1 µM of IVA and 5 μM of OLA were used. The cells were treated for 72 h. Western blot was performed. HSP90 was the loading control. C IVA enhanced ATF6 binding to the promoter region of FBXO24 . The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. ChIP was performed with anti-ATF6. qPCR was employed to determine the enrichment of 3 different regions of FBXO24 promoter in the elute. Results were shown as mean ± SD from 4 independent experiments. One-way ANOVA was employed. D ATF6 inhibition abolished the effect of IVA on FBXO24 induction. 5 μM of ATF6 inhibitor Ceapin-A7 and 0.1 µM of IVA and/or 5 μM of OLA were used for treating the cells for 48 h. qPCR was performed. Results were shown as mean ± SD from 4 independent experiments. E IVA treatment enhanced FBXO24 protein expression. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was used. HSP90 was the loading control. F Knockdown of FBXO24 compromised the effect of IVA on RAD51 down-regulation. The cells were treated with 0.1 µM of IVA and 15 μM of siFBXO24 for 72 h. Western blot was used. HSP90 was the loading control. NT represents no treatment control. *** represent P < 0.001

Journal: Journal of Translational Medicine

Article Title: Ivabradine induces RAD51 degradation, potentiating PARP inhibitor efficacy in non-germline BRCA pathogenic variant triple-negative breast cancer

doi: 10.1186/s12967-025-06902-8

Figure Lengend Snippet: IVA employed ATF6 to induce the expression of FBXO24 to mediate RAD51 down-regulation. A IVA treatment and co-treatment of IVA and OLA reduced the expression of RAD51 only. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was performed. GAPDH was the loading control. B ATF6 inhibition abolished the effect of RAD51 down-regulation mediated by IVA. 5 μM of ATF6 inhibitor Ceapin-A7, 0.1 µM of IVA and 5 μM of OLA were used. The cells were treated for 72 h. Western blot was performed. HSP90 was the loading control. C IVA enhanced ATF6 binding to the promoter region of FBXO24 . The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. ChIP was performed with anti-ATF6. qPCR was employed to determine the enrichment of 3 different regions of FBXO24 promoter in the elute. Results were shown as mean ± SD from 4 independent experiments. One-way ANOVA was employed. D ATF6 inhibition abolished the effect of IVA on FBXO24 induction. 5 μM of ATF6 inhibitor Ceapin-A7 and 0.1 µM of IVA and/or 5 μM of OLA were used for treating the cells for 48 h. qPCR was performed. Results were shown as mean ± SD from 4 independent experiments. E IVA treatment enhanced FBXO24 protein expression. The cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 72 h. Western blot was used. HSP90 was the loading control. F Knockdown of FBXO24 compromised the effect of IVA on RAD51 down-regulation. The cells were treated with 0.1 µM of IVA and 15 μM of siFBXO24 for 72 h. Western blot was used. HSP90 was the loading control. NT represents no treatment control. *** represent P < 0.001

Article Snippet: The PARPi Niraparib (NIRA; HY-10619), ATF6 inhibitor (Ceapin-A7; HY-108434) and Z-VAD-FMK (HY-16658B) were purchased from MedChemExpress and dissolved in DMSO.

Techniques: Expressing, Western Blot, Control, Inhibition, Binding Assay, Knockdown

The ATF6-FBXO24 axis was essential for the efficacy of IVA and OLA co-treatment. A RAD51 interacted with FBXO24. The cells were transfected with pcDNA3.1_myc_RAD51 . 24 h post-transfection, the cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 48 h. CoIP was performed with either anti-mouse IgG or anti-myc antibodies. Western blot was employed to evaluate the level of indicated protein candidates in the immunoprecipitant. B IVA treatment enhanced the degree of ubiquitination on RAD51. The cells were transfected with pcDNA3.1_myc_RAD51 . 24 h post-transfection, the cells were treated with 5 μM of MG132, 0.1 µM of IVA and/or 5 μM of OLA for 48 h. Co-immunoprecipitation was performed with either anti-mouse IgG or anti-MYC antibodies. Western blot was performed using an anti-K48-linkage polyubiquitin antibody. C Knockdown of FBXO24 could compromise the effect of the co-treatment on the degree of K-48 conjugation polyubiquitination of RAD51. The cells were transfected with pcDNA3.1_myc_RAD51 . 24 h post-transfection, the cells were treated with 5 μM of MG132, 15 μM of siCtrl or siFBXO24, 0.1 µM of IVA and 5 μM of OLA for 48 h. Co-immunoprecipitation was performed with either anti-mouse IgG or anti-myc antibodies. Western blot was performed using an anti-K48-linkage polyubiquitin antibody. D FBXO24 knockdown weakened the efficacy of IVA and OLA co-treatment. The cells were treated with 0.1 µM of IVA, 5 μM of OLA and 15 μM of siFBXO24 or 15 μM of siCtrl for 72 h. Cell viability was assayed with CCK8. Results were shown as mean ± SD from 6 independent experiments. Students’ t-test was used. NT represents no chemical treatment. NSR represents no siRNA treatment. *** represent P < 0.001

Journal: Journal of Translational Medicine

Article Title: Ivabradine induces RAD51 degradation, potentiating PARP inhibitor efficacy in non-germline BRCA pathogenic variant triple-negative breast cancer

doi: 10.1186/s12967-025-06902-8

Figure Lengend Snippet: The ATF6-FBXO24 axis was essential for the efficacy of IVA and OLA co-treatment. A RAD51 interacted with FBXO24. The cells were transfected with pcDNA3.1_myc_RAD51 . 24 h post-transfection, the cells were treated with 0.1 µM of IVA and/or 5 μM of OLA for 48 h. CoIP was performed with either anti-mouse IgG or anti-myc antibodies. Western blot was employed to evaluate the level of indicated protein candidates in the immunoprecipitant. B IVA treatment enhanced the degree of ubiquitination on RAD51. The cells were transfected with pcDNA3.1_myc_RAD51 . 24 h post-transfection, the cells were treated with 5 μM of MG132, 0.1 µM of IVA and/or 5 μM of OLA for 48 h. Co-immunoprecipitation was performed with either anti-mouse IgG or anti-MYC antibodies. Western blot was performed using an anti-K48-linkage polyubiquitin antibody. C Knockdown of FBXO24 could compromise the effect of the co-treatment on the degree of K-48 conjugation polyubiquitination of RAD51. The cells were transfected with pcDNA3.1_myc_RAD51 . 24 h post-transfection, the cells were treated with 5 μM of MG132, 15 μM of siCtrl or siFBXO24, 0.1 µM of IVA and 5 μM of OLA for 48 h. Co-immunoprecipitation was performed with either anti-mouse IgG or anti-myc antibodies. Western blot was performed using an anti-K48-linkage polyubiquitin antibody. D FBXO24 knockdown weakened the efficacy of IVA and OLA co-treatment. The cells were treated with 0.1 µM of IVA, 5 μM of OLA and 15 μM of siFBXO24 or 15 μM of siCtrl for 72 h. Cell viability was assayed with CCK8. Results were shown as mean ± SD from 6 independent experiments. Students’ t-test was used. NT represents no chemical treatment. NSR represents no siRNA treatment. *** represent P < 0.001

Article Snippet: The PARPi Niraparib (NIRA; HY-10619), ATF6 inhibitor (Ceapin-A7; HY-108434) and Z-VAD-FMK (HY-16658B) were purchased from MedChemExpress and dissolved in DMSO.

Techniques: Transfection, Western Blot, Ubiquitin Proteomics, Immunoprecipitation, Knockdown, Conjugation Assay