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immunofluorescence staining  (Boster Bio)


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    Boster Bio immunofluorescence staining
    NR1D1 expression and mRNA stability are decreased in ApoA5 -/- hamsters under different nutrient conditions. A-B: The heatmap analysis of the genes, which mRNA expression levels were altered in the livers of both CD (A) and HFD-fed (B) WT and ApoA5 -/- hamsters. C: The mRNA levels of NR1D1 in the livers of WT and ApoA5 -/- hamsters under CD and HFD (n = 5-6/group). D: The mRNA levels of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters treated with BSA or PA (500 μM) (n = 6/group). E: The representative <t>immunofluorescence</t> images of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters. F: Western blot analysis of NR1D1 protein in the liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). G: Western blot analysis of NR1D1 in the nucleus of liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). H: The representative immunofluorescence images of NR1D1 and ApoA5 in HepG2 cells. I: Co-IP analysis of the interaction between ApoA5 and NR1D1 in the livers of CD-fed hamster. J: Analysis of NR1D1 mRNA levels in the cultured primary hepatocytes from the two genotypes after treated with Actinomycin D (2 μg/mL) (n = 3/group). K: RNA pulldown assays were performed by using HepG2 cell lysates and in vitro-transcribed RNAs depicted to test the binding of ApoA5 to Nr1d1 mRNA. HepG2 cells were transfected with ApoA5 plasmid containing a FLAG tag for 48 h. L-M: The heatmap of the changed downstream genes of NR1D1 in the transcriptome data in the livers of WT and ApoA5 -/- hamsters under CD (C) and HFD (D) conditions. Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.
    Immunofluorescence Staining, supplied by Boster Bio, used in various techniques. Bioz Stars score: 96/100, based on 284 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 96 stars, based on 284 article reviews
    immunofluorescence staining - by Bioz Stars, 2026-03
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    Images

    1) Product Images from "Depletion of ApoA5 aggravates spontaneous and diet-induced nonalcoholic fatty liver disease by reducing hepatic NR1D1 in hamsters"

    Article Title: Depletion of ApoA5 aggravates spontaneous and diet-induced nonalcoholic fatty liver disease by reducing hepatic NR1D1 in hamsters

    Journal: Theranostics

    doi: 10.7150/thno.91084

    NR1D1 expression and mRNA stability are decreased in ApoA5 -/- hamsters under different nutrient conditions. A-B: The heatmap analysis of the genes, which mRNA expression levels were altered in the livers of both CD (A) and HFD-fed (B) WT and ApoA5 -/- hamsters. C: The mRNA levels of NR1D1 in the livers of WT and ApoA5 -/- hamsters under CD and HFD (n = 5-6/group). D: The mRNA levels of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters treated with BSA or PA (500 μM) (n = 6/group). E: The representative immunofluorescence images of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters. F: Western blot analysis of NR1D1 protein in the liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). G: Western blot analysis of NR1D1 in the nucleus of liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). H: The representative immunofluorescence images of NR1D1 and ApoA5 in HepG2 cells. I: Co-IP analysis of the interaction between ApoA5 and NR1D1 in the livers of CD-fed hamster. J: Analysis of NR1D1 mRNA levels in the cultured primary hepatocytes from the two genotypes after treated with Actinomycin D (2 μg/mL) (n = 3/group). K: RNA pulldown assays were performed by using HepG2 cell lysates and in vitro-transcribed RNAs depicted to test the binding of ApoA5 to Nr1d1 mRNA. HepG2 cells were transfected with ApoA5 plasmid containing a FLAG tag for 48 h. L-M: The heatmap of the changed downstream genes of NR1D1 in the transcriptome data in the livers of WT and ApoA5 -/- hamsters under CD (C) and HFD (D) conditions. Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.
    Figure Legend Snippet: NR1D1 expression and mRNA stability are decreased in ApoA5 -/- hamsters under different nutrient conditions. A-B: The heatmap analysis of the genes, which mRNA expression levels were altered in the livers of both CD (A) and HFD-fed (B) WT and ApoA5 -/- hamsters. C: The mRNA levels of NR1D1 in the livers of WT and ApoA5 -/- hamsters under CD and HFD (n = 5-6/group). D: The mRNA levels of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters treated with BSA or PA (500 μM) (n = 6/group). E: The representative immunofluorescence images of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters. F: Western blot analysis of NR1D1 protein in the liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). G: Western blot analysis of NR1D1 in the nucleus of liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). H: The representative immunofluorescence images of NR1D1 and ApoA5 in HepG2 cells. I: Co-IP analysis of the interaction between ApoA5 and NR1D1 in the livers of CD-fed hamster. J: Analysis of NR1D1 mRNA levels in the cultured primary hepatocytes from the two genotypes after treated with Actinomycin D (2 μg/mL) (n = 3/group). K: RNA pulldown assays were performed by using HepG2 cell lysates and in vitro-transcribed RNAs depicted to test the binding of ApoA5 to Nr1d1 mRNA. HepG2 cells were transfected with ApoA5 plasmid containing a FLAG tag for 48 h. L-M: The heatmap of the changed downstream genes of NR1D1 in the transcriptome data in the livers of WT and ApoA5 -/- hamsters under CD (C) and HFD (D) conditions. Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.

    Techniques Used: Expressing, Cell Culture, Immunofluorescence, Western Blot, Co-Immunoprecipitation Assay, In Vitro, Binding Assay, Transfection, Plasmid Preparation, FLAG-tag

    Cold exposure improves lipid metabolism disorders caused by ApoA5 deficiency. A: The representative images of UCP1 immunohistochemical staining in BAT sections of 3-month old male WT and ApoA5 -/- hamsters on chow diet. B: The body temperature of the hamsters described in (A) (n = 8/group). C: The expression levels of genes involved in thermogenesis in the BAT of the hamsters described in (A) (n = 5-7/group). D-E: Plasma TG (D) and TC (E) were determined from WT and ApoA5 -/- hamsters after cold exposure for 5 days (n = 4-6/group). F-G: The representative images of HE and UCP1 immunohistochemical staining in BAT and eWAT sections of the animals described in (D-E) and quantitative data (n = 4-6/group). H: The representative images of tyrosine hydroxylase (TH) immunofluorescence staining in eWAT sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). I: The representative images of Oil red O in liver sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). J-K: Plasma TG (J) and TC (K) were determined from WT and ApoA5 -/- hamsters on HFD after cold exposure for 7 days (n = 3-5/group). L: The representative images of Oil red O in liver sections of the hamsters described in (J-K) and quantitative data (n = 3-5/group). Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.
    Figure Legend Snippet: Cold exposure improves lipid metabolism disorders caused by ApoA5 deficiency. A: The representative images of UCP1 immunohistochemical staining in BAT sections of 3-month old male WT and ApoA5 -/- hamsters on chow diet. B: The body temperature of the hamsters described in (A) (n = 8/group). C: The expression levels of genes involved in thermogenesis in the BAT of the hamsters described in (A) (n = 5-7/group). D-E: Plasma TG (D) and TC (E) were determined from WT and ApoA5 -/- hamsters after cold exposure for 5 days (n = 4-6/group). F-G: The representative images of HE and UCP1 immunohistochemical staining in BAT and eWAT sections of the animals described in (D-E) and quantitative data (n = 4-6/group). H: The representative images of tyrosine hydroxylase (TH) immunofluorescence staining in eWAT sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). I: The representative images of Oil red O in liver sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). J-K: Plasma TG (J) and TC (K) were determined from WT and ApoA5 -/- hamsters on HFD after cold exposure for 7 days (n = 3-5/group). L: The representative images of Oil red O in liver sections of the hamsters described in (J-K) and quantitative data (n = 3-5/group). Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.

    Techniques Used: Immunohistochemical staining, Staining, Expressing, Clinical Proteomics, Immunofluorescence



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    NR1D1 expression and mRNA stability are decreased in ApoA5 -/- hamsters under different nutrient conditions. A-B: The heatmap analysis of the genes, which mRNA expression levels were altered in the livers of both CD (A) and HFD-fed (B) WT and ApoA5 -/- hamsters. C: The mRNA levels of NR1D1 in the livers of WT and ApoA5 -/- hamsters under CD and HFD (n = 5-6/group). D: The mRNA levels of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters treated with BSA or PA (500 μM) (n = 6/group). E: The representative <t>immunofluorescence</t> images of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters. F: Western blot analysis of NR1D1 protein in the liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). G: Western blot analysis of NR1D1 in the nucleus of liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). H: The representative immunofluorescence images of NR1D1 and ApoA5 in HepG2 cells. I: Co-IP analysis of the interaction between ApoA5 and NR1D1 in the livers of CD-fed hamster. J: Analysis of NR1D1 mRNA levels in the cultured primary hepatocytes from the two genotypes after treated with Actinomycin D (2 μg/mL) (n = 3/group). K: RNA pulldown assays were performed by using HepG2 cell lysates and in vitro-transcribed RNAs depicted to test the binding of ApoA5 to Nr1d1 mRNA. HepG2 cells were transfected with ApoA5 plasmid containing a FLAG tag for 48 h. L-M: The heatmap of the changed downstream genes of NR1D1 in the transcriptome data in the livers of WT and ApoA5 -/- hamsters under CD (C) and HFD (D) conditions. Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.
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    NR1D1 expression and mRNA stability are decreased in ApoA5 -/- hamsters under different nutrient conditions. A-B: The heatmap analysis of the genes, which mRNA expression levels were altered in the livers of both CD (A) and HFD-fed (B) WT and ApoA5 -/- hamsters. C: The mRNA levels of NR1D1 in the livers of WT and ApoA5 -/- hamsters under CD and HFD (n = 5-6/group). D: The mRNA levels of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters treated with BSA or PA (500 μM) (n = 6/group). E: The representative <t>immunofluorescence</t> images of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters. F: Western blot analysis of NR1D1 protein in the liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). G: Western blot analysis of NR1D1 in the nucleus of liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). H: The representative immunofluorescence images of NR1D1 and ApoA5 in HepG2 cells. I: Co-IP analysis of the interaction between ApoA5 and NR1D1 in the livers of CD-fed hamster. J: Analysis of NR1D1 mRNA levels in the cultured primary hepatocytes from the two genotypes after treated with Actinomycin D (2 μg/mL) (n = 3/group). K: RNA pulldown assays were performed by using HepG2 cell lysates and in vitro-transcribed RNAs depicted to test the binding of ApoA5 to Nr1d1 mRNA. HepG2 cells were transfected with ApoA5 plasmid containing a FLAG tag for 48 h. L-M: The heatmap of the changed downstream genes of NR1D1 in the transcriptome data in the livers of WT and ApoA5 -/- hamsters under CD (C) and HFD (D) conditions. Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.
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    Image Search Results


    Regulation of macrophage polarization by the different modified surfaces in vivo. A) H&E staining of peri‐implant tissue in the femur 5 d after implantation and F) quantitative analysis of the thickness of the fibrous layer. B,C) Immunohistochemical staining of peri‐implant tissue to examine TNF‐α and IL‐10 expression, and G,H) the quantitative results of the corresponding positive areas are shown. D,E) Immunofluorescence staining of peri‐implant tissue to assess macrophage polarization status (green: macrophage‐specific marker (CD68); red: marker of M1 macrophages (CD86); and blue: nucleus of M2 macrophages (CD206)). I,J) The quantitative results are shown for positive cells. The data are presented as the mean ± standard deviation (SD) ( n = 5 per group). Statistical analysis was performed by one‐way ANOVA, and * P < 0.05 and ** P < 0.01 indicate statistical significance.

    Journal: Advanced Science

    Article Title: Mussel‐Derived and Bioclickable Peptide Mimic for Enhanced Interfacial Osseointegration via Synergistic Immunomodulation and Vascularized Bone Regeneration

    doi: 10.1002/advs.202401833

    Figure Lengend Snippet: Regulation of macrophage polarization by the different modified surfaces in vivo. A) H&E staining of peri‐implant tissue in the femur 5 d after implantation and F) quantitative analysis of the thickness of the fibrous layer. B,C) Immunohistochemical staining of peri‐implant tissue to examine TNF‐α and IL‐10 expression, and G,H) the quantitative results of the corresponding positive areas are shown. D,E) Immunofluorescence staining of peri‐implant tissue to assess macrophage polarization status (green: macrophage‐specific marker (CD68); red: marker of M1 macrophages (CD86); and blue: nucleus of M2 macrophages (CD206)). I,J) The quantitative results are shown for positive cells. The data are presented as the mean ± standard deviation (SD) ( n = 5 per group). Statistical analysis was performed by one‐way ANOVA, and * P < 0.05 and ** P < 0.01 indicate statistical significance.

    Article Snippet: To assess macrophage polarization around the implants, immunofluorescence staining for CD68 (a macrophage marker; Abcam, ab201340), CD86 (an M1 marker; Immunoway, YT7823), and CD206 (an M2 marker; Abcam, ab64693) was performed.

    Techniques: Modification, In Vivo, Staining, Immunohistochemical staining, Expressing, Immunofluorescence, Marker, Standard Deviation

    NR1D1 expression and mRNA stability are decreased in ApoA5 -/- hamsters under different nutrient conditions. A-B: The heatmap analysis of the genes, which mRNA expression levels were altered in the livers of both CD (A) and HFD-fed (B) WT and ApoA5 -/- hamsters. C: The mRNA levels of NR1D1 in the livers of WT and ApoA5 -/- hamsters under CD and HFD (n = 5-6/group). D: The mRNA levels of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters treated with BSA or PA (500 μM) (n = 6/group). E: The representative immunofluorescence images of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters. F: Western blot analysis of NR1D1 protein in the liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). G: Western blot analysis of NR1D1 in the nucleus of liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). H: The representative immunofluorescence images of NR1D1 and ApoA5 in HepG2 cells. I: Co-IP analysis of the interaction between ApoA5 and NR1D1 in the livers of CD-fed hamster. J: Analysis of NR1D1 mRNA levels in the cultured primary hepatocytes from the two genotypes after treated with Actinomycin D (2 μg/mL) (n = 3/group). K: RNA pulldown assays were performed by using HepG2 cell lysates and in vitro-transcribed RNAs depicted to test the binding of ApoA5 to Nr1d1 mRNA. HepG2 cells were transfected with ApoA5 plasmid containing a FLAG tag for 48 h. L-M: The heatmap of the changed downstream genes of NR1D1 in the transcriptome data in the livers of WT and ApoA5 -/- hamsters under CD (C) and HFD (D) conditions. Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.

    Journal: Theranostics

    Article Title: Depletion of ApoA5 aggravates spontaneous and diet-induced nonalcoholic fatty liver disease by reducing hepatic NR1D1 in hamsters

    doi: 10.7150/thno.91084

    Figure Lengend Snippet: NR1D1 expression and mRNA stability are decreased in ApoA5 -/- hamsters under different nutrient conditions. A-B: The heatmap analysis of the genes, which mRNA expression levels were altered in the livers of both CD (A) and HFD-fed (B) WT and ApoA5 -/- hamsters. C: The mRNA levels of NR1D1 in the livers of WT and ApoA5 -/- hamsters under CD and HFD (n = 5-6/group). D: The mRNA levels of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters treated with BSA or PA (500 μM) (n = 6/group). E: The representative immunofluorescence images of NR1D1 in the cultured primary hepatocytes of WT and ApoA5 -/- hamsters. F: Western blot analysis of NR1D1 protein in the liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). G: Western blot analysis of NR1D1 in the nucleus of liver samples of CD-fed WT and ApoA5 -/- hamsters and quantitative data (n = 3/group). H: The representative immunofluorescence images of NR1D1 and ApoA5 in HepG2 cells. I: Co-IP analysis of the interaction between ApoA5 and NR1D1 in the livers of CD-fed hamster. J: Analysis of NR1D1 mRNA levels in the cultured primary hepatocytes from the two genotypes after treated with Actinomycin D (2 μg/mL) (n = 3/group). K: RNA pulldown assays were performed by using HepG2 cell lysates and in vitro-transcribed RNAs depicted to test the binding of ApoA5 to Nr1d1 mRNA. HepG2 cells were transfected with ApoA5 plasmid containing a FLAG tag for 48 h. L-M: The heatmap of the changed downstream genes of NR1D1 in the transcriptome data in the livers of WT and ApoA5 -/- hamsters under CD (C) and HFD (D) conditions. Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.

    Article Snippet: Immunofluorescence staining was performed with CD68 antibody (1:200 rabbit polyclonal IgG, BM3639, BOSTER, China) for macrophage in liver, TH (Tyrosine hydroxylase) antibody (1:200 rabbit polyclonal IgG, A12756, ABclonal, China) in WAT and IL-6 (interleukin 6) antibody (1:100 rabbit polyclonal IgG, BA4339, BOSTER, China) in BAT.

    Techniques: Expressing, Cell Culture, Immunofluorescence, Western Blot, Co-Immunoprecipitation Assay, In Vitro, Binding Assay, Transfection, Plasmid Preparation, FLAG-tag

    Cold exposure improves lipid metabolism disorders caused by ApoA5 deficiency. A: The representative images of UCP1 immunohistochemical staining in BAT sections of 3-month old male WT and ApoA5 -/- hamsters on chow diet. B: The body temperature of the hamsters described in (A) (n = 8/group). C: The expression levels of genes involved in thermogenesis in the BAT of the hamsters described in (A) (n = 5-7/group). D-E: Plasma TG (D) and TC (E) were determined from WT and ApoA5 -/- hamsters after cold exposure for 5 days (n = 4-6/group). F-G: The representative images of HE and UCP1 immunohistochemical staining in BAT and eWAT sections of the animals described in (D-E) and quantitative data (n = 4-6/group). H: The representative images of tyrosine hydroxylase (TH) immunofluorescence staining in eWAT sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). I: The representative images of Oil red O in liver sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). J-K: Plasma TG (J) and TC (K) were determined from WT and ApoA5 -/- hamsters on HFD after cold exposure for 7 days (n = 3-5/group). L: The representative images of Oil red O in liver sections of the hamsters described in (J-K) and quantitative data (n = 3-5/group). Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.

    Journal: Theranostics

    Article Title: Depletion of ApoA5 aggravates spontaneous and diet-induced nonalcoholic fatty liver disease by reducing hepatic NR1D1 in hamsters

    doi: 10.7150/thno.91084

    Figure Lengend Snippet: Cold exposure improves lipid metabolism disorders caused by ApoA5 deficiency. A: The representative images of UCP1 immunohistochemical staining in BAT sections of 3-month old male WT and ApoA5 -/- hamsters on chow diet. B: The body temperature of the hamsters described in (A) (n = 8/group). C: The expression levels of genes involved in thermogenesis in the BAT of the hamsters described in (A) (n = 5-7/group). D-E: Plasma TG (D) and TC (E) were determined from WT and ApoA5 -/- hamsters after cold exposure for 5 days (n = 4-6/group). F-G: The representative images of HE and UCP1 immunohistochemical staining in BAT and eWAT sections of the animals described in (D-E) and quantitative data (n = 4-6/group). H: The representative images of tyrosine hydroxylase (TH) immunofluorescence staining in eWAT sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). I: The representative images of Oil red O in liver sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). J-K: Plasma TG (J) and TC (K) were determined from WT and ApoA5 -/- hamsters on HFD after cold exposure for 7 days (n = 3-5/group). L: The representative images of Oil red O in liver sections of the hamsters described in (J-K) and quantitative data (n = 3-5/group). Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.

    Article Snippet: Immunofluorescence staining was performed with CD68 antibody (1:200 rabbit polyclonal IgG, BM3639, BOSTER, China) for macrophage in liver, TH (Tyrosine hydroxylase) antibody (1:200 rabbit polyclonal IgG, A12756, ABclonal, China) in WAT and IL-6 (interleukin 6) antibody (1:100 rabbit polyclonal IgG, BA4339, BOSTER, China) in BAT.

    Techniques: Immunohistochemical staining, Staining, Expressing, Clinical Proteomics, Immunofluorescence