rabbit anti a2a adenosine receptor antibody  (Alomone Labs)


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    Alomone Labs rabbit anti a2a adenosine receptor antibody
    Activation of <t>A2A</t> AR decreases the focal adhesion activity of human brain endothelial cell mediated by decrease in phosphorylation of ERM and focal adhesion kinase (A) Western blot on phosphorylated ERM (p-ERM) and phosphorylated focal adhesion kinase (p-FAK) were performed in Lexiscan treated primary human brain endothelial cells (HBMVEC) upto 30 minutes. (B) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from A) and plotted as graph. (C) Western blot analysis of p-ERM, p-FAK were performed in NECA treated HBMVEC upto 120 minutes. (D) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from C) and plotted as graph. (E) Western blot analysis of p-ERM in Lexiscan treated HCMEC-D3 cells up to 60 minutes. (F) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from E) and plotted as graph. (G) Western blot analysis of p-ERM in NECA treated HCMEC D3 cells up to 120 minutes. (H) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from G) and plotted as graph. In all images M indicates media only control.
    Rabbit Anti A2a Adenosine Receptor Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti a2a adenosine receptor antibody/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti a2a adenosine receptor antibody - by Bioz Stars, 2022-05
    91/100 stars

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    1) Product Images from "A2A adenosine receptor regulates the human blood brain barrier permeability"

    Article Title: A2A adenosine receptor regulates the human blood brain barrier permeability

    Journal: Molecular neurobiology

    doi: 10.1007/s12035-014-8879-2

    Activation of A2A AR decreases the focal adhesion activity of human brain endothelial cell mediated by decrease in phosphorylation of ERM and focal adhesion kinase (A) Western blot on phosphorylated ERM (p-ERM) and phosphorylated focal adhesion kinase (p-FAK) were performed in Lexiscan treated primary human brain endothelial cells (HBMVEC) upto 30 minutes. (B) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from A) and plotted as graph. (C) Western blot analysis of p-ERM, p-FAK were performed in NECA treated HBMVEC upto 120 minutes. (D) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from C) and plotted as graph. (E) Western blot analysis of p-ERM in Lexiscan treated HCMEC-D3 cells up to 60 minutes. (F) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from E) and plotted as graph. (G) Western blot analysis of p-ERM in NECA treated HCMEC D3 cells up to 120 minutes. (H) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from G) and plotted as graph. In all images M indicates media only control.
    Figure Legend Snippet: Activation of A2A AR decreases the focal adhesion activity of human brain endothelial cell mediated by decrease in phosphorylation of ERM and focal adhesion kinase (A) Western blot on phosphorylated ERM (p-ERM) and phosphorylated focal adhesion kinase (p-FAK) were performed in Lexiscan treated primary human brain endothelial cells (HBMVEC) upto 30 minutes. (B) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from A) and plotted as graph. (C) Western blot analysis of p-ERM, p-FAK were performed in NECA treated HBMVEC upto 120 minutes. (D) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from C) and plotted as graph. (E) Western blot analysis of p-ERM in Lexiscan treated HCMEC-D3 cells up to 60 minutes. (F) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from E) and plotted as graph. (G) Western blot analysis of p-ERM in NECA treated HCMEC D3 cells up to 120 minutes. (H) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from G) and plotted as graph. In all images M indicates media only control.

    Techniques Used: Activation Assay, Activity Assay, Western Blot

    A2A AR signaling activates RhoA in human brain endothelial cells and induces stress fiber formation (A) Changes in the level of cyclic AMP (cAMP) by Lexiscan or NECA were determined in human brain endothelial cells. Intracellular cAMP levels in primary human brain endothelial cells were measured using a cAMP screening kit (Applied biosystems) after treatment with 1 uM of Lexiscan or NECA. 1 uM of Forskolin (FSK) was used as a positive control. (B) RhoA pull down assay performed in HBMVEC, or primary human brain endothelial cells with Lexiscan and NECA stimulation up to 15 minutes. M indicates media only control. (C) Densitometric analysis of western blot data from (B). The band intensity from each treatment group was divided by that of control group from each time point. (D and E) Western blot analysis of active RhoA levels using a pull down assay performed in the human brain endothelial cell line. HCMEC D3 cells lysates were activated with Lexiscan (D), or NECA (E). M indicates media only control. (F) Densitometric analysis of western blot data from (D) and (E). Intensity of band from treated group was divided by that of control group from each time point. (G) IFA analysis of stress fiber formation by Lexiscan and NECA treatment in HBMVEC which was visualized with AF568 conjugated phalloidin (Red). Nucleus was counterstained with DAPI (Blue). Induction of stress fiber formation was determined up to 30 minutes. Scale bar indicates 50 um.
    Figure Legend Snippet: A2A AR signaling activates RhoA in human brain endothelial cells and induces stress fiber formation (A) Changes in the level of cyclic AMP (cAMP) by Lexiscan or NECA were determined in human brain endothelial cells. Intracellular cAMP levels in primary human brain endothelial cells were measured using a cAMP screening kit (Applied biosystems) after treatment with 1 uM of Lexiscan or NECA. 1 uM of Forskolin (FSK) was used as a positive control. (B) RhoA pull down assay performed in HBMVEC, or primary human brain endothelial cells with Lexiscan and NECA stimulation up to 15 minutes. M indicates media only control. (C) Densitometric analysis of western blot data from (B). The band intensity from each treatment group was divided by that of control group from each time point. (D and E) Western blot analysis of active RhoA levels using a pull down assay performed in the human brain endothelial cell line. HCMEC D3 cells lysates were activated with Lexiscan (D), or NECA (E). M indicates media only control. (F) Densitometric analysis of western blot data from (D) and (E). Intensity of band from treated group was divided by that of control group from each time point. (G) IFA analysis of stress fiber formation by Lexiscan and NECA treatment in HBMVEC which was visualized with AF568 conjugated phalloidin (Red). Nucleus was counterstained with DAPI (Blue). Induction of stress fiber formation was determined up to 30 minutes. Scale bar indicates 50 um.

    Techniques Used: Positive Control, Pull Down Assay, Western Blot, Immunofluorescence

    Activation of A2A AR decreases expression level of tight and adherens junction molecules in human and mouse brain endothelial cell (A–D) Western blot result of VE-Cadherin and Claudin 5 in primary human brain endothelial cells with Lexiscan and NECA activation. (A and B) Western blot analysis of Claudin-5 and VE-Cadherin was performed on the HBMVEC cells treated with Lexiscan upto 30 minutes (A). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (B). (C and D) Western blot on Claudin-5 and VE-Cadherin was performed on the HBMVEC cells treated with NECA upto 120 minutes (C). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (D). (E–H) Western blot analysis of Claudin-5 and VE-Cadherin levels in mouse brain endothelial cell line (bEnd3). (E and F) Western blot analysis of Claudin-5 and VE-Cadherin was performed on the bEnd 3 cells treated with Lexiscan upto 4 hours (E). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (F). (G and H) Western blot on Claudin-5 and VE-Cadherin was performed on the bEnd 3 cells treated with NECA upto 4 hours (G). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (H). In all western blot images M indicates media only control.
    Figure Legend Snippet: Activation of A2A AR decreases expression level of tight and adherens junction molecules in human and mouse brain endothelial cell (A–D) Western blot result of VE-Cadherin and Claudin 5 in primary human brain endothelial cells with Lexiscan and NECA activation. (A and B) Western blot analysis of Claudin-5 and VE-Cadherin was performed on the HBMVEC cells treated with Lexiscan upto 30 minutes (A). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (B). (C and D) Western blot on Claudin-5 and VE-Cadherin was performed on the HBMVEC cells treated with NECA upto 120 minutes (C). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (D). (E–H) Western blot analysis of Claudin-5 and VE-Cadherin levels in mouse brain endothelial cell line (bEnd3). (E and F) Western blot analysis of Claudin-5 and VE-Cadherin was performed on the bEnd 3 cells treated with Lexiscan upto 4 hours (E). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (F). (G and H) Western blot on Claudin-5 and VE-Cadherin was performed on the bEnd 3 cells treated with NECA upto 4 hours (G). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (H). In all western blot images M indicates media only control.

    Techniques Used: Activation Assay, Expressing, Western Blot

    A2A AR is expressed in primary human brain endothelial cells and human brain endothelial cell line Western blot (A) and immunofluoresecence assay (IFA) (B) show the presence of A2A adenosine receptor (AR) expression on human primary brain endothelial cells (HBMVEC) and human brain endothelial cell line (HCMEC-D3). For IFA, cells were stained with anti-A2A AR antibody (Green) and anti-human CD31 as endothelial cell marker (Red). Nucleus was counter stained with DAPI (Blue). Scale bar indicates 25 um. (C) FACS analysis (Dot-plot and histogram) shows expression of the extracellular enzymes, CD39 and CD73, in HBMVEC and HCMEC-D3.
    Figure Legend Snippet: A2A AR is expressed in primary human brain endothelial cells and human brain endothelial cell line Western blot (A) and immunofluoresecence assay (IFA) (B) show the presence of A2A adenosine receptor (AR) expression on human primary brain endothelial cells (HBMVEC) and human brain endothelial cell line (HCMEC-D3). For IFA, cells were stained with anti-A2A AR antibody (Green) and anti-human CD31 as endothelial cell marker (Red). Nucleus was counter stained with DAPI (Blue). Scale bar indicates 25 um. (C) FACS analysis (Dot-plot and histogram) shows expression of the extracellular enzymes, CD39 and CD73, in HBMVEC and HCMEC-D3.

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

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    Alomone Labs rabbit anti a2a adenosine receptor antibody
    Activation of <t>A2A</t> AR decreases the focal adhesion activity of human brain endothelial cell mediated by decrease in phosphorylation of ERM and focal adhesion kinase (A) Western blot on phosphorylated ERM (p-ERM) and phosphorylated focal adhesion kinase (p-FAK) were performed in Lexiscan treated primary human brain endothelial cells (HBMVEC) upto 30 minutes. (B) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from A) and plotted as graph. (C) Western blot analysis of p-ERM, p-FAK were performed in NECA treated HBMVEC upto 120 minutes. (D) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from C) and plotted as graph. (E) Western blot analysis of p-ERM in Lexiscan treated HCMEC-D3 cells up to 60 minutes. (F) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from E) and plotted as graph. (G) Western blot analysis of p-ERM in NECA treated HCMEC D3 cells up to 120 minutes. (H) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from G) and plotted as graph. In all images M indicates media only control.
    Rabbit Anti A2a Adenosine Receptor Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti a2a adenosine receptor antibody/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti a2a adenosine receptor antibody - by Bioz Stars, 2022-05
    91/100 stars
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    Activation of A2A AR decreases the focal adhesion activity of human brain endothelial cell mediated by decrease in phosphorylation of ERM and focal adhesion kinase (A) Western blot on phosphorylated ERM (p-ERM) and phosphorylated focal adhesion kinase (p-FAK) were performed in Lexiscan treated primary human brain endothelial cells (HBMVEC) upto 30 minutes. (B) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from A) and plotted as graph. (C) Western blot analysis of p-ERM, p-FAK were performed in NECA treated HBMVEC upto 120 minutes. (D) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from C) and plotted as graph. (E) Western blot analysis of p-ERM in Lexiscan treated HCMEC-D3 cells up to 60 minutes. (F) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from E) and plotted as graph. (G) Western blot analysis of p-ERM in NECA treated HCMEC D3 cells up to 120 minutes. (H) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from G) and plotted as graph. In all images M indicates media only control.

    Journal: Molecular neurobiology

    Article Title: A2A adenosine receptor regulates the human blood brain barrier permeability

    doi: 10.1007/s12035-014-8879-2

    Figure Lengend Snippet: Activation of A2A AR decreases the focal adhesion activity of human brain endothelial cell mediated by decrease in phosphorylation of ERM and focal adhesion kinase (A) Western blot on phosphorylated ERM (p-ERM) and phosphorylated focal adhesion kinase (p-FAK) were performed in Lexiscan treated primary human brain endothelial cells (HBMVEC) upto 30 minutes. (B) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from A) and plotted as graph. (C) Western blot analysis of p-ERM, p-FAK were performed in NECA treated HBMVEC upto 120 minutes. (D) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Ratio from treated group was normalized by GAPDH and was divided by the value of control group at each time point (from C) and plotted as graph. (E) Western blot analysis of p-ERM in Lexiscan treated HCMEC-D3 cells up to 60 minutes. (F) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from E) and plotted as graph. (G) Western blot analysis of p-ERM in NECA treated HCMEC D3 cells up to 120 minutes. (H) Intensity of the band of phosphorylated form was divided by that of total protein to obtain the ratio. Normalized ratio by GAPDH from treated group was divided by that of control group at each time point (from G) and plotted as graph. In all images M indicates media only control.

    Article Snippet: Rabbit anti-A2A adenosine receptor antibody was purchased from Alomone labs (Jerusalem, Israel).

    Techniques: Activation Assay, Activity Assay, Western Blot

    A2A AR signaling activates RhoA in human brain endothelial cells and induces stress fiber formation (A) Changes in the level of cyclic AMP (cAMP) by Lexiscan or NECA were determined in human brain endothelial cells. Intracellular cAMP levels in primary human brain endothelial cells were measured using a cAMP screening kit (Applied biosystems) after treatment with 1 uM of Lexiscan or NECA. 1 uM of Forskolin (FSK) was used as a positive control. (B) RhoA pull down assay performed in HBMVEC, or primary human brain endothelial cells with Lexiscan and NECA stimulation up to 15 minutes. M indicates media only control. (C) Densitometric analysis of western blot data from (B). The band intensity from each treatment group was divided by that of control group from each time point. (D and E) Western blot analysis of active RhoA levels using a pull down assay performed in the human brain endothelial cell line. HCMEC D3 cells lysates were activated with Lexiscan (D), or NECA (E). M indicates media only control. (F) Densitometric analysis of western blot data from (D) and (E). Intensity of band from treated group was divided by that of control group from each time point. (G) IFA analysis of stress fiber formation by Lexiscan and NECA treatment in HBMVEC which was visualized with AF568 conjugated phalloidin (Red). Nucleus was counterstained with DAPI (Blue). Induction of stress fiber formation was determined up to 30 minutes. Scale bar indicates 50 um.

    Journal: Molecular neurobiology

    Article Title: A2A adenosine receptor regulates the human blood brain barrier permeability

    doi: 10.1007/s12035-014-8879-2

    Figure Lengend Snippet: A2A AR signaling activates RhoA in human brain endothelial cells and induces stress fiber formation (A) Changes in the level of cyclic AMP (cAMP) by Lexiscan or NECA were determined in human brain endothelial cells. Intracellular cAMP levels in primary human brain endothelial cells were measured using a cAMP screening kit (Applied biosystems) after treatment with 1 uM of Lexiscan or NECA. 1 uM of Forskolin (FSK) was used as a positive control. (B) RhoA pull down assay performed in HBMVEC, or primary human brain endothelial cells with Lexiscan and NECA stimulation up to 15 minutes. M indicates media only control. (C) Densitometric analysis of western blot data from (B). The band intensity from each treatment group was divided by that of control group from each time point. (D and E) Western blot analysis of active RhoA levels using a pull down assay performed in the human brain endothelial cell line. HCMEC D3 cells lysates were activated with Lexiscan (D), or NECA (E). M indicates media only control. (F) Densitometric analysis of western blot data from (D) and (E). Intensity of band from treated group was divided by that of control group from each time point. (G) IFA analysis of stress fiber formation by Lexiscan and NECA treatment in HBMVEC which was visualized with AF568 conjugated phalloidin (Red). Nucleus was counterstained with DAPI (Blue). Induction of stress fiber formation was determined up to 30 minutes. Scale bar indicates 50 um.

    Article Snippet: Rabbit anti-A2A adenosine receptor antibody was purchased from Alomone labs (Jerusalem, Israel).

    Techniques: Positive Control, Pull Down Assay, Western Blot, Immunofluorescence

    Activation of A2A AR decreases expression level of tight and adherens junction molecules in human and mouse brain endothelial cell (A–D) Western blot result of VE-Cadherin and Claudin 5 in primary human brain endothelial cells with Lexiscan and NECA activation. (A and B) Western blot analysis of Claudin-5 and VE-Cadherin was performed on the HBMVEC cells treated with Lexiscan upto 30 minutes (A). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (B). (C and D) Western blot on Claudin-5 and VE-Cadherin was performed on the HBMVEC cells treated with NECA upto 120 minutes (C). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (D). (E–H) Western blot analysis of Claudin-5 and VE-Cadherin levels in mouse brain endothelial cell line (bEnd3). (E and F) Western blot analysis of Claudin-5 and VE-Cadherin was performed on the bEnd 3 cells treated with Lexiscan upto 4 hours (E). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (F). (G and H) Western blot on Claudin-5 and VE-Cadherin was performed on the bEnd 3 cells treated with NECA upto 4 hours (G). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (H). In all western blot images M indicates media only control.

    Journal: Molecular neurobiology

    Article Title: A2A adenosine receptor regulates the human blood brain barrier permeability

    doi: 10.1007/s12035-014-8879-2

    Figure Lengend Snippet: Activation of A2A AR decreases expression level of tight and adherens junction molecules in human and mouse brain endothelial cell (A–D) Western blot result of VE-Cadherin and Claudin 5 in primary human brain endothelial cells with Lexiscan and NECA activation. (A and B) Western blot analysis of Claudin-5 and VE-Cadherin was performed on the HBMVEC cells treated with Lexiscan upto 30 minutes (A). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (B). (C and D) Western blot on Claudin-5 and VE-Cadherin was performed on the HBMVEC cells treated with NECA upto 120 minutes (C). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (D). (E–H) Western blot analysis of Claudin-5 and VE-Cadherin levels in mouse brain endothelial cell line (bEnd3). (E and F) Western blot analysis of Claudin-5 and VE-Cadherin was performed on the bEnd 3 cells treated with Lexiscan upto 4 hours (E). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (F). (G and H) Western blot on Claudin-5 and VE-Cadherin was performed on the bEnd 3 cells treated with NECA upto 4 hours (G). Normalized intensity of band by GAPDH from treated group was divided by that of control group at each time point and plotted as graph (H). In all western blot images M indicates media only control.

    Article Snippet: Rabbit anti-A2A adenosine receptor antibody was purchased from Alomone labs (Jerusalem, Israel).

    Techniques: Activation Assay, Expressing, Western Blot

    A2A AR is expressed in primary human brain endothelial cells and human brain endothelial cell line Western blot (A) and immunofluoresecence assay (IFA) (B) show the presence of A2A adenosine receptor (AR) expression on human primary brain endothelial cells (HBMVEC) and human brain endothelial cell line (HCMEC-D3). For IFA, cells were stained with anti-A2A AR antibody (Green) and anti-human CD31 as endothelial cell marker (Red). Nucleus was counter stained with DAPI (Blue). Scale bar indicates 25 um. (C) FACS analysis (Dot-plot and histogram) shows expression of the extracellular enzymes, CD39 and CD73, in HBMVEC and HCMEC-D3.

    Journal: Molecular neurobiology

    Article Title: A2A adenosine receptor regulates the human blood brain barrier permeability

    doi: 10.1007/s12035-014-8879-2

    Figure Lengend Snippet: A2A AR is expressed in primary human brain endothelial cells and human brain endothelial cell line Western blot (A) and immunofluoresecence assay (IFA) (B) show the presence of A2A adenosine receptor (AR) expression on human primary brain endothelial cells (HBMVEC) and human brain endothelial cell line (HCMEC-D3). For IFA, cells were stained with anti-A2A AR antibody (Green) and anti-human CD31 as endothelial cell marker (Red). Nucleus was counter stained with DAPI (Blue). Scale bar indicates 25 um. (C) FACS analysis (Dot-plot and histogram) shows expression of the extracellular enzymes, CD39 and CD73, in HBMVEC and HCMEC-D3.

    Article Snippet: Rabbit anti-A2A adenosine receptor antibody was purchased from Alomone labs (Jerusalem, Israel).

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