anti gfap  (Boster Bio)


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    Name:
    Anti GFAP Antibody
    Description:

    Catalog Number:
    PA1239
    Price:
    99.0
    Category:
    Primary Antibodies
    Reactivity:
    Human Mouse Rat
    Applications:
    IF, IHC, WB
    Immunogen:
    A synthetic peptide corresponding to a sequence at the C-terminus of human GFAP(417-432aa DGEVIKESKQEHKDVM), identical to the related rat sequence, and different from the related mouse sequence by two amino acids.
    Host:
    Rabbit
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    Structured Review

    Boster Bio anti gfap
    Anti GFAP Antibody

    https://www.bioz.com/result/anti gfap/product/Boster Bio
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti gfap - by Bioz Stars, 2021-07
    93/100 stars

    Images

    1) Product Images from "Graphene oxide suppresses the growth and malignancy of glioblastoma stem cell-like spheroids via epigenetic mechanisms"

    Article Title: Graphene oxide suppresses the growth and malignancy of glioblastoma stem cell-like spheroids via epigenetic mechanisms

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-020-02359-z

    Graphene oxide inhibits the cell viability and promotes the differentiation of U251 GSCs. a U251 cells were cultured in a serum-free environment. Sphere morphology was photographed using light microscopy. Scale bar = 100 μm. b The expression of SOX2, CD133 and OCT4 in glioblastoma stem-like cells was increased during different periods. c Morphological appearance of U251 GSCs with or without treatment with GO for 2 days. The GSC spheres treated with GO showed adherent growth. Scale bar = 100 μm. d An MTT assay showed the cell viability of U251 GSCs with or without treatment with different dosages of GO for 2, 4, and 6 days. e Quantification of the mRNA levels of the stem cell markers SOX2 and differentiation markers (GFAP and TUJ1) in U251 GSCs with or without treatment with 0, 5, 12.5, 25 and 50 μg/ml GO respectively. * p
    Figure Legend Snippet: Graphene oxide inhibits the cell viability and promotes the differentiation of U251 GSCs. a U251 cells were cultured in a serum-free environment. Sphere morphology was photographed using light microscopy. Scale bar = 100 μm. b The expression of SOX2, CD133 and OCT4 in glioblastoma stem-like cells was increased during different periods. c Morphological appearance of U251 GSCs with or without treatment with GO for 2 days. The GSC spheres treated with GO showed adherent growth. Scale bar = 100 μm. d An MTT assay showed the cell viability of U251 GSCs with or without treatment with different dosages of GO for 2, 4, and 6 days. e Quantification of the mRNA levels of the stem cell markers SOX2 and differentiation markers (GFAP and TUJ1) in U251 GSCs with or without treatment with 0, 5, 12.5, 25 and 50 μg/ml GO respectively. * p

    Techniques Used: Cell Culture, Light Microscopy, Expressing, MTT Assay

    Graphene oxide reduces the expression of stem cell markers and promotes the differentiation of GSCs. a Quantification of the mRNA levels of stem cell markers SOX2 and CD133 in GSCs with or without treatment with GO. b The intracellular expression of the differentiation marker GFAP after treatment with 50 μg/ml GO was examined using immunofluorescence staining. Scale bar = 100 μm. c The expression level of the stem cell marker CD133 in cells treated with different concentrations of GO was detected by immunofluorescence staining. Scale bar = 50 μm. d , e Representative immunoblots and relative quantification of OCT4, SOX2, TUJ1 and GFAP in GSCs after treatment with 0, 5, 12.5, 25 and 50 μg/ml GO respectively. * p
    Figure Legend Snippet: Graphene oxide reduces the expression of stem cell markers and promotes the differentiation of GSCs. a Quantification of the mRNA levels of stem cell markers SOX2 and CD133 in GSCs with or without treatment with GO. b The intracellular expression of the differentiation marker GFAP after treatment with 50 μg/ml GO was examined using immunofluorescence staining. Scale bar = 100 μm. c The expression level of the stem cell marker CD133 in cells treated with different concentrations of GO was detected by immunofluorescence staining. Scale bar = 50 μm. d , e Representative immunoblots and relative quantification of OCT4, SOX2, TUJ1 and GFAP in GSCs after treatment with 0, 5, 12.5, 25 and 50 μg/ml GO respectively. * p

    Techniques Used: Expressing, Marker, Immunofluorescence, Staining, Western Blot

    2) Product Images from "RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke"

    Article Title: RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke

    Journal: Cell Death and Differentiation

    doi: 10.1038/s41418-018-0058-y

    RGMa inhibition reduces MCAO/R-induced reactive astrogliosis and glial scar formation in rats and promotes neurological function recovery. a Timeline of experimental design and animal group classification. WB, Western blot. b Representative fluorescence microscope images showing GFAP expression in tissue sections 14 days post reperfusion. Images are representative of three rats per treatment. (i–iii) Composition of low magnification micrographs (× 40). The dotted lines indicate the boundary of glial scar. Scale bar, 1000 μm. (iv–xv) Higher-magnified view of the squared region (R1-R6) in (i–iii) respectively; × 100 (iv–ix), × 200 (x–xv). DAPI (blue) was used to stain cellular nuclei. Scale bar, 100 μm. c Quantification of GFAP expression at R1-R6 (× 200) ( n = 3). IR, immunoreactivity. ** p
    Figure Legend Snippet: RGMa inhibition reduces MCAO/R-induced reactive astrogliosis and glial scar formation in rats and promotes neurological function recovery. a Timeline of experimental design and animal group classification. WB, Western blot. b Representative fluorescence microscope images showing GFAP expression in tissue sections 14 days post reperfusion. Images are representative of three rats per treatment. (i–iii) Composition of low magnification micrographs (× 40). The dotted lines indicate the boundary of glial scar. Scale bar, 1000 μm. (iv–xv) Higher-magnified view of the squared region (R1-R6) in (i–iii) respectively; × 100 (iv–ix), × 200 (x–xv). DAPI (blue) was used to stain cellular nuclei. Scale bar, 100 μm. c Quantification of GFAP expression at R1-R6 (× 200) ( n = 3). IR, immunoreactivity. ** p

    Techniques Used: Inhibition, Western Blot, Fluorescence, Microscopy, Expressing, Staining

    Knockdown of RGMa reduces key steps of TGFβ1-triggered reactive astrogliosis and glial scar formation. a Immunofluorescence of GFAP (red) in culture of primary astrocytes infected with rAd-shRGMa or rAd-HK 3 days before TGFβ1 (10 ng/ml for 24 h) treatment. One representative panel per group out of three independent experiments is shown. b Western blot analysis of GFAP expression in primary astrocytes infected with rAd-shRGMa or rAd-HK, followed by TGFβ1 (10 ng/ml for 3 days) treatment ( n = 3). c , d The migration capability of astrocytes determined by a transwell chamber assay. The astrocytes were cultured in different conditions (Control, TGFβ1, TGFβ1 + rAd-shRGMa, and TGFβ1 + rAd-HK). c Representative fluorescence microscope images of the lower surface of the filter. The cells were stained with DAPI (blue). d Quantification of the cell number of astrocytes that migrated to the lower side of the filter in each group ( n = 3). e The proliferation ability of astrocytes measured by a CCK8 assay ( n = 3). The cultured astrocytes were infected with rAd-shRGMa or rAd-HK before exposure to TGFβ1 (10 ng/ml for 3 days). NS, no significance. f , g Western blot analysis of neurocan f and phosphacan g expression in the supernatant of cultured astrocytes infected with rAd-shRGMa or rAd-HK 3 days before TGFβ1 (10 ng/ml for 3 days) treatment ( n = 3). Scale bar, 100 μm. Data in bar graphs are means ± SEM ( b , d , e , f , g ); one-way ANOVA with Bonferroni post hoc test, ** p
    Figure Legend Snippet: Knockdown of RGMa reduces key steps of TGFβ1-triggered reactive astrogliosis and glial scar formation. a Immunofluorescence of GFAP (red) in culture of primary astrocytes infected with rAd-shRGMa or rAd-HK 3 days before TGFβ1 (10 ng/ml for 24 h) treatment. One representative panel per group out of three independent experiments is shown. b Western blot analysis of GFAP expression in primary astrocytes infected with rAd-shRGMa or rAd-HK, followed by TGFβ1 (10 ng/ml for 3 days) treatment ( n = 3). c , d The migration capability of astrocytes determined by a transwell chamber assay. The astrocytes were cultured in different conditions (Control, TGFβ1, TGFβ1 + rAd-shRGMa, and TGFβ1 + rAd-HK). c Representative fluorescence microscope images of the lower surface of the filter. The cells were stained with DAPI (blue). d Quantification of the cell number of astrocytes that migrated to the lower side of the filter in each group ( n = 3). e The proliferation ability of astrocytes measured by a CCK8 assay ( n = 3). The cultured astrocytes were infected with rAd-shRGMa or rAd-HK before exposure to TGFβ1 (10 ng/ml for 3 days). NS, no significance. f , g Western blot analysis of neurocan f and phosphacan g expression in the supernatant of cultured astrocytes infected with rAd-shRGMa or rAd-HK 3 days before TGFβ1 (10 ng/ml for 3 days) treatment ( n = 3). Scale bar, 100 μm. Data in bar graphs are means ± SEM ( b , d , e , f , g ); one-way ANOVA with Bonferroni post hoc test, ** p

    Techniques Used: Immunofluorescence, Infection, Western Blot, Expressing, Migration, Transwell Chamber Assay, Cell Culture, Fluorescence, Microscopy, Staining, CCK-8 Assay

    TGFβ1 stimulates RGMa protein expression in primary astrocytes. a Western blot analysis for RGMa expression in primary astrocytes treated with or without TGFβ1 (1–100 ng/ml) for 3 days ( n = 3). b Representative fluorescence photographs of RGMa (green) and GFAP (red) expression in cultured astrocytes in the absence or presence of TGFβ1 (10 ng/ml for 3 days). Similar results were obtained using two additional cell batches. c Western blot analysis for RGMa expression in astrocyte cultures pretreated with or without SB431542 (30 μM for 1 h) before TGFβ1 (10 ng/ml for 3 days) stimulation ( n = 3). d Immunostaining of RGMa (green) and GFAP (red) expression in cultured primary astrocytes pretreated with or without SB431542 (30 μM for 1 h) before TGFβ1 (10 ng/ml for 3 days) stimulation. One representative panel per group out of three independent cell cultures is shown. Scale bar, 100 μm. Data in bar graphs are means ± SEM a and c ; one-way ANOVA with Bonferroni post hoc test, ** p
    Figure Legend Snippet: TGFβ1 stimulates RGMa protein expression in primary astrocytes. a Western blot analysis for RGMa expression in primary astrocytes treated with or without TGFβ1 (1–100 ng/ml) for 3 days ( n = 3). b Representative fluorescence photographs of RGMa (green) and GFAP (red) expression in cultured astrocytes in the absence or presence of TGFβ1 (10 ng/ml for 3 days). Similar results were obtained using two additional cell batches. c Western blot analysis for RGMa expression in astrocyte cultures pretreated with or without SB431542 (30 μM for 1 h) before TGFβ1 (10 ng/ml for 3 days) stimulation ( n = 3). d Immunostaining of RGMa (green) and GFAP (red) expression in cultured primary astrocytes pretreated with or without SB431542 (30 μM for 1 h) before TGFβ1 (10 ng/ml for 3 days) stimulation. One representative panel per group out of three independent cell cultures is shown. Scale bar, 100 μm. Data in bar graphs are means ± SEM a and c ; one-way ANOVA with Bonferroni post hoc test, ** p

    Techniques Used: Expressing, Western Blot, Fluorescence, Cell Culture, Immunostaining

    3) Product Images from "RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke"

    Article Title: RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke

    Journal: Cell Death and Differentiation

    doi: 10.1038/s41418-018-0058-y

    RGMa inhibition reduces MCAO/R-induced reactive astrogliosis and glial scar formation in rats and promotes neurological function recovery. a Timeline of experimental design and animal group classification. WB, Western blot. b Representative fluorescence microscope images showing GFAP expression in tissue sections 14 days post reperfusion. Images are representative of three rats per treatment. (i–iii) Composition of low magnification micrographs (× 40). The dotted lines indicate the boundary of glial scar. Scale bar, 1000 μm. (iv–xv) Higher-magnified view of the squared region (R1-R6) in (i–iii) respectively; × 100 (iv–ix), × 200 (x–xv). DAPI (blue) was used to stain cellular nuclei. Scale bar, 100 μm. c Quantification of GFAP expression at R1-R6 (× 200) ( n = 3). IR, immunoreactivity. ** p
    Figure Legend Snippet: RGMa inhibition reduces MCAO/R-induced reactive astrogliosis and glial scar formation in rats and promotes neurological function recovery. a Timeline of experimental design and animal group classification. WB, Western blot. b Representative fluorescence microscope images showing GFAP expression in tissue sections 14 days post reperfusion. Images are representative of three rats per treatment. (i–iii) Composition of low magnification micrographs (× 40). The dotted lines indicate the boundary of glial scar. Scale bar, 1000 μm. (iv–xv) Higher-magnified view of the squared region (R1-R6) in (i–iii) respectively; × 100 (iv–ix), × 200 (x–xv). DAPI (blue) was used to stain cellular nuclei. Scale bar, 100 μm. c Quantification of GFAP expression at R1-R6 (× 200) ( n = 3). IR, immunoreactivity. ** p

    Techniques Used: Inhibition, Western Blot, Fluorescence, Microscopy, Expressing, Staining

    Knockdown of RGMa reduces key steps of TGFβ1-triggered reactive astrogliosis and glial scar formation. a Immunofluorescence of GFAP (red) in culture of primary astrocytes infected with rAd-shRGMa or rAd-HK 3 days before TGFβ1 (10 ng/ml for 24 h) treatment. One representative panel per group out of three independent experiments is shown. b Western blot analysis of GFAP expression in primary astrocytes infected with rAd-shRGMa or rAd-HK, followed by TGFβ1 (10 ng/ml for 3 days) treatment ( n = 3). c , d The migration capability of astrocytes determined by a transwell chamber assay. The astrocytes were cultured in different conditions (Control, TGFβ1, TGFβ1 + rAd-shRGMa, and TGFβ1 + rAd-HK). c Representative fluorescence microscope images of the lower surface of the filter. The cells were stained with DAPI (blue). d Quantification of the cell number of astrocytes that migrated to the lower side of the filter in each group ( n = 3). e The proliferation ability of astrocytes measured by a CCK8 assay ( n = 3). The cultured astrocytes were infected with rAd-shRGMa or rAd-HK before exposure to TGFβ1 (10 ng/ml for 3 days). NS, no significance. f , g Western blot analysis of neurocan f and phosphacan g expression in the supernatant of cultured astrocytes infected with rAd-shRGMa or rAd-HK 3 days before TGFβ1 (10 ng/ml for 3 days) treatment ( n = 3). Scale bar, 100 μm. Data in bar graphs are means ± SEM ( b , d , e , f , g ); one-way ANOVA with Bonferroni post hoc test, ** p
    Figure Legend Snippet: Knockdown of RGMa reduces key steps of TGFβ1-triggered reactive astrogliosis and glial scar formation. a Immunofluorescence of GFAP (red) in culture of primary astrocytes infected with rAd-shRGMa or rAd-HK 3 days before TGFβ1 (10 ng/ml for 24 h) treatment. One representative panel per group out of three independent experiments is shown. b Western blot analysis of GFAP expression in primary astrocytes infected with rAd-shRGMa or rAd-HK, followed by TGFβ1 (10 ng/ml for 3 days) treatment ( n = 3). c , d The migration capability of astrocytes determined by a transwell chamber assay. The astrocytes were cultured in different conditions (Control, TGFβ1, TGFβ1 + rAd-shRGMa, and TGFβ1 + rAd-HK). c Representative fluorescence microscope images of the lower surface of the filter. The cells were stained with DAPI (blue). d Quantification of the cell number of astrocytes that migrated to the lower side of the filter in each group ( n = 3). e The proliferation ability of astrocytes measured by a CCK8 assay ( n = 3). The cultured astrocytes were infected with rAd-shRGMa or rAd-HK before exposure to TGFβ1 (10 ng/ml for 3 days). NS, no significance. f , g Western blot analysis of neurocan f and phosphacan g expression in the supernatant of cultured astrocytes infected with rAd-shRGMa or rAd-HK 3 days before TGFβ1 (10 ng/ml for 3 days) treatment ( n = 3). Scale bar, 100 μm. Data in bar graphs are means ± SEM ( b , d , e , f , g ); one-way ANOVA with Bonferroni post hoc test, ** p

    Techniques Used: Immunofluorescence, Infection, Western Blot, Expressing, Migration, Transwell Chamber Assay, Cell Culture, Fluorescence, Microscopy, Staining, CCK-8 Assay

    TGFβ1 stimulates RGMa protein expression in primary astrocytes. a Western blot analysis for RGMa expression in primary astrocytes treated with or without TGFβ1 (1–100 ng/ml) for 3 days ( n = 3). b Representative fluorescence photographs of RGMa (green) and GFAP (red) expression in cultured astrocytes in the absence or presence of TGFβ1 (10 ng/ml for 3 days). Similar results were obtained using two additional cell batches. c Western blot analysis for RGMa expression in astrocyte cultures pretreated with or without SB431542 (30 μM for 1 h) before TGFβ1 (10 ng/ml for 3 days) stimulation ( n = 3). d Immunostaining of RGMa (green) and GFAP (red) expression in cultured primary astrocytes pretreated with or without SB431542 (30 μM for 1 h) before TGFβ1 (10 ng/ml for 3 days) stimulation. One representative panel per group out of three independent cell cultures is shown. Scale bar, 100 μm. Data in bar graphs are means ± SEM a and c ; one-way ANOVA with Bonferroni post hoc test, ** p
    Figure Legend Snippet: TGFβ1 stimulates RGMa protein expression in primary astrocytes. a Western blot analysis for RGMa expression in primary astrocytes treated with or without TGFβ1 (1–100 ng/ml) for 3 days ( n = 3). b Representative fluorescence photographs of RGMa (green) and GFAP (red) expression in cultured astrocytes in the absence or presence of TGFβ1 (10 ng/ml for 3 days). Similar results were obtained using two additional cell batches. c Western blot analysis for RGMa expression in astrocyte cultures pretreated with or without SB431542 (30 μM for 1 h) before TGFβ1 (10 ng/ml for 3 days) stimulation ( n = 3). d Immunostaining of RGMa (green) and GFAP (red) expression in cultured primary astrocytes pretreated with or without SB431542 (30 μM for 1 h) before TGFβ1 (10 ng/ml for 3 days) stimulation. One representative panel per group out of three independent cell cultures is shown. Scale bar, 100 μm. Data in bar graphs are means ± SEM a and c ; one-way ANOVA with Bonferroni post hoc test, ** p

    Techniques Used: Expressing, Western Blot, Fluorescence, Cell Culture, Immunostaining

    Related Articles

    Incubation:

    Article Title: Graphene oxide suppresses the growth and malignancy of glioblastoma stem cell-like spheroids via epigenetic mechanisms
    Article Snippet: .. We performed incubation with anti-CD133 (1:200; PB0168, Boster) and anti-GFAP (1:200; BA0056, Boster) antibodies overnight, which was followed by incubation with secondary antibody for 1 h. The nuclear DNA was labeled with DAPI. .. Representative images were obtained with an IX71 Olympus fluorescence microscope.

    Article Title: Let-7f promotes the differentiation of neural stem cells in rats
    Article Snippet: For immunofluorescence on differentiated NSCs, the cells were cultured on culture slides for 7 days at 37°C. .. Then NSCs were fixed with 4% paraformaldehyde at room temperature (RT) and permeabilized with 0.1 Triton X-100, followed by blocking with 5% FBS and incubation with the following primary antibodies: rabbit anti-Nestin antibody (Abcam, Cambridge, UK; dilution 1:100), mouse anti-Tuj1 antibody (Beyotime Biotechnology; dilution 1:100), and rabbit anti-GFAP antibody (Boster Biological Technology; dilution 1:100). .. The following secondary antibodies were also applied: anti-rabbit IgG-TRITC (Boster Biological Technology; dilution 1:100), anti-mouse IgG-FITC (Sigma-Aldrich, St.Louis, MO; dilution 1:100), and anti-rabbit IgG-TRITC (Boster Biological Technology; dilution 1:100).

    Article Title: Electro-acupuncture Alleviates METH Withdrawal-induced Spatial Memory Deficits by Restoring Astrocyte-drived Glutamate Uptake in dCA1
    Article Snippet: .. The blots were incubated overnight at 4°C with the primary antibody [rat anti-C3 (1:50; abam, UK), rabbit anti-GFAP (1:1000; Boster, China), rabbit anti-GLT-1 (1:1000; Thermo Fisher Scientific, USA), rabbit anti-GLAST (1:1000; abcam, UK), mouse anti-GS (1:1000; abcam, UK), mouse anti-S100A10 (1:1000; Thermo Fisher Scientific, USA). .. The blots were incubated overnight at 4°C with the primary antibody [rat anti-C3 (1:50; abam, UK), rabbit anti-GFAP (1:1000; Boster, China), rabbit anti-GLT-1 (1:1000; Thermo Fisher Scientific, USA), rabbit anti-GLAST (1:1000; abcam, UK), mouse anti-GS (1:1000; abcam, UK), mouse anti-S100A10 (1:1000; Thermo Fisher Scientific, USA).

    Article Title: RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke
    Article Snippet: On the following day, the sections were washed using PBS and incubated with appropriate secondary antibodies conjugated with Alexa Fluor 488 (1:200, A-21206 Thermo Fisher) or 555 (1:200, A0460 Beyotime; or 1:300, A-21432 Thermo Fisher) for 1 h at 37 °C. .. For cultured astrocyte staining, cells were fixed with 100% methanol for 10 min. After washing with PBS, cells were blocked by 10% normal donkey serum for 1 h at 37 °C and incubated overnight at 4 °C with primary antibodies including anti-RGMa (1:50, ab169761 Abcam) and anti-GFAP (1:100, BM0055 Boster). .. Cells were washed and for 1 h at 37 °C incubation with secondary antibodies conjugated with Alexa Fluor 488 (1:200, A-21206 Thermo Fisher) or 555 (1:200, A0460 Beyotime).

    Labeling:

    Article Title: Graphene oxide suppresses the growth and malignancy of glioblastoma stem cell-like spheroids via epigenetic mechanisms
    Article Snippet: .. We performed incubation with anti-CD133 (1:200; PB0168, Boster) and anti-GFAP (1:200; BA0056, Boster) antibodies overnight, which was followed by incubation with secondary antibody for 1 h. The nuclear DNA was labeled with DAPI. .. Representative images were obtained with an IX71 Olympus fluorescence microscope.

    Blocking Assay:

    Article Title: Let-7f promotes the differentiation of neural stem cells in rats
    Article Snippet: For immunofluorescence on differentiated NSCs, the cells were cultured on culture slides for 7 days at 37°C. .. Then NSCs were fixed with 4% paraformaldehyde at room temperature (RT) and permeabilized with 0.1 Triton X-100, followed by blocking with 5% FBS and incubation with the following primary antibodies: rabbit anti-Nestin antibody (Abcam, Cambridge, UK; dilution 1:100), mouse anti-Tuj1 antibody (Beyotime Biotechnology; dilution 1:100), and rabbit anti-GFAP antibody (Boster Biological Technology; dilution 1:100). .. The following secondary antibodies were also applied: anti-rabbit IgG-TRITC (Boster Biological Technology; dilution 1:100), anti-mouse IgG-FITC (Sigma-Aldrich, St.Louis, MO; dilution 1:100), and anti-rabbit IgG-TRITC (Boster Biological Technology; dilution 1:100).

    Cell Culture:

    Article Title: RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke
    Article Snippet: On the following day, the sections were washed using PBS and incubated with appropriate secondary antibodies conjugated with Alexa Fluor 488 (1:200, A-21206 Thermo Fisher) or 555 (1:200, A0460 Beyotime; or 1:300, A-21432 Thermo Fisher) for 1 h at 37 °C. .. For cultured astrocyte staining, cells were fixed with 100% methanol for 10 min. After washing with PBS, cells were blocked by 10% normal donkey serum for 1 h at 37 °C and incubated overnight at 4 °C with primary antibodies including anti-RGMa (1:50, ab169761 Abcam) and anti-GFAP (1:100, BM0055 Boster). .. Cells were washed and for 1 h at 37 °C incubation with secondary antibodies conjugated with Alexa Fluor 488 (1:200, A-21206 Thermo Fisher) or 555 (1:200, A0460 Beyotime).

    Staining:

    Article Title: RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke
    Article Snippet: On the following day, the sections were washed using PBS and incubated with appropriate secondary antibodies conjugated with Alexa Fluor 488 (1:200, A-21206 Thermo Fisher) or 555 (1:200, A0460 Beyotime; or 1:300, A-21432 Thermo Fisher) for 1 h at 37 °C. .. For cultured astrocyte staining, cells were fixed with 100% methanol for 10 min. After washing with PBS, cells were blocked by 10% normal donkey serum for 1 h at 37 °C and incubated overnight at 4 °C with primary antibodies including anti-RGMa (1:50, ab169761 Abcam) and anti-GFAP (1:100, BM0055 Boster). .. Cells were washed and for 1 h at 37 °C incubation with secondary antibodies conjugated with Alexa Fluor 488 (1:200, A-21206 Thermo Fisher) or 555 (1:200, A0460 Beyotime).

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  • 94
    Boster Bio mouse anti glial fibrillary acidic protein gfap
    Localization of <t>OLFM3</t> in the human neocortex and in the mouse cortex and hippocampus. (A–C) OLFM3 (green) and MAP2 (red) were co-expressed (yellow) in the human neocortex (A) , mouse cortex (B) , and mouse hippocampus (C) , while no co-localization of OLFM3 and <t>GFAP</t> (red) was detected (D–F) . (G–I) Representative images show that OLFM3 expression (green) overlapped (yellow) with that of the excitatory postsynaptic marker PSD95 (red) but not the excitatory presynaptic marker vGlut1 (purple) in the human neocortex (G) and mouse cortex (H) and hippocampus (I) . DAPI (blue) indicates cell nuclei. White squares indicate positive cells, and the scale bar represents 20 or 50 μm.
    Mouse Anti Glial Fibrillary Acidic Protein Gfap, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti glial fibrillary acidic protein gfap/product/Boster Bio
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse anti glial fibrillary acidic protein gfap - by Bioz Stars, 2021-07
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    92
    Boster Bio rabbit anti glial fibrillary acidic protein gfap
    Morphological and immunocytochemical characteristics of the hippocampal NVU. (A) Hippocampal neurons, astrocytes and <t>microvascular</t> endothelial cells under an inverted light microscope. (B) Neurons are positive for NSE (arrows), astrocytes express <t>GFAP</t> (arrows), and brain microvascular endothelial cells are positive for CD31 (arrows). Scale bars: 100 μm. NVU: Neurovascular unit; NSE: neuron-specific enolase; GFAP: glial fibrillary acidic protein.
    Rabbit Anti Glial Fibrillary Acidic Protein Gfap, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti glial fibrillary acidic protein gfap/product/Boster Bio
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti glial fibrillary acidic protein gfap - by Bioz Stars, 2021-07
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    93
    Boster Bio rabbit anti gfap
    EA rescued METH-related neurotoxicity via normalizing the function of astrocyte. A. Expression of <t>C3</t> in the dCA1 during METH withdrawal. (A1), Top panels: immunohistochemistry staining for C3 (green), <t>GFAP</t> (red) and DAPI (blue) in the hippocampus of SAL and METH group mice. White arrows indicate representative cells which were showed at a higher power view in the white box. Bottom panels: left, the proportion of C3 and GFAP double-label cells; middle, the proportion of reactive astrocytes; right, numbers of GFAP-positive cells per mm 2 in SAL and METH groups. (A2), Western blots (top) and quantification (bottom) of C3 and GFAP protein levels in the dCA1 of SAL and METH groups. (A3), Top panels: immunohistochemistry staining for C3 (green), GFAP (red) and DAPI (blue) in the hippocampus of M+SEA and M+EA group mice. Bottom panels: left, the proportion of C3 and GFAP double-label cells; middle, the proportion of reactive astrocytes; right, number of GFAP-positive cells per mm 2 . (A4), Western blots (top) and quantification (bottom) of C3 and GFAP protein levels in the dCA1 of M+SEA and M+EA group. B, GLT-1, GLAST and GS expression levels in the dCA1 during METH withdrawal. (B1), Immunohistochemistry staining (left, GLT-1/GLAST/GS-green; GFAP-red and DAPI-blue) and colocalized ratio (right) for GLT-1, GLAST and GS in the hippocampus of SAL and METH group mice. (B2), Western blots (top) and quantification (bottom) of GLT-1, GLAST and GS protein levels in the dCA1 of SAL and METH group. (B3), Immunohistochemistry staining (left) and colocalized ratio (right) for GLT-1, GLAST and GS of M+SEA and M+EA group. (B4), Western blots (top) and quantification (bottom) of GLT-1, GLAST and GS protein levels in the dCA1 of M+SEA and M+EA group. Data are Mean ± S.E.M.
    Rabbit Anti Gfap, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti gfap/product/Boster Bio
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti gfap - by Bioz Stars, 2021-07
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    Image Search Results


    Localization of OLFM3 in the human neocortex and in the mouse cortex and hippocampus. (A–C) OLFM3 (green) and MAP2 (red) were co-expressed (yellow) in the human neocortex (A) , mouse cortex (B) , and mouse hippocampus (C) , while no co-localization of OLFM3 and GFAP (red) was detected (D–F) . (G–I) Representative images show that OLFM3 expression (green) overlapped (yellow) with that of the excitatory postsynaptic marker PSD95 (red) but not the excitatory presynaptic marker vGlut1 (purple) in the human neocortex (G) and mouse cortex (H) and hippocampus (I) . DAPI (blue) indicates cell nuclei. White squares indicate positive cells, and the scale bar represents 20 or 50 μm.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Olfactomedin-3 Enhances Seizure Activity by Interacting With AMPA Receptors in Epilepsy Models

    doi: 10.3389/fcell.2020.00722

    Figure Lengend Snippet: Localization of OLFM3 in the human neocortex and in the mouse cortex and hippocampus. (A–C) OLFM3 (green) and MAP2 (red) were co-expressed (yellow) in the human neocortex (A) , mouse cortex (B) , and mouse hippocampus (C) , while no co-localization of OLFM3 and GFAP (red) was detected (D–F) . (G–I) Representative images show that OLFM3 expression (green) overlapped (yellow) with that of the excitatory postsynaptic marker PSD95 (red) but not the excitatory presynaptic marker vGlut1 (purple) in the human neocortex (G) and mouse cortex (H) and hippocampus (I) . DAPI (blue) indicates cell nuclei. White squares indicate positive cells, and the scale bar represents 20 or 50 μm.

    Article Snippet: The following primary antibodies were used: rabbit anti-OLFM3 (1:50, Proteintech, Wuhan, China), mouse anti-glial fibrillary acidic protein (GFAP) (1:50, Boster Bioengineering, Wuhan, China), guinea pig anti-microtubule-associated protein 2 (MAP2) (1:200, Sysy, Göttingen, Germany), guinea pig anti-vGlut1(1:200, Sysy, Göttingen, Germany), mouse anti-PSD95 (1:100, Abcam, United States), mouse anti-GluA1 (1:50, Santa Cruz Biotechnology, United States), mouse anti-GluA2 (1:100, Abcam, United States), Alexa Fluor 488-conjugated goat anti-rabbit IgG antibody (1:50, Zhongshan Golden Bridge, Inc., Beijing, China), Alexa Fluor 594-conjugated goat anti-mouse IgG antibody (1:200, Zhongshan Golden Bridge Inc., Beijing, China), and Alexa Fluor 633-conjugated goat anti-guinea pig IgG antibody (1:50, Abcam, United States).

    Techniques: Expressing, Marker

    Morphological and immunocytochemical characteristics of the hippocampal NVU. (A) Hippocampal neurons, astrocytes and microvascular endothelial cells under an inverted light microscope. (B) Neurons are positive for NSE (arrows), astrocytes express GFAP (arrows), and brain microvascular endothelial cells are positive for CD31 (arrows). Scale bars: 100 μm. NVU: Neurovascular unit; NSE: neuron-specific enolase; GFAP: glial fibrillary acidic protein.

    Journal: Neural Regeneration Research

    Article Title: Structural and functional damage to the hippocampal neurovascular unit in diabetes-related depression

    doi: 10.4103/1673-5374.244794

    Figure Lengend Snippet: Morphological and immunocytochemical characteristics of the hippocampal NVU. (A) Hippocampal neurons, astrocytes and microvascular endothelial cells under an inverted light microscope. (B) Neurons are positive for NSE (arrows), astrocytes express GFAP (arrows), and brain microvascular endothelial cells are positive for CD31 (arrows). Scale bars: 100 μm. NVU: Neurovascular unit; NSE: neuron-specific enolase; GFAP: glial fibrillary acidic protein.

    Article Snippet: Astrocytes and brain microvascular endothelial cells were labeled with rabbit anti-glial fibrillary acidic protein (GFAP) (1:100; Boster) and rabbit anti-PECAM-1/CD31 (1:100; Boster) antibodies.

    Techniques: Light Microscopy

    EA rescued METH-related neurotoxicity via normalizing the function of astrocyte. A. Expression of C3 in the dCA1 during METH withdrawal. (A1), Top panels: immunohistochemistry staining for C3 (green), GFAP (red) and DAPI (blue) in the hippocampus of SAL and METH group mice. White arrows indicate representative cells which were showed at a higher power view in the white box. Bottom panels: left, the proportion of C3 and GFAP double-label cells; middle, the proportion of reactive astrocytes; right, numbers of GFAP-positive cells per mm 2 in SAL and METH groups. (A2), Western blots (top) and quantification (bottom) of C3 and GFAP protein levels in the dCA1 of SAL and METH groups. (A3), Top panels: immunohistochemistry staining for C3 (green), GFAP (red) and DAPI (blue) in the hippocampus of M+SEA and M+EA group mice. Bottom panels: left, the proportion of C3 and GFAP double-label cells; middle, the proportion of reactive astrocytes; right, number of GFAP-positive cells per mm 2 . (A4), Western blots (top) and quantification (bottom) of C3 and GFAP protein levels in the dCA1 of M+SEA and M+EA group. B, GLT-1, GLAST and GS expression levels in the dCA1 during METH withdrawal. (B1), Immunohistochemistry staining (left, GLT-1/GLAST/GS-green; GFAP-red and DAPI-blue) and colocalized ratio (right) for GLT-1, GLAST and GS in the hippocampus of SAL and METH group mice. (B2), Western blots (top) and quantification (bottom) of GLT-1, GLAST and GS protein levels in the dCA1 of SAL and METH group. (B3), Immunohistochemistry staining (left) and colocalized ratio (right) for GLT-1, GLAST and GS of M+SEA and M+EA group. (B4), Western blots (top) and quantification (bottom) of GLT-1, GLAST and GS protein levels in the dCA1 of M+SEA and M+EA group. Data are Mean ± S.E.M.

    Journal: bioRxiv

    Article Title: Electro-acupuncture Alleviates METH Withdrawal-induced Spatial Memory Deficits by Restoring Astrocyte-drived Glutamate Uptake in dCA1

    doi: 10.1101/2020.05.20.106153

    Figure Lengend Snippet: EA rescued METH-related neurotoxicity via normalizing the function of astrocyte. A. Expression of C3 in the dCA1 during METH withdrawal. (A1), Top panels: immunohistochemistry staining for C3 (green), GFAP (red) and DAPI (blue) in the hippocampus of SAL and METH group mice. White arrows indicate representative cells which were showed at a higher power view in the white box. Bottom panels: left, the proportion of C3 and GFAP double-label cells; middle, the proportion of reactive astrocytes; right, numbers of GFAP-positive cells per mm 2 in SAL and METH groups. (A2), Western blots (top) and quantification (bottom) of C3 and GFAP protein levels in the dCA1 of SAL and METH groups. (A3), Top panels: immunohistochemistry staining for C3 (green), GFAP (red) and DAPI (blue) in the hippocampus of M+SEA and M+EA group mice. Bottom panels: left, the proportion of C3 and GFAP double-label cells; middle, the proportion of reactive astrocytes; right, number of GFAP-positive cells per mm 2 . (A4), Western blots (top) and quantification (bottom) of C3 and GFAP protein levels in the dCA1 of M+SEA and M+EA group. B, GLT-1, GLAST and GS expression levels in the dCA1 during METH withdrawal. (B1), Immunohistochemistry staining (left, GLT-1/GLAST/GS-green; GFAP-red and DAPI-blue) and colocalized ratio (right) for GLT-1, GLAST and GS in the hippocampus of SAL and METH group mice. (B2), Western blots (top) and quantification (bottom) of GLT-1, GLAST and GS protein levels in the dCA1 of SAL and METH group. (B3), Immunohistochemistry staining (left) and colocalized ratio (right) for GLT-1, GLAST and GS of M+SEA and M+EA group. (B4), Western blots (top) and quantification (bottom) of GLT-1, GLAST and GS protein levels in the dCA1 of M+SEA and M+EA group. Data are Mean ± S.E.M.

    Article Snippet: The following primary antibodies were used in these experiments: rat anti-C3 (1:200; abcam, UK), mouse anti-S100A10 (1:200; Thermo Fisher Scientific, USA), rabbit anti-GFAP (1:300; Boster, China), rat anti-GFAP(1:500, Thermo Fisher Scientific, USA), rabbit anti-GLT-1 (1:300; Cell Signaling Technology, USA), rabbit anti-GLAST (1:300; Thermo Fisher Scientific, USA), mouse anti-GS (1:500; abcam, UK), rabbit anti-c-Fos (1:2000; Cell Signaling Technology, USA), rabbit anti-SYP1 (Synaptotagmin-1, 1;500; Signalway Antibody, USA), mouse anti-VGLUT-1 (1;500; 1:200; abcam, UK), rabbit anti-NeuN (1:100; MERCK, Germany).

    Techniques: Expressing, Immunohistochemistry, Staining, Mouse Assay, Western Blot

    A1-like astrocytes showed decreased capacity of Glu uptake. A, Glu clearance in primary cultured astrocytes. (A1), Representative micrographs (left) and quantification (right) for GFAP staining in primary astrocytes. (A2), Top panels: immunohistochemistry micrographs for C3 (green), GFAP (red) and DAPI (blue) of control and A1 group. Bottom panels: left, ratio of C3 positive astrocytes; right, mRNA expression levels of C3. (A3), Ratio of Glu clearance after 1h application of Glu (100μM) in the control and A1 group. B, GLT-1, GLAST and GS expression in the primary cultured astrocytes. (B1) , Immunohistochemistry micrographs (left, GLT-1/GLAST/GS-red; C3-green and DAPI-blue) and quantification (right) for GLT-1, GS and GLAST of control and A1 group. (B2), Western blots (top) and quantification (bottom) of GLT-1, GS and GLAST protein levels of control and A1 group. Data are Mean ± S.E.M.

    Journal: bioRxiv

    Article Title: Electro-acupuncture Alleviates METH Withdrawal-induced Spatial Memory Deficits by Restoring Astrocyte-drived Glutamate Uptake in dCA1

    doi: 10.1101/2020.05.20.106153

    Figure Lengend Snippet: A1-like astrocytes showed decreased capacity of Glu uptake. A, Glu clearance in primary cultured astrocytes. (A1), Representative micrographs (left) and quantification (right) for GFAP staining in primary astrocytes. (A2), Top panels: immunohistochemistry micrographs for C3 (green), GFAP (red) and DAPI (blue) of control and A1 group. Bottom panels: left, ratio of C3 positive astrocytes; right, mRNA expression levels of C3. (A3), Ratio of Glu clearance after 1h application of Glu (100μM) in the control and A1 group. B, GLT-1, GLAST and GS expression in the primary cultured astrocytes. (B1) , Immunohistochemistry micrographs (left, GLT-1/GLAST/GS-red; C3-green and DAPI-blue) and quantification (right) for GLT-1, GS and GLAST of control and A1 group. (B2), Western blots (top) and quantification (bottom) of GLT-1, GS and GLAST protein levels of control and A1 group. Data are Mean ± S.E.M.

    Article Snippet: The following primary antibodies were used in these experiments: rat anti-C3 (1:200; abcam, UK), mouse anti-S100A10 (1:200; Thermo Fisher Scientific, USA), rabbit anti-GFAP (1:300; Boster, China), rat anti-GFAP(1:500, Thermo Fisher Scientific, USA), rabbit anti-GLT-1 (1:300; Cell Signaling Technology, USA), rabbit anti-GLAST (1:300; Thermo Fisher Scientific, USA), mouse anti-GS (1:500; abcam, UK), rabbit anti-c-Fos (1:2000; Cell Signaling Technology, USA), rabbit anti-SYP1 (Synaptotagmin-1, 1;500; Signalway Antibody, USA), mouse anti-VGLUT-1 (1;500; 1:200; abcam, UK), rabbit anti-NeuN (1:100; MERCK, Germany).

    Techniques: Cell Culture, Staining, Immunohistochemistry, Expressing, Western Blot

    Graphene oxide inhibits the cell viability and promotes the differentiation of U251 GSCs. a U251 cells were cultured in a serum-free environment. Sphere morphology was photographed using light microscopy. Scale bar = 100 μm. b The expression of SOX2, CD133 and OCT4 in glioblastoma stem-like cells was increased during different periods. c Morphological appearance of U251 GSCs with or without treatment with GO for 2 days. The GSC spheres treated with GO showed adherent growth. Scale bar = 100 μm. d An MTT assay showed the cell viability of U251 GSCs with or without treatment with different dosages of GO for 2, 4, and 6 days. e Quantification of the mRNA levels of the stem cell markers SOX2 and differentiation markers (GFAP and TUJ1) in U251 GSCs with or without treatment with 0, 5, 12.5, 25 and 50 μg/ml GO respectively. * p

    Journal: Journal of Translational Medicine

    Article Title: Graphene oxide suppresses the growth and malignancy of glioblastoma stem cell-like spheroids via epigenetic mechanisms

    doi: 10.1186/s12967-020-02359-z

    Figure Lengend Snippet: Graphene oxide inhibits the cell viability and promotes the differentiation of U251 GSCs. a U251 cells were cultured in a serum-free environment. Sphere morphology was photographed using light microscopy. Scale bar = 100 μm. b The expression of SOX2, CD133 and OCT4 in glioblastoma stem-like cells was increased during different periods. c Morphological appearance of U251 GSCs with or without treatment with GO for 2 days. The GSC spheres treated with GO showed adherent growth. Scale bar = 100 μm. d An MTT assay showed the cell viability of U251 GSCs with or without treatment with different dosages of GO for 2, 4, and 6 days. e Quantification of the mRNA levels of the stem cell markers SOX2 and differentiation markers (GFAP and TUJ1) in U251 GSCs with or without treatment with 0, 5, 12.5, 25 and 50 μg/ml GO respectively. * p

    Article Snippet: We performed incubation with anti-CD133 (1:200; PB0168, Boster) and anti-GFAP (1:200; BA0056, Boster) antibodies overnight, which was followed by incubation with secondary antibody for 1 h. The nuclear DNA was labeled with DAPI.

    Techniques: Cell Culture, Light Microscopy, Expressing, MTT Assay

    Graphene oxide reduces the expression of stem cell markers and promotes the differentiation of GSCs. a Quantification of the mRNA levels of stem cell markers SOX2 and CD133 in GSCs with or without treatment with GO. b The intracellular expression of the differentiation marker GFAP after treatment with 50 μg/ml GO was examined using immunofluorescence staining. Scale bar = 100 μm. c The expression level of the stem cell marker CD133 in cells treated with different concentrations of GO was detected by immunofluorescence staining. Scale bar = 50 μm. d , e Representative immunoblots and relative quantification of OCT4, SOX2, TUJ1 and GFAP in GSCs after treatment with 0, 5, 12.5, 25 and 50 μg/ml GO respectively. * p

    Journal: Journal of Translational Medicine

    Article Title: Graphene oxide suppresses the growth and malignancy of glioblastoma stem cell-like spheroids via epigenetic mechanisms

    doi: 10.1186/s12967-020-02359-z

    Figure Lengend Snippet: Graphene oxide reduces the expression of stem cell markers and promotes the differentiation of GSCs. a Quantification of the mRNA levels of stem cell markers SOX2 and CD133 in GSCs with or without treatment with GO. b The intracellular expression of the differentiation marker GFAP after treatment with 50 μg/ml GO was examined using immunofluorescence staining. Scale bar = 100 μm. c The expression level of the stem cell marker CD133 in cells treated with different concentrations of GO was detected by immunofluorescence staining. Scale bar = 50 μm. d , e Representative immunoblots and relative quantification of OCT4, SOX2, TUJ1 and GFAP in GSCs after treatment with 0, 5, 12.5, 25 and 50 μg/ml GO respectively. * p

    Article Snippet: We performed incubation with anti-CD133 (1:200; PB0168, Boster) and anti-GFAP (1:200; BA0056, Boster) antibodies overnight, which was followed by incubation with secondary antibody for 1 h. The nuclear DNA was labeled with DAPI.

    Techniques: Expressing, Marker, Immunofluorescence, Staining, Western Blot