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hdac7 (BPS Bioscience)

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BPS Bioscience hdac7
Hdac7, supplied by BPS Bioscience, used in various techniques. Bioz Stars score: 94/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hdac7/HDAC7%2C+GST-tag+Recombinant/pmc13125535-601-68-73
Average 94 stars, based on 16 article reviews

hdac7 - by Bioz Stars, 2026-10

94/100 stars

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Article Title: Inhibition of class IIa histone deacetylase activity by gallic acid, sulforaphane, TMP269, and panobinostat.
Article Snippet: Histone deacetylase (HDAC) inhibitors are gaining increasing attention as potential therapeutics for cardiovascular diseases as well as cancer.. We recently reported that the class II HDAC inhibitor, MC1568, and the phytochemical, gallic acid, lowered high blood pressure in mouse models of hypertension.. We hypothesized that class II HDACs may be involved in the regulation of hypertension.

Article Title: Preclinical Characterization of SDFZ‐8, a Highly Potent HDAC1 Inhibitor, for Cancer Immunotherapy
Article Snippet: .. In detail, the HeLa nuclear extract, HDAC1 (BPS BIOSCIENCE INC, 50051), HDAC2 (BPS BIOSCIENCE Inc; 50052), HDAC3/NCOR1 complex (BPS BIOSCIENCE Inc; 50003), HDAC4 (BPS BIOSCIENCE Inc; 50004), HDAC5 (BPS BIOSCIENCE Inc; 50005), HDAC6 (BPS BIOSCIENCE Inc; 50006), HDAC7 (BPS BIOSCIENCE Inc; 50007), HDAC8 (BPS BIOSCIENCE Inc; 50008), HDAC9 (BPS BIOSCIENCE Inc; 50009), HDAC10 (BPS BIOSCIENCE Inc; 50010), or HDAC11 (BPS BIOSCIENCE Inc; 50011) was diluted to the proper concentrations according to the relative enzymatic activity and the linear range of the plate reader and mixed with different concentrations of drugs. ..

Enzymatic Assay:

Article Title: Histone deacetylase inhibitor LMK235 attenuates vascular constriction and aortic remodelling in hypertension
Article Snippet: .. We used fluorogenic HDAC1 (#50061), HDAC2 (#50062), HDAC3 (#50063), HDAC4 (#50064), HDAC5 (#50065), HDAC6 (#50076), HDAC7 (#50067), HDAC8 (#50068) and HDAC9 (#50069) enzyme assay kits from BPS Bioscience (San Diego, CA, USA). ..

Recombinant:

Article Title: Novel function of HATs and HDACs in homologous recombination through acetylation of human RAD52 at double-strand break sites
Article Snippet: .. The following recombinant human HDAC proteins were used: HDAC1 (BPS Bioscience, #50001, Lot 81110), HDAC2 (BPS Bioscience, #50002, Lot 81010), HDAC3-NCOR2 (BPS Bioscience, #50003, Lot 80917), HDAC8 (BPS Bioscience, #50008, Lot 81020), HDAC4 (BPS Bioscience, #50004, Lot 2000), HDAC5 (BPS Bioscience, #50045, Lot 80613-2), HDAC6 (BPS Bioscience, #50006, Lot 80926), HDAC7 (BPS Bioscience, #50007, Lot 2002), HDAC9 (BPS Bioscience, #50009, Lot 2000), HDAC10 (BPS Bioscience, #50010, Lot 80902), SIRT1 (BPS Bioscience, #50012, Lot 2001), SIRT2 (BPS Bioscience, #50013, Lot 2000), SIRT3 (BPS Bioscience, #50014, Lot 2003), SIRT4 (BPS Bioscience, #50015, Lot 2007), SIRT5 (BPS Bioscience, #50016, Lot 80903), SIRT6 (BPS Bioscience, #50017, Lot 80902), and SIRT7 (Abnova, # H00051547-P01, Lot 0980305). ..

Incubation:

Article Title: 1,3,4-oxadiazole derivatives as histone deacetylase inhibitors
Article Snippet: .. Study compound and HDAC7 (BPS Bioscience 50007) enzyme 5 nM was added in a 384 well Microplate (Geriner 784209) and incubated during 5 minutes at RT. .. Later Acetylated Peptide B (Perkin Elmer CLS960007) 2 μM was added and incubated during 1 hour at RT.

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Retrospective clinical analysis indicates that HDAC7 is associated with the immunotherapy response in BCa. A Retrospective analysis of the IMvigor210 cohort identified HDAC1 and HDAC7 as BCa immunotherapy response-associated HDACs. B Flowchart illustrating the screening and follow-up of BCa patients who received adjuvant immunotherapy at our center, with analysis of the correlation between HDAC1 or HDAC7 expression and immunotherapy response. C Correlation analysis of HDAC1 or HDAC7 expression with the prognosis of BCa patients receiving adjuvant immunotherapy ( n = 20). D Querying the TISIDB database revealed a negative correlation between HDAC7 expression and immunotherapy response in BCa. E Western blot analysis of HDAC7 expression in BCa tissues and adjacent non-tumor tissues. F IHC of HDAC7 expression in BCa tissues and adjacent non-tumor tissues. G qRT-PCR analysis of HDAC7 expression in 40 paired BCa tissues and adjacent non-tumor tissues (* P < 0.05). H Correlation between HDAC7 expression and overall prognosis in 40 BCa patients. I qRT-PCR analysis of HDAC7 expression in 7 BCa cell lines and one normal urothelial cell line (* P < 0.05, ** P < 0.01, *** P < 0.001). Data are mean ± SD, n = 3

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: Retrospective clinical analysis indicates that HDAC7 is associated with the immunotherapy response in BCa. A Retrospective analysis of the IMvigor210 cohort identified HDAC1 and HDAC7 as BCa immunotherapy response-associated HDACs. B Flowchart illustrating the screening and follow-up of BCa patients who received adjuvant immunotherapy at our center, with analysis of the correlation between HDAC1 or HDAC7 expression and immunotherapy response. C Correlation analysis of HDAC1 or HDAC7 expression with the prognosis of BCa patients receiving adjuvant immunotherapy ( n = 20). D Querying the TISIDB database revealed a negative correlation between HDAC7 expression and immunotherapy response in BCa. E Western blot analysis of HDAC7 expression in BCa tissues and adjacent non-tumor tissues. F IHC of HDAC7 expression in BCa tissues and adjacent non-tumor tissues. G qRT-PCR analysis of HDAC7 expression in 40 paired BCa tissues and adjacent non-tumor tissues (* P < 0.05). H Correlation between HDAC7 expression and overall prognosis in 40 BCa patients. I qRT-PCR analysis of HDAC7 expression in 7 BCa cell lines and one normal urothelial cell line (* P < 0.05, ** P < 0.01, *** P < 0.001). Data are mean ± SD, n = 3

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Adjuvant, Expressing, Western Blot, Quantitative RT-PCR

HDAC7 inhibits CD8 + T cell chemotaxis and anti-tumor activity in vitro. A Analysis of IMvigor210 cohort data shows negative correlation between HDAC7 expression and CD8 + T cell chemotaxis. B Flow cytometry confirms the efficiency of CD8 + T cell sorting using CD3 and CD8 antibodies. C Microscopy of CD8 + T cell morphology before and after activation. D Schematic of the co-culture model. E In vitro co-culture shows that HDAC7 inhibits CD8 + T cell chemotaxis (** P < 0.01, *** P < 0.001). F HDAC7 knockdown in T24 cells increases IFN-γ and granzyme B production by CD8 + T cells (* P < 0.05, ** P < 0.01). (G) HDAC7 overexpression in UMUC3 cells inhibits IFN-γ and granzyme B production by CD8 + T cells (** P < 0.01). H CD8 + T cell cytotoxicity is enhanced when co-cultured with HDAC7 knockdown T24 cells and reduced when co-cultured with HDAC7-overexpressing UMUC3 cells. Data are mean ± SD, n = 3

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: HDAC7 inhibits CD8 + T cell chemotaxis and anti-tumor activity in vitro. A Analysis of IMvigor210 cohort data shows negative correlation between HDAC7 expression and CD8 + T cell chemotaxis. B Flow cytometry confirms the efficiency of CD8 + T cell sorting using CD3 and CD8 antibodies. C Microscopy of CD8 + T cell morphology before and after activation. D Schematic of the co-culture model. E In vitro co-culture shows that HDAC7 inhibits CD8 + T cell chemotaxis (** P < 0.01, *** P < 0.001). F HDAC7 knockdown in T24 cells increases IFN-γ and granzyme B production by CD8 + T cells (* P < 0.05, ** P < 0.01). (G) HDAC7 overexpression in UMUC3 cells inhibits IFN-γ and granzyme B production by CD8 + T cells (** P < 0.01). H CD8 + T cell cytotoxicity is enhanced when co-cultured with HDAC7 knockdown T24 cells and reduced when co-cultured with HDAC7-overexpressing UMUC3 cells. Data are mean ± SD, n = 3

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Chemotaxis Assay, Activity Assay, In Vitro, Expressing, Flow Cytometry, FACS, Microscopy, Activation Assay, Co-Culture Assay, Knockdown, Over Expression, Cell Culture

HDAC7 inhibits CD8 + T cell chemotaxis and immunotherapy sensitivity in BCa in vivo. A Schematic of the HuNOG mouse model and experimental design for studying HDAC7’s effect on CD8 + T cell chemotaxis and immunotherapy response. B Flow cytometry analysis of human CD45 positivity in HuNOG mice. C Representative tumor images from HuNOG mice injected with HDAC7 knockdown or control T24 cells and treated with PD-1 or IgG antibodies ( n = 3). D Tumor volume in HuNOG mice measured every 3 days (** P < 0.01, *** P < 0.001). E Tumor weight assessment in HuNOG mice (** P < 0.01). F IHC analysis of CD3 and CD8 in tumors from HuNOG mice, showing increased CD8 + T cell infiltration with HDAC7 knockdown. G – H. Flow cytometry of CD8, IFN-γ, and granzyme B in tumor tissues, confirming that HDAC7 knockdown enhances CD8 + T cell infiltration and anti-tumor activity. Data are mean ± SD, n = 3

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: HDAC7 inhibits CD8 + T cell chemotaxis and immunotherapy sensitivity in BCa in vivo. A Schematic of the HuNOG mouse model and experimental design for studying HDAC7’s effect on CD8 + T cell chemotaxis and immunotherapy response. B Flow cytometry analysis of human CD45 positivity in HuNOG mice. C Representative tumor images from HuNOG mice injected with HDAC7 knockdown or control T24 cells and treated with PD-1 or IgG antibodies ( n = 3). D Tumor volume in HuNOG mice measured every 3 days (** P < 0.01, *** P < 0.001). E Tumor weight assessment in HuNOG mice (** P < 0.01). F IHC analysis of CD3 and CD8 in tumors from HuNOG mice, showing increased CD8 + T cell infiltration with HDAC7 knockdown. G – H. Flow cytometry of CD8, IFN-γ, and granzyme B in tumor tissues, confirming that HDAC7 knockdown enhances CD8 + T cell infiltration and anti-tumor activity. Data are mean ± SD, n = 3

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Chemotaxis Assay, In Vivo, Flow Cytometry, Injection, Knockdown, Control, Activity Assay

HDAC7 inhibits CCL5 expression and impedes CD8 + T cell infiltration in BCa. A Heat map of mRNA sequencing in three pairs of HDAC7 knockdown and control T24 cells. B Volcano plot of mRNA sequencing showing differentially expressed genes, including CCL5. C GSEA indicates enrichment of differentially expressed genes in the T cell chemotaxis pathway. D Analysis of the IMvigor210 cohort shows a negative correlation between HDAC7 and CCL5 expression. E – F Correlation between CCL5 expression and immune cell infiltration across cancers. G Pearson correlation between HDAC7 and CCL5 expression in 40 BCa tissues. H – I qRT-PCR analysis in T24 and UMUC3 cells demonstrates that HDAC7 knockdown upregulates, whereas overexpression downregulates, CCL5 expression (* P < 0.05, ** P < 0.01, *** P < 0.001). J – K ELISA shows that HDAC7 inhibits CCL5 protein expression (* P < 0.05, ** P < 0.01). Data are mean ± SD, n = 3

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: HDAC7 inhibits CCL5 expression and impedes CD8 + T cell infiltration in BCa. A Heat map of mRNA sequencing in three pairs of HDAC7 knockdown and control T24 cells. B Volcano plot of mRNA sequencing showing differentially expressed genes, including CCL5. C GSEA indicates enrichment of differentially expressed genes in the T cell chemotaxis pathway. D Analysis of the IMvigor210 cohort shows a negative correlation between HDAC7 and CCL5 expression. E – F Correlation between CCL5 expression and immune cell infiltration across cancers. G Pearson correlation between HDAC7 and CCL5 expression in 40 BCa tissues. H – I qRT-PCR analysis in T24 and UMUC3 cells demonstrates that HDAC7 knockdown upregulates, whereas overexpression downregulates, CCL5 expression (* P < 0.05, ** P < 0.01, *** P < 0.001). J – K ELISA shows that HDAC7 inhibits CCL5 protein expression (* P < 0.05, ** P < 0.01). Data are mean ± SD, n = 3

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Expressing, Sequencing, Knockdown, Control, Chemotaxis Assay, Quantitative RT-PCR, Over Expression, Enzyme-linked Immunosorbent Assay

HDAC7 targets SRSF7 via non-histone deacetylation to regulate CCL5 expression. A-B ChIP-qPCR with H3K9ac and H3K27ac antibodies examines HDAC7’s effect on acetylation in the CCL5 promoter region. C CO-IP and mass spectrometry identify HDAC7 binding to SRSF7. D Integration of mass spectrometry and RBPsuite predictions identifies SRSF7 as the mediator of HDAC7-regulated CCL5 expression. E CO-IP confirms HDAC7–SRSF7 interaction. F – G HDOCK analysis reveals HDAC7 binding to SRSF7 at Lys24, a potential deacetylation site. H – I Western blot analysis of the effects of HDAC7 on SRSF7 acetylation (Lys24) and protein expression in T24 and UMUC3 cells. J – K CO-IP analysis of how SRSF7 Lys24 mutation affects HDAC7–SRSF7 binding in T24 cells. Data are mean ± SD, n = 3

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: HDAC7 targets SRSF7 via non-histone deacetylation to regulate CCL5 expression. A-B ChIP-qPCR with H3K9ac and H3K27ac antibodies examines HDAC7’s effect on acetylation in the CCL5 promoter region. C CO-IP and mass spectrometry identify HDAC7 binding to SRSF7. D Integration of mass spectrometry and RBPsuite predictions identifies SRSF7 as the mediator of HDAC7-regulated CCL5 expression. E CO-IP confirms HDAC7–SRSF7 interaction. F – G HDOCK analysis reveals HDAC7 binding to SRSF7 at Lys24, a potential deacetylation site. H – I Western blot analysis of the effects of HDAC7 on SRSF7 acetylation (Lys24) and protein expression in T24 and UMUC3 cells. J – K CO-IP analysis of how SRSF7 Lys24 mutation affects HDAC7–SRSF7 binding in T24 cells. Data are mean ± SD, n = 3

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Expressing, ChIP-qPCR, Co-Immunoprecipitation Assay, Mass Spectrometry, Binding Assay, Western Blot, Mutagenesis

HDAC7 deacetylates SRSF7, promoting BTRC-induced ubiquitination and degradation of SRSF7. A PhosphoSitePlus analysis predicts acetylation and ubiquitination of SRSF7 at Lys24. B – C Ubibrowser and HDOCK predict BTRC binding to SRSF7 at Lys24. D CO-IP confirms BTRC–SRSF7 interaction. E CO-IP shows that HDAC7 knockdown promotes SRSF7 expression and reduces BTRC-SRSF7 binding in T24 cells. CO-IP shows that HDAC7 overexpression inhibits SRSF7 expression and increases BTRC-SRSF7 binding in UMUC3 cells. F CO-IP reveals that HDAC7 knockdown inhibits SRSF7 ubiquitination in T24 cells. G In T24 cells, HDAC7 overexpression increases SRSF7 ubiquitination, which is reduced by concurrent BTRC knockdown. H – I Western blot analysis shows that HDAC7 overexpression inhibits SRSF7 expression, which is restored by BTRC knockdown in T24 and UMUC3 cells. CO-IP analysis of SRSF7 Lys24 mutation on BTRC–SRSF7 binding in T24 cells. Data are mean ± SD, n = 3

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: HDAC7 deacetylates SRSF7, promoting BTRC-induced ubiquitination and degradation of SRSF7. A PhosphoSitePlus analysis predicts acetylation and ubiquitination of SRSF7 at Lys24. B – C Ubibrowser and HDOCK predict BTRC binding to SRSF7 at Lys24. D CO-IP confirms BTRC–SRSF7 interaction. E CO-IP shows that HDAC7 knockdown promotes SRSF7 expression and reduces BTRC-SRSF7 binding in T24 cells. CO-IP shows that HDAC7 overexpression inhibits SRSF7 expression and increases BTRC-SRSF7 binding in UMUC3 cells. F CO-IP reveals that HDAC7 knockdown inhibits SRSF7 ubiquitination in T24 cells. G In T24 cells, HDAC7 overexpression increases SRSF7 ubiquitination, which is reduced by concurrent BTRC knockdown. H – I Western blot analysis shows that HDAC7 overexpression inhibits SRSF7 expression, which is restored by BTRC knockdown in T24 and UMUC3 cells. CO-IP analysis of SRSF7 Lys24 mutation on BTRC–SRSF7 binding in T24 cells. Data are mean ± SD, n = 3

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Ubiquitin Proteomics, Binding Assay, Co-Immunoprecipitation Assay, Knockdown, Expressing, Over Expression, Western Blot, Mutagenesis

SRSF7 inhibits exon skipping of CCL5 pre-mRNA, thereby promoting mRNA maturation. A Analysis of alternative splicing (AS-Novel) in transcriptome sequencing data showed that exon skipping (ES) events accounted for 67.55% of all events. B AS-Novel analysis identified exon 2 (E2) skipping in CCL5. C ESE finder 3.0 predicted that CCL5 E2 contains exonic splicing enhancer (ESE) regions. D RIP assay confirmed the binding between SRSF7 and CCL5 pre-mRNA (*** P < 0.001). E Primers spanning E2 and targeting E2-skipping were designed; PCR amplification and agarose gel electrophoresis were used to assess changes in CCL5 alternative splicing following SRSF7 knockdown in T24 cells. F – G qRT-PCR showed that SRSF7 knockdown inhibited CCL5 expression in T24 and UMUC3 cells (* P < 0.05, *** P < 0.001). H – I ELISA showed reduced CCL5 protein production following SRSF7 knockdown in T24 and UMUC3 cells (** P < 0.01, *** P < 0.001). J – K qRT-PCR and ELISA-based rescue experiments demonstrated that HDAC7 knockdown increases CCL5 expression, which is repressed when SRSF7 is simultaneously knocked down in T24 cells (* P < 0.05, ** P < 0.01). Data are mean ± SD, n = 3

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: SRSF7 inhibits exon skipping of CCL5 pre-mRNA, thereby promoting mRNA maturation. A Analysis of alternative splicing (AS-Novel) in transcriptome sequencing data showed that exon skipping (ES) events accounted for 67.55% of all events. B AS-Novel analysis identified exon 2 (E2) skipping in CCL5. C ESE finder 3.0 predicted that CCL5 E2 contains exonic splicing enhancer (ESE) regions. D RIP assay confirmed the binding between SRSF7 and CCL5 pre-mRNA (*** P < 0.001). E Primers spanning E2 and targeting E2-skipping were designed; PCR amplification and agarose gel electrophoresis were used to assess changes in CCL5 alternative splicing following SRSF7 knockdown in T24 cells. F – G qRT-PCR showed that SRSF7 knockdown inhibited CCL5 expression in T24 and UMUC3 cells (* P < 0.05, *** P < 0.001). H – I ELISA showed reduced CCL5 protein production following SRSF7 knockdown in T24 and UMUC3 cells (** P < 0.01, *** P < 0.001). J – K qRT-PCR and ELISA-based rescue experiments demonstrated that HDAC7 knockdown increases CCL5 expression, which is repressed when SRSF7 is simultaneously knocked down in T24 cells (* P < 0.05, ** P < 0.01). Data are mean ± SD, n = 3

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Alternative Splicing, Sequencing, Binding Assay, Amplification, Agarose Gel Electrophoresis, Knockdown, Quantitative RT-PCR, Expressing, Enzyme-linked Immunosorbent Assay

Virtual screening identifies Pinocembrin as a specific HDAC7 inhibitor. A Workflow of virtual screening for HDAC7 inhibitors. B Chemical structure of Pinocembrin and its predicted binding score with HDAC7. C Schematic diagrams showing Pinocembrin binding to HDAC7 in cartoon and surface representations. D Three-dimensional (3D) and two-dimensional (2D) views of Pinocembrin binding to HDAC7. In the 3D diagram, the C backbone of HDAC7 is green, N atoms blue, O atoms magenta, H atoms white, and Pinocembrin sky blue. Purple dashed lines indicate hydrogen bond lengths, with longer lines representing weaker interactions. E–F. MST experiments evaluate the binding affinity of Pinocembrin to HDAC7. G–H. T24 and MB49 cells were treated with increasing concentrations of Pinocembrin (10, 50, 100, 200 µM); HDAC activity was assessed in cells with different HDAC7 expression levels using an HDAC Activity Assay Kit (* P < 0.05, ** P < 0.01, *** P < 0.001). Data are mean ± SD, n = 3

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: Virtual screening identifies Pinocembrin as a specific HDAC7 inhibitor. A Workflow of virtual screening for HDAC7 inhibitors. B Chemical structure of Pinocembrin and its predicted binding score with HDAC7. C Schematic diagrams showing Pinocembrin binding to HDAC7 in cartoon and surface representations. D Three-dimensional (3D) and two-dimensional (2D) views of Pinocembrin binding to HDAC7. In the 3D diagram, the C backbone of HDAC7 is green, N atoms blue, O atoms magenta, H atoms white, and Pinocembrin sky blue. Purple dashed lines indicate hydrogen bond lengths, with longer lines representing weaker interactions. E–F. MST experiments evaluate the binding affinity of Pinocembrin to HDAC7. G–H. T24 and MB49 cells were treated with increasing concentrations of Pinocembrin (10, 50, 100, 200 µM); HDAC activity was assessed in cells with different HDAC7 expression levels using an HDAC Activity Assay Kit (* P < 0.05, ** P < 0.01, *** P < 0.001). Data are mean ± SD, n = 3

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Binding Assay, Activity Assay, Expressing, HDAC Activity Assay

Schematic model of the Pinocembrin/HDAC7/BTRC/SRSF7/CCL5 regulatory and functional network

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin

doi: 10.1186/s13046-025-03585-3

Figure Lengend Snippet: Schematic model of the Pinocembrin/HDAC7/BTRC/SRSF7/CCL5 regulatory and functional network

Article Snippet: HDAC7 recombinant protein was obtained from SIGNALCHEM (cat. H89-31G), and Pinocembrin was obtained from the MedChemExpress (CAS: 205370-59−8).

Techniques: Functional Assay

Effect of lead secosteroid–2-pyrazoline hybrids 3f , 3j , and 3k on signaling pathways in MCF-7 breast cancer cells. Antibodies against androgen receptor (AR), estrogen receptor α (ERα), GREB1, S6K, and its phosphorylated form (p-S6K), Bcl-2, and its phosphorylated form (p-Bcl-2), and α-tubulin were used for immunoblotting.

Journal: Biomedicines

Article Title: Secosteroid–2-Pyrazoline Hybrids: Design, Synthesis, Biological Evaluation and Development of Therapeutic Combinations Against ERα-Positive Breast Cancer Cells

doi: 10.3390/biomedicines13123057

Figure Lengend Snippet: Effect of lead secosteroid–2-pyrazoline hybrids 3f , 3j , and 3k on signaling pathways in MCF-7 breast cancer cells. Antibodies against androgen receptor (AR), estrogen receptor α (ERα), GREB1, S6K, and its phosphorylated form (p-S6K), Bcl-2, and its phosphorylated form (p-Bcl-2), and α-tubulin were used for immunoblotting.

Article Snippet: Primary antibodies against androgen receptor (AR), estrogen receptor α (ERα), GREB1, S6K, and its phosphorylated form (p-S6K), Bcl-2, and its phosphorylated form (p-Bcl-2), and α-tubulin were employed (Cell Signaling Technology, Danvers, MA, USA). α-Tubulin served as the internal loading control.

Techniques: Protein-Protein interactions, Western Blot

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hdac7 (BPS Bioscience)

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