Journal: Current Issues in Molecular Biology

Article Title: IGFBP5 Promotes Atherosclerosis in APOE −/− Mice Through Phenotypic Transformation of VSMCs

doi: 10.3390/cimb47070555

Figure Lengend Snippet: Overexpression of IGFBP5 does not influence food consumption by and the body weight of ApoE −/− mice. ( A ) IGFBP5 mRNA expression level in skeletal muscle of ApoE −/− mice at 10 weeks of experimental treatment ( n = 3). ( B ) Plasma IGFBP5 protein levels at 10 weeks of experimental treatment ( n = 3). ( C ) Weight change curve ( n = 15). ( D ) Comparison of average daily food intake during the entire experimental treatment among groups ( n = 15). Data are expressed as the mean ± SEM. * p < 0.05. NS means no significant difference.

Article Snippet: The primary antibody used in this experiment was a rabbit anti- IGFBP5 antibody (1:500, #55205-1-AP; Proteintech Group, Chicago, IL, USA).

Techniques: Over Expression, Expressing, Clinical Proteomics, Comparison

Journal: Current Issues in Molecular Biology

Article Title: IGFBP5 Promotes Atherosclerosis in APOE −/− Mice Through Phenotypic Transformation of VSMCs

doi: 10.3390/cimb47070555

Figure Lengend Snippet: Overexpression of IGFBP5 enhances the development of atherosclerotic plaques in ApoE −/− mice. Oil Red O staining of the aorta ( A ) and statistical quantification ( B ). ( C ) H&E staining (up panel) and Oil Red O staining (down panel) of cardiac outflow tract sections. Scale bar: 500 μm. ( D ) Statistical quantification of neutral lipids in the plaques of the cardiac outflow tract sections stained with Oil Red O ( n = 10). Data are expressed as the mean ± SEM. * p < 0.05. NS means no significant difference.

Article Snippet: The primary antibody used in this experiment was a rabbit anti- IGFBP5 antibody (1:500, #55205-1-AP; Proteintech Group, Chicago, IL, USA).

Techniques: Over Expression, Staining

Journal: Current Issues in Molecular Biology

Article Title: IGFBP5 Promotes Atherosclerosis in APOE −/− Mice Through Phenotypic Transformation of VSMCs

doi: 10.3390/cimb47070555

Figure Lengend Snippet: Effect of overexpression of IGFBP5 on blood lipid levels in ApoE −/− mice. Plasma was collected from each group of mice ( n = 15) at week 0, 4, 8, and 12 of treatment to measure total cholesterol (TC) ( A ), total triglycerides (TG) ( B ), low-density lipoprotein cholesterol (LDL-C) ( C ), and high-density lipoprotein cholesterol (HDL-C) ( D ) levels. Data are expressed as the mean ± SEM.

Article Snippet: The primary antibody used in this experiment was a rabbit anti- IGFBP5 antibody (1:500, #55205-1-AP; Proteintech Group, Chicago, IL, USA).

Techniques: Over Expression, Clinical Proteomics

Journal: Current Issues in Molecular Biology

Article Title: IGFBP5 Promotes Atherosclerosis in APOE −/− Mice Through Phenotypic Transformation of VSMCs

doi: 10.3390/cimb47070555

Figure Lengend Snippet: Transcriptome analysis of aortic tissues in ApoE −/− mice following overexpression of IGFBP5 . ( A , B ) Heatmap representing global gene expression in aortic tissues of AAV-GFP and AAV- IGFBP5 mice after 12 weeks of being fed a HFD ( n = 4).

Article Snippet: The primary antibody used in this experiment was a rabbit anti- IGFBP5 antibody (1:500, #55205-1-AP; Proteintech Group, Chicago, IL, USA).

Techniques: Over Expression, Gene Expression

Journal: Current Issues in Molecular Biology

Article Title: IGFBP5 Promotes Atherosclerosis in APOE −/− Mice Through Phenotypic Transformation of VSMCs

doi: 10.3390/cimb47070555

Figure Lengend Snippet: Gene Ontology analyses of the differentially expression genes in aortic tissues in ApoE −/− mice following overexpression of IGFBP5 . ( A ) Gene Ontology analyses of the differentially expression genes in aortic of AAV-GFP and AAV- IGFBP5 mice after 12 weeks of HFD ( n = 4). ( B ) GO analysis was performed based on three categories: biological process (BP), molecular function (MF), and cellular component (CC).

Article Snippet: The primary antibody used in this experiment was a rabbit anti- IGFBP5 antibody (1:500, #55205-1-AP; Proteintech Group, Chicago, IL, USA).

Techniques: Expressing, Over Expression

Journal: Current Issues in Molecular Biology

Article Title: IGFBP5 Promotes Atherosclerosis in APOE −/− Mice Through Phenotypic Transformation of VSMCs

doi: 10.3390/cimb47070555

Figure Lengend Snippet: Overexpression of IGFBP5 induces VSMCs to adopt a proliferative state. ( A ) Flow cytometric analysis of cell cycle distribution of immortalized mouse vascular smooth muscle cell line treated with different concentrations of IGFBP5 during proliferation ( n = 3). ( B ) Cell cycle distribution statistics ( n = 3). ( C ) The CCK-8 kit was used to detect the effect of different concentrations of IGFBP5 on VSMC proliferation for 24 h ( n = 5). ( D ) Effects of different concentrations of IGFBP5 on cell migration in cell scratch assays ( n = 3). ( E ) Statistics of relative distance of cell migration ( n = 3). ( F ) Real-time qPCR analysis of ACTA2 , MYH11 , TAGLN , CNN1 and KLF4 transcription expression in immortalized mouse vascular smooth muscle cells treated with different concentrations of IGFBP5 ( n = 3). GAPDH was used as a control. Data are expressed as the mean ± SEM. * p < 0.05.

Article Snippet: The primary antibody used in this experiment was a rabbit anti- IGFBP5 antibody (1:500, #55205-1-AP; Proteintech Group, Chicago, IL, USA).

Techniques: Over Expression, CCK-8 Assay, Migration, Expressing, Control

Journal: Journal of Nanobiotechnology

Article Title: Apoptotic vesicles from macrophages exacerbate periodontal bone resorption in periodontitis via delivering miR-143-3p targeting Igfbp5

doi: 10.1186/s12951-024-02934-2

Figure Lengend Snippet: MiR-143-3p inhibited the osteogenic differentiation of BMSCs through targeting Igfbp5 . ( A ) Prediction of miR-143-5p target genes by databases. ( B ) Gene sequences for the dual-luciferase reporter assay. ( C ) Fluorescence intensity of the dual-luciferase reporter assay. ( D ) IGFBP5 expression levels in BMSCs. Effects of mimic and inhibitor on IGFBP5 mRNA ( E ) and protein ( F ) levels. ( G ) Immunofluorescence images of IGFBP5 in periodontal tissues of mice with periodontitis. Scale bar: 200 μm. ( H ) Relative fluorescence intensity of IGFBP5 in bone tissue. Effects of IGFBP5 and its inhibitor on mRNA levels of BMSC mineralization markers ( I ), ALP activity ( J ), ARS and ALP staining ( K ), and protein levels of mineralization markers ( L ). n = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: Recombined IGFBP5 (HY-P70408), NBI-31,772 (HY-110135) and Z-VAD(OMe)-FMK (HY-16658) were purchased from MedChemExpress.

Techniques: Luciferase, Reporter Assay, Fluorescence, Expressing, Immunofluorescence, Activity Assay, Staining

Journal: Journal of Nanobiotechnology

Article Title: Apoptotic vesicles from macrophages exacerbate periodontal bone resorption in periodontitis via delivering miR-143-3p targeting Igfbp5

doi: 10.1186/s12951-024-02934-2

Figure Lengend Snippet: Schematic representation of macrophage-derived ApoVs inhibiting BMSC differentiation and exacerbate periodontal resorption via miR-143-3p/Igfbp5 signaling axis

Article Snippet: Recombined IGFBP5 (HY-P70408), NBI-31,772 (HY-110135) and Z-VAD(OMe)-FMK (HY-16658) were purchased from MedChemExpress.

Techniques: Derivative Assay

Journal: Clinical and Translational Medicine

Article Title: Deletion of endothelial IGFBP5 protects against ischaemic hindlimb injury by promoting angiogenesis

doi: 10.1002/ctm2.1725

Figure Lengend Snippet: Insulin‐like growth factor‐binding protein 5 (IGFBP5) knockdown promotes tube formation, cell proliferation and migration in human umbilical vein endothelial cells (HUVECs). (A) Representative heatmap, (B) volcano plot and (C) Gene Ontology (GO) biological process enrichment pathway in IGFBP5 shRNA (sh‐IGFBP5)‐ or control shRNA (sh‐NC)‐transfected HUVECs. (D) Representative images and (E) quantification of tube formation in sh‐NC‐ and sh‐IGFBP5‐transfected HUVECs ( n = 5 in each group). (F) Representative immunofluorescence images and (G) quantification of 5‐ethynyl‐2′‐deoxyuridine (EdU, green)‐stained HUVECs transfected with sh‐NC or sh‐IGFBP5 ( n = 5 in each group). (H) Representative images and (I) quantification of flow cytometry for cell cycle in sh‐NC‐ or sh‐IGFBP5‐transfected HUVECs ( n = 5 in each group). (J) Representative images and (K) quantification of wound healing assay in sh‐NC‐ or sh‐IGFBP5‐transfected HUVECs ( n = 5 in each group). (L) Representative images and (M) quantification of transwell assay in sh‐NC‐ or sh‐IGFBP5‐transfected HUVECs ( n = 5 in each group). (N) Representative Western blotting images and (O) quantification of IGFBP5, p‐IGF1R and IGF1R expression in sh‐NC‐ or sh‐IGFBP5‐transfected HUVECs. (P) Representative Western blotting images and (Q) quantification of p‐Erk1/2, Erk1/2, p‐Akt and Akt expression in sh‐NC‐ or sh‐IGFBP5‐transfected HUVECs ( n = 6 in each group).

Article Snippet: To investigate the role of the IGF1R, sh‐NC and sh‐IGFBP5, HUVECs were treated with PPP (AXK1717, Cat#: HY‐15494, MedChemExpress) for 24 h. Rot/AA (inhibitors of complexes I and III) and 2‐deoxy‐D‐glucose (2‐DG, rate‐limiting enzymes in glycolysis) were kept at room temperature prior to use.

Techniques: Binding Assay, Knockdown, Migration, shRNA, Control, Transfection, Immunofluorescence, Staining, Flow Cytometry, Wound Healing Assay, Transwell Assay, Western Blot, Expressing

Journal: Clinical and Translational Medicine

Article Title: Deletion of endothelial IGFBP5 protects against ischaemic hindlimb injury by promoting angiogenesis

doi: 10.1002/ctm2.1725

Figure Lengend Snippet: Insulin‐like growth factor‐binding protein 5 (IGFBP5) deficiency promotes glycolysis through IGF1R. (A) OCR and (B) ECAR profiles in sh‐NC‐ and sh‐IGFBP5‐infected human umbilical vein endothelial cells (HUVECs) ( n = 8 in each group). (C) Quantification of ATP production in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs. (D) OCR and (E) ECAR profiles showing the glycolytic function in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs ( n = 8 in each group). (F) Quantification of glycolytic function parameters in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs ( n = 8 in each group). (G) Western blotting images and (H) quantification of the expression of lactate dehydrogenase (LDH), PKM1 and PKM2 in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs. (I) OCR, (J) ECAR, (K) proton efflux rate (PER) and (L) glycoPER profiles showing glycolytic function in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs in the presence or absence of IGF1R inhibitor picropodophyllin (PPP) ( n = 6 in each group). (M) Quantification of glycolytic function parameters in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs in the presence or absence of PPP ( n = 8 in each group). (N) Western blot images and (O) quantification of the expression of LDH, PKM1 and PKM2 in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs in the presence or absence of IGF1R inhibitor PPP ( n = 6 in each group).

Article Snippet: To investigate the role of the IGF1R, sh‐NC and sh‐IGFBP5, HUVECs were treated with PPP (AXK1717, Cat#: HY‐15494, MedChemExpress) for 24 h. Rot/AA (inhibitors of complexes I and III) and 2‐deoxy‐D‐glucose (2‐DG, rate‐limiting enzymes in glycolysis) were kept at room temperature prior to use.

Techniques: Binding Assay, Infection, Western Blot, Expressing

Journal: Clinical and Translational Medicine

Article Title: Deletion of endothelial IGFBP5 protects against ischaemic hindlimb injury by promoting angiogenesis

doi: 10.1002/ctm2.1725

Figure Lengend Snippet: Deletion of insulin‐like growth factor‐binding protein 5 (IGFBP5) increases HIF1α expression by suppressing ubiquitination via ubiquitin ligase Von Hippel‐Lindau (VHL). (A) Western blotting images and quantification of HIF1α in sh‐NC‐ and sh‐IGFBP5‐infected human umbilical vein endothelial cells (HUVECs) ( n = 6 in each group). (B) Western blotting images and quantification of HIF1α in NC‐overexpression (OE‐NC)‐ and IGFBP5‐overexpression (OE‐IGFBP5)‐transfected HUVECs ( n = 6 in each group). (C) The stability of HIF1α expression in sh‐NC‐ and sh‐IGFBP5‐transfected HUVECs in the presence of 20 μg/mL cycloheximide (CHX) determined by Western blot ( n = 5 in each group). (D) The stability of HIF1α expression in OE‐NC‐ and OE‐IGFBP5‐transfected HUVECs in the presence of MG132 (MG) determined by Western blot. (E) Western blotting images of total ubiquitin, K48 ubiquitin and K63 ubiquitin of HIF1α in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs ( n = 3). (F) Western blotting images and quantification of VHL in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs ( n = 5 in each group). (G) Co‐immunoprecipitation of the interaction between VHL and HIF1α detected by Western blot in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs ( n = 3). (H) Western blot images and quantification of HIF1α expression in sh‐NC‐ and sh‐IGFBP5‐infected HUVECs in the presence or absence of IGF1R inhibitor picropodophyllin (PPP) ( n = 5 in each group).

Article Snippet: To investigate the role of the IGF1R, sh‐NC and sh‐IGFBP5, HUVECs were treated with PPP (AXK1717, Cat#: HY‐15494, MedChemExpress) for 24 h. Rot/AA (inhibitors of complexes I and III) and 2‐deoxy‐D‐glucose (2‐DG, rate‐limiting enzymes in glycolysis) were kept at room temperature prior to use.

Techniques: Binding Assay, Expressing, Ubiquitin Proteomics, Western Blot, Infection, Over Expression, Transfection, Immunoprecipitation

Journal: Clinical and Translational Medicine

Article Title: Deletion of endothelial IGFBP5 protects against ischaemic hindlimb injury by promoting angiogenesis

doi: 10.1002/ctm2.1725

Figure Lengend Snippet: Endothelial cell (EC)‐specific deletion of IGF1R abolished IGFBP5 EKO ‐attenuated limb ischaemia. (A) Representative images detected by laser Doppler‐based tissue perfusion system in IGFBP5 EKO mice, which were infected with AAV2/9‐sh‐NC or AAV‐sh‐IGF1R after ischaemia induction (0 W) and 4 weeks after ischaemia (4 W). (B) Quantification of blood flow in the hindlimb of IGFBP5 EKO mice infected with AAV2/9‐sh‐NC or AAV‐sh‐IGF1R before (−1 D) and after ischaemia induction at 0 days, and 1, 2, 3 and 4 weeks ( n = 8 in each group). (C) Percentage of limb salvage, foot necrosis and limb loss in sham or ischaemic IGFBP5 EKO mice infected with AAV2/9‐sh‐NC or AAV2/9‐sh‐IGF1R 4 weeks after ischaemia induction ( n = 8 in each group). (D) Representative images of immunofluorescence staining, and quantification of CD31 (red) and DAPI (blue) in sham or ischaemic IGFBP5 EKO mice infected with AAV2/9‐sh‐NC or AAV2/9‐sh‐IGF1R 4 weeks after ischaemia induction ( n = 5 in each group). (E) Representative images of haematoxylin‒eosin and picrosirius red staining, and quantification of fibrosis area in gastrocnemius of the hindlimb in ischaemic or sham in IGFBP5 EKO mice infected with AAV2/9‐sh‐NC or AAV2/9‐sh‐IGF1R 4 weeks after ischaemia induction ( n = 5 in each group). (F) Representative immunofluorescence staining images and quantification of dihydroethidium (DHE) staining for reactive oxygen species (ROS) detection in gastrocnemius of the hindlimb in sham or ischaemic IGFBP5 EKO mice infected with AAV2/9‐sh‐NC or AAV2/9‐sh‐IGF1R 4 weeks after ischaemia induction ( n = 5 in each group). (G) Representative immunofluorescence staining images and quantification of TUNEL staining in gastrocnemius of the hindlimb in sham or ischaemic IGFBP5 EKO mice infected with AAV2/9‐sh‐NC or AAV2/9‐sh‐IGF1R 4 weeks after ischaemia induction ( n = 5 in each group).

Article Snippet: To investigate the role of the IGF1R, sh‐NC and sh‐IGFBP5, HUVECs were treated with PPP (AXK1717, Cat#: HY‐15494, MedChemExpress) for 24 h. Rot/AA (inhibitors of complexes I and III) and 2‐deoxy‐D‐glucose (2‐DG, rate‐limiting enzymes in glycolysis) were kept at room temperature prior to use.

Techniques: Infection, Immunofluorescence, Staining, TUNEL Assay

Journal: BMC Veterinary Research

Article Title: Chi-miR-3031 regulates beta-casein via the PI3K/AKT-mTOR signaling pathway in goat mammary epithelial cells (GMECs)

doi: 10.1186/s12917-018-1695-6

Figure Lengend Snippet: Increasing chi-miR-3031 and siRNA-IGFBP5 levels notably decreased IGFBP5 mRNA expression. a : Effect of chi-miR-3031 on IGFBP5 mRNA. b : Effect of siRNA-IGFBP5 on IGFBP5 mRNA. P < 0.01 is shown as **. MC: Chi-miR-3031 mimic. NC: Negative control

Article Snippet: Subsequently, the membranes were incubated overnight at 4 °C with a rabbit anti-IGFBP5 polyclonal antibody (1:300, Boster, USA), a rabbit anti-mTOR polyclonal antibody (1:100, Boster, USA), a rabbit anti-p-mTOR polyclonal antibody (1:100, Boster, USA) or a mouse β-actin monoclonal primary antibody (1:1000, Beyotime, Jiangsu, China).

Techniques: Expressing, Negative Control

Journal: BMC Veterinary Research

Article Title: Chi-miR-3031 regulates beta-casein via the PI3K/AKT-mTOR signaling pathway in goat mammary epithelial cells (GMECs)

doi: 10.1186/s12917-018-1695-6

Figure Lengend Snippet: Effects of chi-miR-3031 and siRNA-IGFBP5 on IGFBP5 protein levels. a : Western blot analysis results. b : Densitometric quantification of western blot results. Protein levels were normalized to β-actin. P < 0.05 is shown as *, and P < 0.01 is shown as **. MC: Chi-miR-3031 mimic. NC: Negative control

Article Snippet: Subsequently, the membranes were incubated overnight at 4 °C with a rabbit anti-IGFBP5 polyclonal antibody (1:300, Boster, USA), a rabbit anti-mTOR polyclonal antibody (1:100, Boster, USA), a rabbit anti-p-mTOR polyclonal antibody (1:100, Boster, USA) or a mouse β-actin monoclonal primary antibody (1:1000, Beyotime, Jiangsu, China).

Techniques: Western Blot, Negative Control

Journal: BMC Veterinary Research

Article Title: Chi-miR-3031 regulates beta-casein via the PI3K/AKT-mTOR signaling pathway in goat mammary epithelial cells (GMECs)

doi: 10.1186/s12917-018-1695-6

Figure Lengend Snippet: Protein expression levels of κ-casein ( a ) and β-casein ( b ) in GMECs transfected with MC, NC and siRNA-IGFBP5. P < 0.05 is shown as *, and P < 0.01 is shown as **. MC: Chi-miR-3031 mimic. NC: Negative control

Article Snippet: Subsequently, the membranes were incubated overnight at 4 °C with a rabbit anti-IGFBP5 polyclonal antibody (1:300, Boster, USA), a rabbit anti-mTOR polyclonal antibody (1:100, Boster, USA), a rabbit anti-p-mTOR polyclonal antibody (1:100, Boster, USA) or a mouse β-actin monoclonal primary antibody (1:1000, Beyotime, Jiangsu, China).

Techniques: Expressing, Transfection, Negative Control

Journal: BMC Veterinary Research

Article Title: Chi-miR-3031 regulates beta-casein via the PI3K/AKT-mTOR signaling pathway in goat mammary epithelial cells (GMECs)

doi: 10.1186/s12917-018-1695-6

Figure Lengend Snippet: Effects of chi-miR-3031 and siRNA-IGFBP5 on p-mTOR protein levels. a : Western blot analysis results. b : Densitometric quantification of western blot results. P < 0.05 is shown as *, and P < 0.01 is shown as **. MC: Chi-miR-3031 mimic. NC: Negative control

Article Snippet: Subsequently, the membranes were incubated overnight at 4 °C with a rabbit anti-IGFBP5 polyclonal antibody (1:300, Boster, USA), a rabbit anti-mTOR polyclonal antibody (1:100, Boster, USA), a rabbit anti-p-mTOR polyclonal antibody (1:100, Boster, USA) or a mouse β-actin monoclonal primary antibody (1:1000, Beyotime, Jiangsu, China).

Techniques: Western Blot, Negative Control

Journal: BMC Veterinary Research

Article Title: Chi-miR-3031 regulates beta-casein via the PI3K/AKT-mTOR signaling pathway in goat mammary epithelial cells (GMECs)

doi: 10.1186/s12917-018-1695-6

Figure Lengend Snippet: Primer information for RT-qPCR

Article Snippet: Subsequently, the membranes were incubated overnight at 4 °C with a rabbit anti-IGFBP5 polyclonal antibody (1:300, Boster, USA), a rabbit anti-mTOR polyclonal antibody (1:100, Boster, USA), a rabbit anti-p-mTOR polyclonal antibody (1:100, Boster, USA) or a mouse β-actin monoclonal primary antibody (1:1000, Beyotime, Jiangsu, China).

Techniques: Sequencing

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Expressions of IGFBP-5, cFLIP in cervical intraepithelial neoplasia, cervical carcinoma and their clinical significances: a molecular pathology

doi: 10.1186/1756-9966-28-70

Figure Lengend Snippet: The relationship between expression of IGFBP-5 and cFLIP and clinicopathological parameters in CC

Article Snippet: Primary antibodies used in this study include IGFBP-5 rabbit anti-human polyclonal antibody (Boster Co., Ltd., Wuhan) and cFLIP rabbit anti-human polyclonal antibody (American Neomarker Co.).

Techniques: Expressing

Journal: Experimental Hematology & Oncology

Article Title: Physical activity improves outcomes of combined lenvatinib plus anti-PD-1 therapy in unresectable hepatocellular carcinoma: a retrospective study and mouse model

doi: 10.1186/s40164-022-00275-0

Figure Lengend Snippet: Immunohistochemical staining and analysis of subcutaneous tumors. Immunohistochemical staining was conducted on subcutaneous tumor tissue microarray. H-score were calculated to quantify the expression levels of marker proteins. Representative images captured at 40 ×. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Foxp3 forkhead box protein p3, CTLA4 cytotoxic T-lymphocyte-associated protein 4, TIGIT T cell immunoreceptor with Ig and ITIM domains, TIM3 T-cell immunoglobulin mucin-3, VISTA V domain-containing Ig suppressor of T-cell activation

Article Snippet: Primary Abs used for immunohistochemical staining included: anti-CD4 Ab (#25229, CST), anti-CD8α Ab (#98941,CST), anti-Forkhead box protein p3 (Foxp3) Ab (ab253297, Abcam), anti-F4/80 Ab (#70076, CST), anti-CTLA4 Ab (A00020, Boster), anti-T cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) Ab (A01962, Boster), anti-TIM3 Ab (ab241332, Abcam) and, anti-V domain-containing Ig suppressor of T-cell activation (VISTA) Ab (#54979, CST).

Techniques: Immunohistochemical staining, Staining, Microarray, Expressing, Marker, Activation Assay

Journal: Journal of Functional Foods

Article Title: Noni (Morinda citrifolia L.) fruit polysaccharide ameliorated high-fat diet-induced obesity by modulating gut microbiota and improving bile acid metabolism

doi: 10.1016/j.jff.2023.105408

Figure Lengend Snippet: Fig. 2. Effect of NFP on bile acids synthesis in mice under a high-fat diet. (A) The content of TBA in the liver. (B) The expression of CYP7A1 in the liver. (C) Relative protein expression levels of liver FXR. (D) Relative protein expression levels of liver SHP. (E) Bargraph of liver bile acid-related protein expression. (F) Bargraph of intestinal bile acid-related protein expression. (G) Relative protein expression levels of colonic FXR. (H) Relative expression levels of colonic FGF15. (I) Relative expression levels of colonic TGR5. Data are shown as mean ± SEM (n = 5); *p < 0.05, **p < 0.01 versus the NC group; #p < 0.05, ##p < 0.01 versus the HFD group.

Article Snippet: The antibodies GAPDH (BA2913), SHP (A03866-1), and TGR5 (A01958-1) for Western blot detection were purchased from Boster Bioengineering Co., Ltd. (California, USA).

Techniques: Expressing