brd4 inhibitor jq  (MedChemExpress)

Journal: PLOS One

Article Title: SHP2 improved Late-onset fetal growth restriction via modulating ROS/BRD4/PI3K/YAP/PIGF signaling induced angiogenesis

doi: 10.1371/journal.pone.0342649

Figure Lengend Snippet: A: Boxplot of sample normalization for the FGR dataset GSE147776 ; B: Volcano plot of differentially expressed genes for the FGR dataset GSE147776 ; C: Heatmap of differentially expressed gene clustering for the FGR dataset GSE147776 ; Da: GO enrichment bubble plot of DEGs; Db: GO enrichment bar plot of DEGs; Ea: KEGG enrichment bubble plot of DEGs; Eb: KEGG enrichment lollipop plot of DEGs; F: Scatter plot of BRD4 and KEAP1 correlation; G: Scatter plot of KEAP1 and Nrf2 correlation; H: Heatmap of molecular interactions among BRD4, NOX4, NOX2, Nrf2, SHP2, P53, VEGFR, PI3K, CREB, JNK, and P38; I: Lollipop plot of YAP and effector factor correlations (CREB, VEGF, VEGFR2, SOX9, OCT4, SOX2, Ki-67, Nrf2).

Article Snippet: BRD4 inhibitor JQ-1, SHP2 inhibitor PHPS1, PI3K agonist 740 Y-P, and YAP inhibitor Verteporfin were purchased from MCE.

Techniques:

Journal: PLOS One

Article Title: SHP2 improved Late-onset fetal growth restriction via modulating ROS/BRD4/PI3K/YAP/PIGF signaling induced angiogenesis

doi: 10.1371/journal.pone.0342649

Figure Lengend Snippet: A: Western blot analysis of NOX4, nuclear BRD4, p-SHP2, p-PI3K, nuclear YAP, Nrf2, and PIGF protein expressions in EPCs in the following six groups: NC group, Model group, Model + JQ-1 group, Model + JQ-1 + PHPS1 group, Model + JQ-1 + PHPS1 + 740Y-P group, and Model + JQ-1 + PHPS1 + 740Y-P + Verteporfin group, GAPDH as the control protein; B: Statistical analysis of relative protein expression levels. N = 3; Data are expressed as mean ± standard deviation; Different lowercase letters on the same column indicate significant differences between groups at P < 0.05, while different uppercase letters indicate significant differences at P < 0.01.

Article Snippet: BRD4 inhibitor JQ-1, SHP2 inhibitor PHPS1, PI3K agonist 740 Y-P, and YAP inhibitor Verteporfin were purchased from MCE.

Techniques: Western Blot, Control, Expressing, Standard Deviation

Journal: PLOS One

Article Title: SHP2 improved Late-onset fetal growth restriction via modulating ROS/BRD4/PI3K/YAP/PIGF signaling induced angiogenesis

doi: 10.1371/journal.pone.0342649

Figure Lengend Snippet: A: Western blot analysis of VEGF and HIF1α protein expressions in EPCs in the following six groups: NC group, Model group, Model + JQ-1 group, Model + JQ-1 + PHPS1 group, Model + JQ-1 + PHPS1 + 740Y-P group, and Model + JQ-1 + PHPS1 + 740Y-P + Verteporfin group, along with statistical analysis of relative protein expression levels. GAPDH as the control protein; B: Tube formation assay measuring vascular intersections, total vessel length, and vessel branch length, along with statistical analysis of number of neovessels visual field. N = 3; Data are expressed as mean ± standard deviation; Different lowercase letters on the same column indicate significant differences between groups at P < 0.05, while different uppercase letters indicate significant differences at P < 0.01.

Article Snippet: BRD4 inhibitor JQ-1, SHP2 inhibitor PHPS1, PI3K agonist 740 Y-P, and YAP inhibitor Verteporfin were purchased from MCE.

Techniques: Western Blot, Expressing, Control, Tube Formation Assay, Standard Deviation

Journal: PLOS One

Article Title: SHP2 improved Late-onset fetal growth restriction via modulating ROS/BRD4/PI3K/YAP/PIGF signaling induced angiogenesis

doi: 10.1371/journal.pone.0342649

Figure Lengend Snippet: A: Western blot analysis of OCT4, SOX2, and C-Myc protein expressions in EPCs in the following six groups: NC group, Model group, Model + JQ-1 group, Model + JQ-1 + PHPS1 group, Model + JQ-1 + PHPS1 + 740Y-P group, and Model + JQ-1 + PHPS1 + 740Y-P + Verteporfin group, along with statistical analysis of relative protein expression levels. GAPDH as the control protein; B: Colony formation assay observing EPCs proliferation, along with statistical analysis of number of cloned cells; C: Flow cytometry analysis of the cell cycle, along with statistical analysis of cell cycle distribution; D: Flow cytometry analysis of cell apoptosis, along with statistical analysis of apoptosis rate. N = 3; Data are expressed as mean ± standard deviation; Different lowercase letters on the same column indicate significant differences between groups at P < 0.05, while different uppercase letters indicate significant differences at P < 0.01.

Article Snippet: BRD4 inhibitor JQ-1, SHP2 inhibitor PHPS1, PI3K agonist 740 Y-P, and YAP inhibitor Verteporfin were purchased from MCE.

Techniques: Western Blot, Expressing, Control, Colony Assay, Clone Assay, Flow Cytometry, Standard Deviation

Journal: PLOS One

Article Title: SHP2 improved Late-onset fetal growth restriction via modulating ROS/BRD4/PI3K/YAP/PIGF signaling induced angiogenesis

doi: 10.1371/journal.pone.0342649

Figure Lengend Snippet: SHP2 induces endothelial progenitor cell activation by regulating ROS/BRD4 and PI3K/YAP/PIGF, improving late-onset fetal growth restriction.

Article Snippet: BRD4 inhibitor JQ-1, SHP2 inhibitor PHPS1, PI3K agonist 740 Y-P, and YAP inhibitor Verteporfin were purchased from MCE.

Techniques: Activation Assay

Journal: International Journal of Molecular Sciences

Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells

doi: 10.3390/ijms26168074

Figure Lengend Snippet: TGF-β-induced BRD4 expression along with SMC markers in 10T1/2 cells. ( A , B ), TGF-β-induced BRD4 and SMC marker expression dose dependently in 10T1/2 cells. Serum-starved 10T1/2 cells were treated with vehicle or different concentrations of TGF-β as indicated for 48 h. BRD4 and VSMC markers (α-SMA and SM22α) were detected by Western blotting (WB, ( A )) and quantified in ( B ). Tubulin served as the loading control. *, p < 0.05 compared to vehicle group (0 ng/mL, ( B )), n = 3 independent experiments. ( C , D ), 10T1/2 cells were starved for 24 h, followed by vehicle or TGF-β (5 ng/mL) induction for various times as indicated. WB ( C ) and qPCR ( D ) were performed to detect BRD4 and SMC marker protein and mRNA expression, respectively. *, p < 0.05 compared to vehicle group (0 h, ( D )), n = 3 replicates. Cyclophilin was the internal control for qPCR.

Article Snippet: The small molecular inhibitor of BRD4 JQ1 (HY-13030) and degraders ARV-825 (HY-16954) and dBET1 (HY-101838) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Marker, Western Blot, Control

Journal: International Journal of Molecular Sciences

Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells

doi: 10.3390/ijms26168074

Figure Lengend Snippet: BRD4 knockdown attenuated TGF-β-induced differentiation of 10T1/2 cells to SMCs. ( A ), 10T1/2 cells were transfected with scramble or siBRD4, followed by treatment with vehicle or TGF-β (5 ng/mL) for an additional 48 h. The expression of BRD4 and SMC markers was detected by WB ( A ). ( B ) is the quantification of A based on 3 independent experiments. *, p < 0.05 compared to vehicle-treated scramble; #, p < 0.05 compared to TGF-β-treated scramble.

Article Snippet: The small molecular inhibitor of BRD4 JQ1 (HY-13030) and degraders ARV-825 (HY-16954) and dBET1 (HY-101838) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Knockdown, Transfection, Expressing

Journal: International Journal of Molecular Sciences

Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells

doi: 10.3390/ijms26168074

Figure Lengend Snippet: BRD4 inhibitor JQ1 inhibited TGF-β-induced differentiation of 10T1/2 cells into SMCs. ( A , B ), serum-starved 10T1/2 cells were pretreated with different doses of JQ1, followed by TGF-β treatment for an additional 48 h, and cells were then harvested for WB analysis of SMC markers. Tubulin was used as the loading control. B is the quantification of A based on 3 independent experiments. *, p < 0.05 compared to vehicle control; #, p < 0.05 compared to TGF-β treatment alone group. ( C ), Serum-starved 10T1/2 cells were pretreated with different doses of JQ1, followed by TGF-β treatment for an additional 16 h before cells were harvested for qPCR analysis of SMC markers. Cyclophilin was used as an internal control. *, p < 0.05 compared to vehicle control; #, p < 0.05 compared to TGF-β treatment alone group. n = 3 replicates.

Article Snippet: The small molecular inhibitor of BRD4 JQ1 (HY-13030) and degraders ARV-825 (HY-16954) and dBET1 (HY-101838) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Control

Journal: International Journal of Molecular Sciences

Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells

doi: 10.3390/ijms26168074

Figure Lengend Snippet: BRD4 degraders inhibited TGF-β-induced differentiation of 10T1/2 cells into SMCs. ( A , C ), Serum-starved 10T1/2 cells were pretreated with different doses of ARV-825 (ARV, ( A )) or dBET1 ( C ), followed by TGF-β treatment (5 ng/mL) for an additional 48 h, and the cells were then harvested for WB analysis of SMC markers. Tubulin was used as the loading control. ( B , D ) are the quantification of ( A , C ), respectively, based on 3 independent experiments. *, p < 0.05 compared to vehicle control; #, p < 0.05 compared to TGF-β treatment alone group.

Article Snippet: The small molecular inhibitor of BRD4 JQ1 (HY-13030) and degraders ARV-825 (HY-16954) and dBET1 (HY-101838) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Control

Journal: International Journal of Molecular Sciences

Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells

doi: 10.3390/ijms26168074

Figure Lengend Snippet: BRD4 knockdown inhibited TGF-β-induced TAZ expression in 10T1/2 cells. ( A , B ), Serum-starved 10T1/2 cells were treated with TGF-β treatment (5 ng/mL) for different times as indicated before the cells were harvested for WB ( A ) and qPCR ( B ) analysis of TAZ. Tubulin was used as the loading control. Cyclophilin was used as the internal control for qPCR analysis in B. *, p < 0.05 compared to control (0 h), n = 3 replicates. ( C ), 10T1/2 cells were transfected with scramble control or siBRD4, followed by treatment with vehicle or TGF-β (5 ng/mL) for an additional 8 h. The cells were then harvested for analysis of given protein by WB. ( D ) is the quantification of C based on 3 independent experiments. *, p < 0.05 compared to the vehicle-treated scramble; #, p < 0.05 compared to TGF-β-treated scramble.

Article Snippet: The small molecular inhibitor of BRD4 JQ1 (HY-13030) and degraders ARV-825 (HY-16954) and dBET1 (HY-101838) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Knockdown, Expressing, Control, Transfection

Journal: International Journal of Molecular Sciences

Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells

doi: 10.3390/ijms26168074

Figure Lengend Snippet: BRD4 inhibitors suppressed TGF-β-induced TAZ expression in 10T1/2 cells. ( A ), serum-starved 10T1/2 cells were pretreated with JQ1 (2 µM), dBET1 (100 nM), or ARV-825 (ARV, 100 nM), followed by TGF-β treatment (5 ng/mL) for an additional 8 h. The cells were then harvested for WB analysis of TAZ. Tubulin was used as the loading control. ( B ) is the quantification of A based on 3 independent experiments. *, p < 0.05 compared with vehicle control; #, p < 0.05 compared to TGF-β treatment alone group. ( C – E ), serum-starved 10T1/2 cells were pretreated with different doses of JQ1 ( C ), ARV-825 (ARV, ( D )) or dBET1 ( E ), followed by TGF-β treatment (5 ng/mL) for an additional 8 h to detect TAZ through WB.

Article Snippet: The small molecular inhibitor of BRD4 JQ1 (HY-13030) and degraders ARV-825 (HY-16954) and dBET1 (HY-101838) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Control

Journal: International Journal of Molecular Sciences

Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells

doi: 10.3390/ijms26168074

Figure Lengend Snippet: Myocardin is involved in BRD4 mediated10T1/2 differentiation into SMCs. ( A ) Serum-starved 10T1/2 cells were treated with TGF-β (5 ng/mL) for various times to detect Myocardin expression through WB. ( B ) is the quantification of A based on three independent experiments. *, p < 0.05 compared with control (0 h). ( C ) 10T1/2 cells were transfected with scramble control or siBRD4, followed by treatment with vehicle or TGF-β (5 ng/mL) for an additional 24 h. Myocardin expression was detected through WB. ( D ) is the quantification of C based on three independent experiments. *, p < 0.05 compared with the vehicle-treated scramble; #, p < 0.05 compared with TGF-β-treated scramble. ( E ) serum-starved 10T1/2 cells were pretreated with JQ1 (2 µM), dBET1 (100 nM), or ARV-825 (100 nM), followed by TGF-β treatment (5 ng/mL) for an additional 24 h. The cells were then harvested for WB analysis of myocardin. ( F ) is the quantification of E based on three independent experiments. *, p < 0.05 compared to vehicle control; #, p < 0.05 compared to TGF-β treatment alone group.

Article Snippet: The small molecular inhibitor of BRD4 JQ1 (HY-13030) and degraders ARV-825 (HY-16954) and dBET1 (HY-101838) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Control, Transfection

Journal: International Journal of Molecular Sciences

Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells

doi: 10.3390/ijms26168074

Figure Lengend Snippet: BRD4 inhibition reduced the nuclear levels of Smad3 induced by TGF-β in 10T1/2 cells. ( A ) Serum-starved 10T1/2 cells were pretreated with ARV-825 (100 nM) for 30 min, followed by TGF-β treatment (5 ng/mL) for an additional 2 h, and cells were then subject to immunofluorescence staining of Smad3. Images were taken at 200×. ( B ) Serum-starved 10T1/2 cells were pretreated with JQ1 (1 µM) or ARV-825 (100 nM), followed by TGF-β treatment (5 ng/mL) for an additional 2 h, and cells were then subject to fractionation WB analysis of Smad3. Tubulin and Lamin B1 were used as loading controls for the cytoplasm and nucleus, respectively.

Article Snippet: The small molecular inhibitor of BRD4 JQ1 (HY-13030) and degraders ARV-825 (HY-16954) and dBET1 (HY-101838) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Inhibition, Immunofluorescence, Staining, Fractionation

Journal: International immunopharmacology

Article Title: USP22/BRD4 mediated hedgehog pathway activation contributes to airway remodeling in asthma.

doi: 10.1016/j.intimp.2025.114538

Figure Lengend Snippet: Fig. 1. TGF-β1 promotes ASMCs proliferation and induces USP22, BRD4, GLI1, OPN upregulation. A ASMCs were treated with different concentrations of TGF-β1 (0–100 ng/ml) for 48 h, and cell viability was evaluated using the Cell Counting Kit-8(CCK-8) assay (n = 6 per group). B ASMCs were treated with 30 ng/ml TGF-β1 for the indicated time (0–72 h), and cell viability was evaluated using the CCK-8 assay (n = 6 per group). C ASMCs were incubated with 30 ng/ml TGF-β1 for 48 h, and cell proliferation was measured by EdU incorporation assay (scale bar = 100 μm, n = 3 per group). D ASMCs were incubated with 30 ng/ml TGF-β1 for 48 h, USP22, BRD4, GLI1, OPN protein levels were examined by immunoblotting (n = 3 per group). E ASMCs were stimulated with 30 ng/ml TGF-β1 for 48 h, BRD4 mRNA level was examined by qRT-PCR (n = 3 per group). * P < 0.05.

Article Snippet: All OVA-sensitized rats were randomly divided into 6 groups (n = 5 rats/group) and treated as follows: OVA model group; OVA + DMSO group: received vehicle DMSO by daily intraperitoneal injection; OVA + TGF-β receptor inhibitor SB-431542 group: received SB-431542 (10 mg/kg, Aladdin, Shanghai, China) by daily intraperitoneal injection [24]; OVA + USP22 inhibitor Usp22i-S02 group: received Usp22i-S02 (14 mg/kg, Selleck, USA, E1330) by daily intraperitoneal injection [25]; OVA + BRD4 inhibitor JQ-1 group: received JQ-1 (25 mg/kg, MedChemExpress, USA, HY-13030) by intraperitoneal injection three times a week [26,27]; OVA + GLI1 inhibitor GANT61 group: received GANT61 (10 mg/kg, MedChemExpress, USA, HY-13901) every 2 days by intraperitoneal injection [28]; OVA + OPN inhibitor group: received OPN expression inhibitor 1 (5 mg/kg, MedChemExpress, USA, HY-146064) every 3 days by intraperitoneal injection.

Techniques: Cell Counting, CCK-8 Assay, Incubation, Western Blot, Quantitative RT-PCR

Journal: International immunopharmacology

Article Title: USP22/BRD4 mediated hedgehog pathway activation contributes to airway remodeling in asthma.

doi: 10.1016/j.intimp.2025.114538

Figure Lengend Snippet: Fig. 2. USP22 mediates the upregulation of BRD4, GLI1 and OPN in TGF-β1 treated ASMCs. A ASMCs were transfected with USP22 siRNA or NC siRNA for 48 h, the protein level of USP22 was examined using immunoblotting (n = 3 per group). B ASMCs were pre-transfected with USP22 siRNA or NC siRNA for 24 h and then stimulated with 30 ng/ml TGF-β1 for 48 h, BRD4, GLI1, OPN protein levels were analyzed using immunoblotting (n = 3 per group). C ASMCs were stimulated with TGF-β1 for 48 h, and proteasome inhibitor MG132 (10 μM) was added 8 h before the end of TGF-β1 stimulation. Immunoprecipitation assay was accomplished with anti-BRD4, or anti-IgG antibody and the endogenously precipitated complexes were detected with anti-ubiquitin antibody. D ASMCs were pre-transfected with USP22 siRNA or NC siRNA and then stimulated with TGF-β1 for 48 h, the ubiquitination levels of BRD4 were examined by immunoprecipitation assay. E Co- immunoprecipitation assay of the interaction between USP22 and BRD4 in ASMCs following immunoprecipitation with anti-USP22, anti-BRD4 or anti-IgG anti body and then the endogenously precipitated complexes were detected with anti-USP22 or anti-BRD4 antibody. * P < 0.05.

Article Snippet: All OVA-sensitized rats were randomly divided into 6 groups (n = 5 rats/group) and treated as follows: OVA model group; OVA + DMSO group: received vehicle DMSO by daily intraperitoneal injection; OVA + TGF-β receptor inhibitor SB-431542 group: received SB-431542 (10 mg/kg, Aladdin, Shanghai, China) by daily intraperitoneal injection [24]; OVA + USP22 inhibitor Usp22i-S02 group: received Usp22i-S02 (14 mg/kg, Selleck, USA, E1330) by daily intraperitoneal injection [25]; OVA + BRD4 inhibitor JQ-1 group: received JQ-1 (25 mg/kg, MedChemExpress, USA, HY-13030) by intraperitoneal injection three times a week [26,27]; OVA + GLI1 inhibitor GANT61 group: received GANT61 (10 mg/kg, MedChemExpress, USA, HY-13901) every 2 days by intraperitoneal injection [28]; OVA + OPN inhibitor group: received OPN expression inhibitor 1 (5 mg/kg, MedChemExpress, USA, HY-146064) every 3 days by intraperitoneal injection.

Techniques: Transfection, Western Blot, Immunoprecipitation, Ubiquitin Proteomics, Co-Immunoprecipitation Assay

Journal: International immunopharmacology

Article Title: USP22/BRD4 mediated hedgehog pathway activation contributes to airway remodeling in asthma.

doi: 10.1016/j.intimp.2025.114538

Figure Lengend Snippet: Fig. 3. BRD4 mediates TGF-β1-induced upregulation of GLI1 and OPN. A ASMCs were pre-treated with 0.5 μM JQ-1 for 1 h and then stimulated with 30 ng/ml TGF- β1 for 48 h, GLI1 and OPN protein levels were examined by immunoblotting (n = 3 per group). B ASMCs were transfected with GLI1 siRNA or NC siRNA for 48 h, the protein level of GLI1 was examined using immunoblotting (n = 3 per group). C ASMCs were exposed to 30 ng/ml TGF-β1 for 48 h with prior the transfection of GLI1 siRNA or NC siRNA for 24 h. Protein levels of OPN was measured by immunoblotting (n = 3 per group). * P < 0.05.

Article Snippet: All OVA-sensitized rats were randomly divided into 6 groups (n = 5 rats/group) and treated as follows: OVA model group; OVA + DMSO group: received vehicle DMSO by daily intraperitoneal injection; OVA + TGF-β receptor inhibitor SB-431542 group: received SB-431542 (10 mg/kg, Aladdin, Shanghai, China) by daily intraperitoneal injection [24]; OVA + USP22 inhibitor Usp22i-S02 group: received Usp22i-S02 (14 mg/kg, Selleck, USA, E1330) by daily intraperitoneal injection [25]; OVA + BRD4 inhibitor JQ-1 group: received JQ-1 (25 mg/kg, MedChemExpress, USA, HY-13030) by intraperitoneal injection three times a week [26,27]; OVA + GLI1 inhibitor GANT61 group: received GANT61 (10 mg/kg, MedChemExpress, USA, HY-13901) every 2 days by intraperitoneal injection [28]; OVA + OPN inhibitor group: received OPN expression inhibitor 1 (5 mg/kg, MedChemExpress, USA, HY-146064) every 3 days by intraperitoneal injection.

Techniques: Western Blot, Transfection

Journal: International immunopharmacology

Article Title: USP22/BRD4 mediated hedgehog pathway activation contributes to airway remodeling in asthma.

doi: 10.1016/j.intimp.2025.114538

Figure Lengend Snippet: Fig. 4. USP22/BRD4/GLI1/OPN axis mediates TGF-β1-induced ASMCs proliferation. ASMCs were pre-transfected with USP22 siRNA or GLI1 siRNA or NC siRNA for 24 h, or pre-treated with JQ-1 (0.5 μM) for 1 h, and then stimulated with 30 ng/ml TGF-β1 for 48 h, cell proliferation was detected by EdU incorporation assay (scale bar = 100 μm) (n = 3 per group). * P < 0.05.

Article Snippet: All OVA-sensitized rats were randomly divided into 6 groups (n = 5 rats/group) and treated as follows: OVA model group; OVA + DMSO group: received vehicle DMSO by daily intraperitoneal injection; OVA + TGF-β receptor inhibitor SB-431542 group: received SB-431542 (10 mg/kg, Aladdin, Shanghai, China) by daily intraperitoneal injection [24]; OVA + USP22 inhibitor Usp22i-S02 group: received Usp22i-S02 (14 mg/kg, Selleck, USA, E1330) by daily intraperitoneal injection [25]; OVA + BRD4 inhibitor JQ-1 group: received JQ-1 (25 mg/kg, MedChemExpress, USA, HY-13030) by intraperitoneal injection three times a week [26,27]; OVA + GLI1 inhibitor GANT61 group: received GANT61 (10 mg/kg, MedChemExpress, USA, HY-13901) every 2 days by intraperitoneal injection [28]; OVA + OPN inhibitor group: received OPN expression inhibitor 1 (5 mg/kg, MedChemExpress, USA, HY-146064) every 3 days by intraperitoneal injection.

Techniques: Transfection

Journal: International immunopharmacology

Article Title: USP22/BRD4 mediated hedgehog pathway activation contributes to airway remodeling in asthma.

doi: 10.1016/j.intimp.2025.114538

Figure Lengend Snippet: Fig. 5. Targeting TGF-β1/USP22/BRD4/GLI1/OPN axis regulates relevant downstream molecules expressions in asthmatic rats. A schematic diagram of the OVA- sensitized chronic rat asthma model (n = 5 per group). B Concentrations of TGF-β1 in rat lung tissues were measured by Elisa (n = 3 per group). C Protein levels of USP22, BRD4, GLI1 and OPN were assessed by immunoblotting in lung tissues of control and asthma models (n = 3 per group). D Protein levels of USP22, BRD4, GLI1 and OPN were examined by immunoblotting in lung tissues of control, asthma models with or without prior treatment of SB-431542 (n = 3 per group). E Protein levels of BRD4, GLI1 and OPN were determined by immunoblotting in lung tissues of control, asthma models with or without prior treatment of Usp22i-s02 (n = 3 per group). F Protein level of GLI1 and OPN were detected by immunoblotting in lung tissues of control, asthma models with or without prior treatment of JQ-1 (n = 3 per group). G Protein level of OPN were evaluated by immunoblotting in lung tissues of control, asthma models with or without prior treatment of GANT61 (n = 3 per group). * P < 0.05.

Article Snippet: All OVA-sensitized rats were randomly divided into 6 groups (n = 5 rats/group) and treated as follows: OVA model group; OVA + DMSO group: received vehicle DMSO by daily intraperitoneal injection; OVA + TGF-β receptor inhibitor SB-431542 group: received SB-431542 (10 mg/kg, Aladdin, Shanghai, China) by daily intraperitoneal injection [24]; OVA + USP22 inhibitor Usp22i-S02 group: received Usp22i-S02 (14 mg/kg, Selleck, USA, E1330) by daily intraperitoneal injection [25]; OVA + BRD4 inhibitor JQ-1 group: received JQ-1 (25 mg/kg, MedChemExpress, USA, HY-13030) by intraperitoneal injection three times a week [26,27]; OVA + GLI1 inhibitor GANT61 group: received GANT61 (10 mg/kg, MedChemExpress, USA, HY-13901) every 2 days by intraperitoneal injection [28]; OVA + OPN inhibitor group: received OPN expression inhibitor 1 (5 mg/kg, MedChemExpress, USA, HY-146064) every 3 days by intraperitoneal injection.

Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Control

Journal: International immunopharmacology

Article Title: USP22/BRD4 mediated hedgehog pathway activation contributes to airway remodeling in asthma.

doi: 10.1016/j.intimp.2025.114538

Figure Lengend Snippet: Fig. 6. Inhibition of TGF-β1/USP22/BRD4/GLI1/OPN axis alleviates the airway remodeling of asthma. Concentrations of IL-4 (A), IL-5 (B) and IL-13 (C) in rat lung tissues were measured by Elisa (n = 3 per group). D Respiratory resistance (Rrs) was measured with inhalation of designated doses of nebulized methacholine chloride (0–100 mg/ml) using a FlexiVent animal ventilator (n = 3 per group). E Bronchial wall thickness shown by hematoxylin and eosin (H&E) staining, epithelial goblet cell proliferation shown by Periodic Acid-Schiff (PAS) staining, subepithelial collagen fiber deposition shown by Masson staining and bronchial musculari zation shown by α-smooth muscle actin (α-SMA) staining, scale bar = 100 μm. F Changes in airway wall thickness (Wat/Pbm) (n = 4 per group). G Changes of PAS- positive epithelium cells (%) (n = 4 per group). H Changes of subepithelial collagen fiber deposition (Wcol/Pbm) (n = 4 per group). I Muscularization quantification (α-SMA positive area/Pbm) (n = 4 per group). * P < 0.05.

Article Snippet: All OVA-sensitized rats were randomly divided into 6 groups (n = 5 rats/group) and treated as follows: OVA model group; OVA + DMSO group: received vehicle DMSO by daily intraperitoneal injection; OVA + TGF-β receptor inhibitor SB-431542 group: received SB-431542 (10 mg/kg, Aladdin, Shanghai, China) by daily intraperitoneal injection [24]; OVA + USP22 inhibitor Usp22i-S02 group: received Usp22i-S02 (14 mg/kg, Selleck, USA, E1330) by daily intraperitoneal injection [25]; OVA + BRD4 inhibitor JQ-1 group: received JQ-1 (25 mg/kg, MedChemExpress, USA, HY-13030) by intraperitoneal injection three times a week [26,27]; OVA + GLI1 inhibitor GANT61 group: received GANT61 (10 mg/kg, MedChemExpress, USA, HY-13901) every 2 days by intraperitoneal injection [28]; OVA + OPN inhibitor group: received OPN expression inhibitor 1 (5 mg/kg, MedChemExpress, USA, HY-146064) every 3 days by intraperitoneal injection.

Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Staining

Journal: Communications biology

Article Title: USP35 promotes the growth of ER positive breast cancer by inhibiting ferroptosis via BRD4-SLC7A11 axis.

doi: 10.1038/s42003-025-07513-1

Figure Lengend Snippet: Fig. 8 | A working model of USP35 regulating ferroptosis in ER+ breast cancer tumors. USP35 interacts with and deubiquitinates BRD4, stabilizing the protein level of BRD4 that regulates SLC7A11. This interaction leads to USP35-invoked upregu- lating SLC7A11 expression, inhibiting ferroptosis, and promoting cell growth in ER+ breast cancer.

Article Snippet: Breast cancer cells MCF-7 (8000 per well) and ZR-75-1 (12,000 per well) were cultured in 24-well tissue culture plates and treated with DMSO or 5 μM (+ )-JQ-1 (BRD4 inhibitor) (Selleck) for 3 d. After one week of culturing, cells were fixed with 10% neutral formalin and stained with 0.5% crystal violet solution.

Techniques: Expressing