gfap  (Boster Bio)


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    Name:
    Anti GFAP Antibody
    Description:

    Catalog Number:
    MA1045
    Price:
    99.0
    Category:
    Primary Antibodies
    Reactivity:
    Human Pig Rat
    Applications:
    IF, IHC-P, IHC-F, WB
    Immunogen:
    GFAP from pig spinal cord.
    Host:
    Mouse
    Isotype:
    Mouse IgG1
    Buy from Supplier


    Structured Review

    Boster Bio gfap
    Anti GFAP Antibody

    https://www.bioz.com/result/gfap/product/Boster Bio
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    gfap - by Bioz Stars, 2021-07
    95/100 stars

    Images

    1) Product Images from "Reversion of malignant phenotypes of human glioblastoma cells by β-elemene through β-catenin-mediated regulation of stemness-, differentiation- and epithelial-to-mesenchymal transition-related molecules"

    Article Title: Reversion of malignant phenotypes of human glioblastoma cells by β-elemene through β-catenin-mediated regulation of stemness-, differentiation- and epithelial-to-mesenchymal transition-related molecules

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-015-0727-2

    β -Elemene regulation of stemness-, differentiation- and EMT-related effectors in vivo. a Western blot assays were performed on the aforementioned glioblastoma xenografts in the β -elemene- and NaCl-treated groups. Expression levels of CD133, ABCG2, N-cadherin and β -catenin were significantly downregulated and expression levels of E-cadherin, GFAP, Notch1 and SHH were upregulated by β -elemene. Interestingly, the expression level of vimentin in the β -elemene-treated group was significantly lower than that in the NaCl-treated group; this result was opposite that for the in vitro procedure. b The results are representative of three independent experiments, and the values are presented as the mean ± SD (* p
    Figure Legend Snippet: β -Elemene regulation of stemness-, differentiation- and EMT-related effectors in vivo. a Western blot assays were performed on the aforementioned glioblastoma xenografts in the β -elemene- and NaCl-treated groups. Expression levels of CD133, ABCG2, N-cadherin and β -catenin were significantly downregulated and expression levels of E-cadherin, GFAP, Notch1 and SHH were upregulated by β -elemene. Interestingly, the expression level of vimentin in the β -elemene-treated group was significantly lower than that in the NaCl-treated group; this result was opposite that for the in vitro procedure. b The results are representative of three independent experiments, and the values are presented as the mean ± SD (* p

    Techniques Used: In Vivo, Western Blot, Expressing, In Vitro

    β -Elemene regulated the expression of stemness markers and differentiation-related effectors in glioblastoma cells. a CD133 + and ABCG2 + cells were sparsely distributed throughout both G1 and G2 tissues, and both CD133 and ABCG2 were localized to both the cytoplasm and cytomembrane. The expression of GFAP was higher in the G1 tissue than in the G2 tissue. b β -Elemene decreased the expression levels of CD133 and ABCG2 and increased the expression levels of GFAP, Notch1 and SHH in a dose-dependent manner. c The results of ( b ) were semi-quantitatively estimated using Gel-Pro Analyzer 4.0 software and are illustrated graphically. The results are representative of three independent experiments, and the values are presented as the mean ± SD (* p
    Figure Legend Snippet: β -Elemene regulated the expression of stemness markers and differentiation-related effectors in glioblastoma cells. a CD133 + and ABCG2 + cells were sparsely distributed throughout both G1 and G2 tissues, and both CD133 and ABCG2 were localized to both the cytoplasm and cytomembrane. The expression of GFAP was higher in the G1 tissue than in the G2 tissue. b β -Elemene decreased the expression levels of CD133 and ABCG2 and increased the expression levels of GFAP, Notch1 and SHH in a dose-dependent manner. c The results of ( b ) were semi-quantitatively estimated using Gel-Pro Analyzer 4.0 software and are illustrated graphically. The results are representative of three independent experiments, and the values are presented as the mean ± SD (* p

    Techniques Used: Expressing, Software

    Related Articles

    Western Blot:

    Article Title: Reversion of malignant phenotypes of human glioblastoma cells by β-elemene through β-catenin-mediated regulation of stemness-, differentiation- and epithelial-to-mesenchymal transition-related molecules
    Article Snippet: .. Antibodies against CD133, ABCG2 and GFAP that were used for Western blot and immunohistochemistry analyses were purchased from Boster Co., Ltd. (Wuhan, China). .. GAPDH antibody was obtained from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA), and the antibodies against Notch1, SHH, β -catenin, vimentin, E-cadherin and N-cadherin were purchased from Cell Signaling Technology, Inc. (Danvers, MA, USA).

    Immunohistochemistry:

    Article Title: Reversion of malignant phenotypes of human glioblastoma cells by β-elemene through β-catenin-mediated regulation of stemness-, differentiation- and epithelial-to-mesenchymal transition-related molecules
    Article Snippet: .. Antibodies against CD133, ABCG2 and GFAP that were used for Western blot and immunohistochemistry analyses were purchased from Boster Co., Ltd. (Wuhan, China). .. GAPDH antibody was obtained from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA), and the antibodies against Notch1, SHH, β -catenin, vimentin, E-cadherin and N-cadherin were purchased from Cell Signaling Technology, Inc. (Danvers, MA, USA).

    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).

    Incubation:

    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).

    Article Title: RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke
    Article Snippet: .. Then the sections were incubated overnight at 4 °C with specific primary antibodies as follows: anti-GFAP (1:100, BM0055 Boster, Wuhan, China), anti-RGMa (1:50, ab26287 Abcam), anti-NeuN (1:50, MAB377 Millipore), anti-Nestin (1:100, ab11306 Abcam), anti-CC1 (1:50, ab16794 Abcam), anti-NG2 (1:100, ab50009 Abcam), anti-Iba1 (1:50, NB100-1028 Novus, Littleton, CO, USA), anti-CD31 (1:50, ab64543 Abcam), anti-αSMA (1:50, ab21027 Abcam), anti-fibronectin (1:50, 610077 BD Biosciences, Franklin Lakes, NJ, USA), anti-collagen I (1:100, ab90395 Abcam), anti-neurocan (1:100, N0913 Sigma-Aldrich), and anti-phosphacan (1:100, P8874 Sigma-Aldrich). .. 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.

    Article Title: Bone marrow-derived mesenchymal stem cells differentiate into nerve-like cells in vitro after transfection with brain-derived neurotrophic factor gene
    Article Snippet: Detection of BDNF, nestin, NSE, and GFAP by immunocytochemistry. .. Immunocytochemistry was performed using the SABC method (Shi et al. ): the culture medium was removed from adherent cells, and the cells were then fixed in 4% paraformaldehyde, incubated in a mixture of 30% hydrogen peroxide and pure methanol, incubated in goat serum, and then incubated with the anti-BDNF, anti-nestin, anti-NSE, and anti-GFAP (1:300 dilution for all; Wuhan Boster, Wuhan, China) primary antibodies overnight in a 4°C refrigerator. .. The following day, incubation with the HRP-labeled rabbit anti-mouse secondary antibody (Wuhan Boster, Wuhan, China) was performed after rewarming of the samples, followed by staining with streptavidin-biotin complex (SABC; Wuhan Boster) and 3,3′-diaminobenzidine (DAB; Wuhan Boster) and counterstaining with hematoxylin.

    Article Title: Role of Elevated Thrombospondin-1 in Kainic Acid-Induced Status Epilepticus
    Article Snippet: .. The blocked membranes were incubated with rabbit anti-GFAP IgG (1:1000; BM0055, Boster), mouse anti-CS56 IgG (1:1000; ab11570, EMD Millipore) or rabbit anti-TSP-1 (1:100; ab85762, Abcam), mouse monoclonal anti-TGF-β1 (1:800; ab64751, Abcam), rabbit anti-Smad2/3/pSmad2/3 monoclonal antibodies (1:2000; ab47083 and ab40854, Abcam; Ser_465/467, Cell Signaling Technology, Boston, MA, USA; ab52903, Abcam), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH; 1:3000; AB-P-R001, Zhejiang Kangcheng Biotech, Jiaxing, China) at room temperature for 2 h and then at 4°C overnight. ..

    Article Title: Electroacupuncture Suppresses the NF-κB Signaling Pathway by Upregulating Cylindromatosis to Alleviate Inflammatory Injury in Cerebral Ischemia/Reperfusion Rats
    Article Snippet: .. Sections were subsequently incubated with prepared primary antibodies at 4°C overnight as follows: Anti-NeuN mouse (labeled neurons, MAB377, Millipore, 1:100), anti-GFAP mouse (labeled astrocytes, BM0055, Boster, 1:100), anti-Iba1 goat (to label microglia, NB100-1028SS, Novus, 1:50), anti-CYLD rabbit (11110-1-AP, Proteintech, 1:100), anti-CYLD mouse (SC-74435, Santa Cruz, 1:100), anti-NF-κB p65 rabbit (#8242, Cell Signaling Technology, 1:50) and anti-CX3CL1 rabbit (ab25088, Abcam, 1:100). .. After rewarming for 1 h at 37°C, sections were incubated with secondary antibodies for 1 h at 37°C in the dark: Alexa Fluor 594-conjugated goat anti-rabbit IgG (H + L) (SA00006-4, Proteintech, 1:200), Alexa Fluor 594-conjugated donkey anti-rabbit IgG (H + L) (SA00006-8, Proteintech, 1:200), Alexa Fluor 488-conjugated goat anti-mouse IgG (H + L) (SA00006-1, Proteintech, 1:200), FITC-conjugated Affinipure donkey anti-goat IgG (H + L) (SA00003-3, Proteintech, 1:200).

    Immunocytochemistry:

    Article Title: Bone marrow-derived mesenchymal stem cells differentiate into nerve-like cells in vitro after transfection with brain-derived neurotrophic factor gene
    Article Snippet: Detection of BDNF, nestin, NSE, and GFAP by immunocytochemistry. .. Immunocytochemistry was performed using the SABC method (Shi et al. ): the culture medium was removed from adherent cells, and the cells were then fixed in 4% paraformaldehyde, incubated in a mixture of 30% hydrogen peroxide and pure methanol, incubated in goat serum, and then incubated with the anti-BDNF, anti-nestin, anti-NSE, and anti-GFAP (1:300 dilution for all; Wuhan Boster, Wuhan, China) primary antibodies overnight in a 4°C refrigerator. .. The following day, incubation with the HRP-labeled rabbit anti-mouse secondary antibody (Wuhan Boster, Wuhan, China) was performed after rewarming of the samples, followed by staining with streptavidin-biotin complex (SABC; Wuhan Boster) and 3,3′-diaminobenzidine (DAB; Wuhan Boster) and counterstaining with hematoxylin.

    Labeling:

    Article Title: Electroacupuncture Suppresses the NF-κB Signaling Pathway by Upregulating Cylindromatosis to Alleviate Inflammatory Injury in Cerebral Ischemia/Reperfusion Rats
    Article Snippet: .. Sections were subsequently incubated with prepared primary antibodies at 4°C overnight as follows: Anti-NeuN mouse (labeled neurons, MAB377, Millipore, 1:100), anti-GFAP mouse (labeled astrocytes, BM0055, Boster, 1:100), anti-Iba1 goat (to label microglia, NB100-1028SS, Novus, 1:50), anti-CYLD rabbit (11110-1-AP, Proteintech, 1:100), anti-CYLD mouse (SC-74435, Santa Cruz, 1:100), anti-NF-κB p65 rabbit (#8242, Cell Signaling Technology, 1:50) and anti-CX3CL1 rabbit (ab25088, Abcam, 1:100). .. After rewarming for 1 h at 37°C, sections were incubated with secondary antibodies for 1 h at 37°C in the dark: Alexa Fluor 594-conjugated goat anti-rabbit IgG (H + L) (SA00006-4, Proteintech, 1:200), Alexa Fluor 594-conjugated donkey anti-rabbit IgG (H + L) (SA00006-8, Proteintech, 1:200), Alexa Fluor 488-conjugated goat anti-mouse IgG (H + L) (SA00006-1, Proteintech, 1:200), FITC-conjugated Affinipure donkey anti-goat IgG (H + L) (SA00003-3, Proteintech, 1:200).

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    Boster Bio anti gfap
    Immunocytochemical analysis of BMSCs and <t>BDNF-BMSCs</t> (brown staining highlighted by arrows , magnification ×200). ( A1 – A4 ) Non-induced BMSCs expressed low levels of BDNF, nestin, NSE, and <t>GFAP.</t> ( B1 – B4 ) Low levels of BDNF, nestin, NSE, and GFAP were also detected in induced BMSCs. ( C1 – C4 ) The number of cells positively co-stained with BDNF, nestin, NSE, and GFAP in non-induced BDNF-BMSCs was significantly higher than that in BMSCs. Over 98% of non-induced BDNF-BMSCs were positively stained for BDNF. ( D1 – D4 ) Over 98% of induced BDNF-BMSCs were positively stained for BDNF. More cells positively co-stained for nestin, NSE, and GFAP were detected in induced BDNF-BMSCs than in non-induced BDNF-BMSCs. ( E ) Rates of positive immunostaining in BMSCs and BDNF-BMSCs, as determined by immunocytochemistry for BDNF, nestin, NSE, and GFAP (%; mean ± SD). # P
    Anti Gfap, supplied by Boster Bio, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti gfap/product/Boster Bio
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti gfap - by Bioz Stars, 2021-07
    95/100 stars
      Buy from Supplier

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    Immunocytochemical analysis of BMSCs and BDNF-BMSCs (brown staining highlighted by arrows , magnification ×200). ( A1 – A4 ) Non-induced BMSCs expressed low levels of BDNF, nestin, NSE, and GFAP. ( B1 – B4 ) Low levels of BDNF, nestin, NSE, and GFAP were also detected in induced BMSCs. ( C1 – C4 ) The number of cells positively co-stained with BDNF, nestin, NSE, and GFAP in non-induced BDNF-BMSCs was significantly higher than that in BMSCs. Over 98% of non-induced BDNF-BMSCs were positively stained for BDNF. ( D1 – D4 ) Over 98% of induced BDNF-BMSCs were positively stained for BDNF. More cells positively co-stained for nestin, NSE, and GFAP were detected in induced BDNF-BMSCs than in non-induced BDNF-BMSCs. ( E ) Rates of positive immunostaining in BMSCs and BDNF-BMSCs, as determined by immunocytochemistry for BDNF, nestin, NSE, and GFAP (%; mean ± SD). # P

    Journal: In Vitro Cellular & Developmental Biology. Animal

    Article Title: Bone marrow-derived mesenchymal stem cells differentiate into nerve-like cells in vitro after transfection with brain-derived neurotrophic factor gene

    doi: 10.1007/s11626-015-9875-1

    Figure Lengend Snippet: Immunocytochemical analysis of BMSCs and BDNF-BMSCs (brown staining highlighted by arrows , magnification ×200). ( A1 – A4 ) Non-induced BMSCs expressed low levels of BDNF, nestin, NSE, and GFAP. ( B1 – B4 ) Low levels of BDNF, nestin, NSE, and GFAP were also detected in induced BMSCs. ( C1 – C4 ) The number of cells positively co-stained with BDNF, nestin, NSE, and GFAP in non-induced BDNF-BMSCs was significantly higher than that in BMSCs. Over 98% of non-induced BDNF-BMSCs were positively stained for BDNF. ( D1 – D4 ) Over 98% of induced BDNF-BMSCs were positively stained for BDNF. More cells positively co-stained for nestin, NSE, and GFAP were detected in induced BDNF-BMSCs than in non-induced BDNF-BMSCs. ( E ) Rates of positive immunostaining in BMSCs and BDNF-BMSCs, as determined by immunocytochemistry for BDNF, nestin, NSE, and GFAP (%; mean ± SD). # P

    Article Snippet: Immunocytochemistry was performed using the SABC method (Shi et al. ): the culture medium was removed from adherent cells, and the cells were then fixed in 4% paraformaldehyde, incubated in a mixture of 30% hydrogen peroxide and pure methanol, incubated in goat serum, and then incubated with the anti-BDNF, anti-nestin, anti-NSE, and anti-GFAP (1:300 dilution for all; Wuhan Boster, Wuhan, China) primary antibodies overnight in a 4°C refrigerator.

    Techniques: Staining, Immunostaining, Immunocytochemistry

    mRNA expression of BMSCs and BDNF-BMSCs. BDNF, nestin, NSE, and GFAP mRNA expression of BMSCs and BDNF-BMSCs determined by RT-PCR (mean ± SD). # P

    Journal: In Vitro Cellular & Developmental Biology. Animal

    Article Title: Bone marrow-derived mesenchymal stem cells differentiate into nerve-like cells in vitro after transfection with brain-derived neurotrophic factor gene

    doi: 10.1007/s11626-015-9875-1

    Figure Lengend Snippet: mRNA expression of BMSCs and BDNF-BMSCs. BDNF, nestin, NSE, and GFAP mRNA expression of BMSCs and BDNF-BMSCs determined by RT-PCR (mean ± SD). # P

    Article Snippet: Immunocytochemistry was performed using the SABC method (Shi et al. ): the culture medium was removed from adherent cells, and the cells were then fixed in 4% paraformaldehyde, incubated in a mixture of 30% hydrogen peroxide and pure methanol, incubated in goat serum, and then incubated with the anti-BDNF, anti-nestin, anti-NSE, and anti-GFAP (1:300 dilution for all; Wuhan Boster, Wuhan, China) primary antibodies overnight in a 4°C refrigerator.

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction

    β -Elemene regulation of stemness-, differentiation- and EMT-related effectors in vivo. a Western blot assays were performed on the aforementioned glioblastoma xenografts in the β -elemene- and NaCl-treated groups. Expression levels of CD133, ABCG2, N-cadherin and β -catenin were significantly downregulated and expression levels of E-cadherin, GFAP, Notch1 and SHH were upregulated by β -elemene. Interestingly, the expression level of vimentin in the β -elemene-treated group was significantly lower than that in the NaCl-treated group; this result was opposite that for the in vitro procedure. b The results are representative of three independent experiments, and the values are presented as the mean ± SD (* p

    Journal: Journal of Translational Medicine

    Article Title: Reversion of malignant phenotypes of human glioblastoma cells by β-elemene through β-catenin-mediated regulation of stemness-, differentiation- and epithelial-to-mesenchymal transition-related molecules

    doi: 10.1186/s12967-015-0727-2

    Figure Lengend Snippet: β -Elemene regulation of stemness-, differentiation- and EMT-related effectors in vivo. a Western blot assays were performed on the aforementioned glioblastoma xenografts in the β -elemene- and NaCl-treated groups. Expression levels of CD133, ABCG2, N-cadherin and β -catenin were significantly downregulated and expression levels of E-cadherin, GFAP, Notch1 and SHH were upregulated by β -elemene. Interestingly, the expression level of vimentin in the β -elemene-treated group was significantly lower than that in the NaCl-treated group; this result was opposite that for the in vitro procedure. b The results are representative of three independent experiments, and the values are presented as the mean ± SD (* p

    Article Snippet: Antibodies against CD133, ABCG2 and GFAP that were used for Western blot and immunohistochemistry analyses were purchased from Boster Co., Ltd. (Wuhan, China).

    Techniques: In Vivo, Western Blot, Expressing, In Vitro

    β -Elemene regulated the expression of stemness markers and differentiation-related effectors in glioblastoma cells. a CD133 + and ABCG2 + cells were sparsely distributed throughout both G1 and G2 tissues, and both CD133 and ABCG2 were localized to both the cytoplasm and cytomembrane. The expression of GFAP was higher in the G1 tissue than in the G2 tissue. b β -Elemene decreased the expression levels of CD133 and ABCG2 and increased the expression levels of GFAP, Notch1 and SHH in a dose-dependent manner. c The results of ( b ) were semi-quantitatively estimated using Gel-Pro Analyzer 4.0 software and are illustrated graphically. The results are representative of three independent experiments, and the values are presented as the mean ± SD (* p

    Journal: Journal of Translational Medicine

    Article Title: Reversion of malignant phenotypes of human glioblastoma cells by β-elemene through β-catenin-mediated regulation of stemness-, differentiation- and epithelial-to-mesenchymal transition-related molecules

    doi: 10.1186/s12967-015-0727-2

    Figure Lengend Snippet: β -Elemene regulated the expression of stemness markers and differentiation-related effectors in glioblastoma cells. a CD133 + and ABCG2 + cells were sparsely distributed throughout both G1 and G2 tissues, and both CD133 and ABCG2 were localized to both the cytoplasm and cytomembrane. The expression of GFAP was higher in the G1 tissue than in the G2 tissue. b β -Elemene decreased the expression levels of CD133 and ABCG2 and increased the expression levels of GFAP, Notch1 and SHH in a dose-dependent manner. c The results of ( b ) were semi-quantitatively estimated using Gel-Pro Analyzer 4.0 software and are illustrated graphically. The results are representative of three independent experiments, and the values are presented as the mean ± SD (* p

    Article Snippet: Antibodies against CD133, ABCG2 and GFAP that were used for Western blot and immunohistochemistry analyses were purchased from Boster Co., Ltd. (Wuhan, China).

    Techniques: Expressing, Software

    Brain-specific serine/threonine-protein kinase 1 (SAD-B) is localized in the epileptic brain. A , Immunofluorescence labelling of SAD-B (red), MAP2 (violet), and GFAP (green) in the cortex of patients with temporal lobe epilepsy (TLE) showing that SAD-B was co-localized with MAP2 but not with GFAP. Scale bar: 50 μm (400×). B , Immunofluorescence labelling of SAD-B (red), MAP2 (violet), and GFAP (green) in the CA1 region of the hippocampus or cortex of an epileptic rat showing that SAD-B was co-localized with MAP2, but not with GFAP. Scale bar: 50 μm (400×). White arrows: SAD-B; yellow arrows: GFAP.

    Journal: Brazilian Journal of Medical and Biological Research

    Article Title: SAD-B modulates epileptic seizure by regulating AMPA receptors in patients with temporal lobe epilepsy and in the PTZ-induced epileptic model

    doi: 10.1590/1414-431X20199175

    Figure Lengend Snippet: Brain-specific serine/threonine-protein kinase 1 (SAD-B) is localized in the epileptic brain. A , Immunofluorescence labelling of SAD-B (red), MAP2 (violet), and GFAP (green) in the cortex of patients with temporal lobe epilepsy (TLE) showing that SAD-B was co-localized with MAP2 but not with GFAP. Scale bar: 50 μm (400×). B , Immunofluorescence labelling of SAD-B (red), MAP2 (violet), and GFAP (green) in the CA1 region of the hippocampus or cortex of an epileptic rat showing that SAD-B was co-localized with MAP2, but not with GFAP. Scale bar: 50 μm (400×). White arrows: SAD-B; yellow arrows: GFAP.

    Article Snippet: The primary antibodies included mouse anti-SAD-B (diluted 1:100, Cat. No. ab206298; Abcam, UK), chicken anti-microtubule-associated protein 2 (MAP2) (1:200, Cat. No. ab5392; Abcam), and rabbit anti-glial fibrillary acidic protein (GFAP) (1:50, Cat. No. BM0055; Boster, China).

    Techniques: Immunofluorescence

    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

    Journal: Cell Death and Differentiation

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

    doi: 10.1038/s41418-018-0058-y

    Figure Lengend 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

    Article Snippet: Then the sections were incubated overnight at 4 °C with specific primary antibodies as follows: anti-GFAP (1:100, BM0055 Boster, Wuhan, China), anti-RGMa (1:50, ab26287 Abcam), anti-NeuN (1:50, MAB377 Millipore), anti-Nestin (1:100, ab11306 Abcam), anti-CC1 (1:50, ab16794 Abcam), anti-NG2 (1:100, ab50009 Abcam), anti-Iba1 (1:50, NB100-1028 Novus, Littleton, CO, USA), anti-CD31 (1:50, ab64543 Abcam), anti-αSMA (1:50, ab21027 Abcam), anti-fibronectin (1:50, 610077 BD Biosciences, Franklin Lakes, NJ, USA), anti-collagen I (1:100, ab90395 Abcam), anti-neurocan (1:100, N0913 Sigma-Aldrich), and anti-phosphacan (1:100, P8874 Sigma-Aldrich).

    Techniques: 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

    Journal: Cell Death and Differentiation

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

    doi: 10.1038/s41418-018-0058-y

    Figure Lengend 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

    Article Snippet: Then the sections were incubated overnight at 4 °C with specific primary antibodies as follows: anti-GFAP (1:100, BM0055 Boster, Wuhan, China), anti-RGMa (1:50, ab26287 Abcam), anti-NeuN (1:50, MAB377 Millipore), anti-Nestin (1:100, ab11306 Abcam), anti-CC1 (1:50, ab16794 Abcam), anti-NG2 (1:100, ab50009 Abcam), anti-Iba1 (1:50, NB100-1028 Novus, Littleton, CO, USA), anti-CD31 (1:50, ab64543 Abcam), anti-αSMA (1:50, ab21027 Abcam), anti-fibronectin (1:50, 610077 BD Biosciences, Franklin Lakes, NJ, USA), anti-collagen I (1:100, ab90395 Abcam), anti-neurocan (1:100, N0913 Sigma-Aldrich), and anti-phosphacan (1:100, P8874 Sigma-Aldrich).

    Techniques: 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

    Journal: Cell Death and Differentiation

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

    doi: 10.1038/s41418-018-0058-y

    Figure Lengend 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

    Article Snippet: Then the sections were incubated overnight at 4 °C with specific primary antibodies as follows: anti-GFAP (1:100, BM0055 Boster, Wuhan, China), anti-RGMa (1:50, ab26287 Abcam), anti-NeuN (1:50, MAB377 Millipore), anti-Nestin (1:100, ab11306 Abcam), anti-CC1 (1:50, ab16794 Abcam), anti-NG2 (1:100, ab50009 Abcam), anti-Iba1 (1:50, NB100-1028 Novus, Littleton, CO, USA), anti-CD31 (1:50, ab64543 Abcam), anti-αSMA (1:50, ab21027 Abcam), anti-fibronectin (1:50, 610077 BD Biosciences, Franklin Lakes, NJ, USA), anti-collagen I (1:100, ab90395 Abcam), anti-neurocan (1:100, N0913 Sigma-Aldrich), and anti-phosphacan (1:100, P8874 Sigma-Aldrich).

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