mouse monoclonal anti at1r antibody (Santa Cruz Biotechnology)

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Santa Cruz Biotechnology mouse monoclonal anti at1r antibody

Fig. 1 Human AT1 and AT2 receptors interact in a heterologous expression system. a–c Immunocytochemistry assays were performed in HEK- 293T cells expressing <t>AT1R-YFP</t> (1 μg cDNA), which was detected by its own yellow fluorescence (green), and AT2R-Rluc (1 μg cDNA), which was detected by a mouse anti-Rluc antibody and a secondary Cy3 anti-mouse antibody (red). Colocalization is shown in yellow. Cell nuclei were stained with Hoechst (blue). Scale bar: 20 μm. d BRET assays were performed in HEK-293T cells transfected with a constant amount of cDNA for AT2R-Rluc (0.9 μg) or σ1R-Rluc (0.75 μg) (as negative control) and increasing amounts of cDNA for AT1R-YFP (0.5 to 4 μg) or AT2R-YFP (0.1 to 4 μg) (as negative control). Values are the mean ± S.E.M. of 8 independent experiments performed in duplicates. e Schematic representation of BRET assay: the occurrence of energy transfer depends on the distance between the BRET donor (Rluc) and the BRET acceptor (YFP)

Mouse Monoclonal Anti At1r Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 616 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/transfer+function+of+a+linearized+model/AT1+Antibody/pm32807174-147-27-33
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mouse monoclonal anti at1r antibody - by Bioz Stars, 2026-09

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1) Product Images from "Angiotensin AT 1 and AT 2 receptor heteromer expression in the hemilesioned rat model of Parkinson's disease that increases with levodopa-induced dyskinesia."

Article Title: Angiotensin AT 1 and AT 2 receptor heteromer expression in the hemilesioned rat model of Parkinson's disease that increases with levodopa-induced dyskinesia.

Journal: Journal of neuroinflammation

doi: 10.1186/s12974-020-01908-z

Figure Legend Snippet: Fig. 1 Human AT1 and AT2 receptors interact in a heterologous expression system. a–c Immunocytochemistry assays were performed in HEK- 293T cells expressing AT1R-YFP (1 μg cDNA), which was detected by its own yellow fluorescence (green), and AT2R-Rluc (1 μg cDNA), which was detected by a mouse anti-Rluc antibody and a secondary Cy3 anti-mouse antibody (red). Colocalization is shown in yellow. Cell nuclei were stained with Hoechst (blue). Scale bar: 20 μm. d BRET assays were performed in HEK-293T cells transfected with a constant amount of cDNA for AT2R-Rluc (0.9 μg) or σ1R-Rluc (0.75 μg) (as negative control) and increasing amounts of cDNA for AT1R-YFP (0.5 to 4 μg) or AT2R-YFP (0.1 to 4 μg) (as negative control). Values are the mean ± S.E.M. of 8 independent experiments performed in duplicates. e Schematic representation of BRET assay: the occurrence of energy transfer depends on the distance between the BRET donor (Rluc) and the BRET acceptor (YFP)

Techniques Used: Expressing, Immunocytochemistry, Fluorescence, Staining, Transfection, Negative Control, Bioluminescence Resonance Energy Transfer

Fig. 2 Functional characterization in HEK-293T cells expressing the AT1R-AT2R heteromer. HEK-293T cells were pretreated with selective receptor antagonists (300 nM candesartan for AT1R or 1 μM PD123319 for AT2R) and subsequently treated with selective agonists (100 nM angiotensin II for AT1R and 300 nM CGP-42112A for AT2R) a–c Cytosolic calcium detection assay were performed in HEK-293T cells transfected with the cDNAs for an engineered calcium sensor, 6GCaMP (1 μg), AT1R (1 μg), and/or AT2R (1 μg). Values are the mean ± S.E.M. of 5 independent experiments performed in duplicates. d–f Intracellular cAMP levels were determined by TR-FRET as described in Methods. HEK-293T cells were transfected with cDNAs for AT1R (1 μg) and/or AT2R (1 μg). When Gi coupling was assessed, decreases in [cAMP] were determined using 0.5 μM forskolin added 15 min after the agonists stimulation. Values are the mean ± S.E.M. of 6 independent experiments performed in triplicates. In cAMP one-way ANOVA followed by Bonferroni’s multiple comparison post-hoc test were used for statistical analysis. Signaling output was the dependent variable and the different treatments were the independent variables. (*p < 0.05, **p < 0.01, ***p < 0.001 versus forskolin treatment; +++p < 0.001 versus Ang II treatment; &&&p < 0.001 versus CGP-42112A treatment)

Figure Legend Snippet: Fig. 2 Functional characterization in HEK-293T cells expressing the AT1R-AT2R heteromer. HEK-293T cells were pretreated with selective receptor antagonists (300 nM candesartan for AT1R or 1 μM PD123319 for AT2R) and subsequently treated with selective agonists (100 nM angiotensin II for AT1R and 300 nM CGP-42112A for AT2R) a–c Cytosolic calcium detection assay were performed in HEK-293T cells transfected with the cDNAs for an engineered calcium sensor, 6GCaMP (1 μg), AT1R (1 μg), and/or AT2R (1 μg). Values are the mean ± S.E.M. of 5 independent experiments performed in duplicates. d–f Intracellular cAMP levels were determined by TR-FRET as described in Methods. HEK-293T cells were transfected with cDNAs for AT1R (1 μg) and/or AT2R (1 μg). When Gi coupling was assessed, decreases in [cAMP] were determined using 0.5 μM forskolin added 15 min after the agonists stimulation. Values are the mean ± S.E.M. of 6 independent experiments performed in triplicates. In cAMP one-way ANOVA followed by Bonferroni’s multiple comparison post-hoc test were used for statistical analysis. Signaling output was the dependent variable and the different treatments were the independent variables. (*p < 0.05, **p < 0.01, ***p < 0.001 versus forskolin treatment; +++p < 0.001 versus Ang II treatment; &&&p < 0.001 versus CGP-42112A treatment)

Techniques Used: Functional Assay, Expressing, Detection Assay, Transfection, Comparison

Fig. 4 AT1R-AT2R heteromer functionality in primary cultures of striatal neurons. For cAMP (a) or ERK1/2 phosphorylation (b), cells were pretreated (15 min) with selective receptor antagonists (300 nM candesartan for AT1R or 1 μM PD123319 for AT2R) and subsequently treated with selective agonists (100 nM angiotensin II for AT1R and/or 300 nM CGP-42112A for AT2R). Values are the mean ± S.E.M. of 5 independent experiments performed in triplicates. One-way ANOVA followed by Bonferroni’s multiple comparison post-hoc test were used for statistical analysis. Signaling output was the dependent variable and the different treatments were the independent variables. (&p < 0.05 versus CGP-42112A treatment; *p < 0.05, **p < 0.01, ***p < 0.001 versus forskolin treatment in cAMP determinations or versus vehicle treatment (basal) in pERK determinations)

Figure Legend Snippet: Fig. 4 AT1R-AT2R heteromer functionality in primary cultures of striatal neurons. For cAMP (a) or ERK1/2 phosphorylation (b), cells were pretreated (15 min) with selective receptor antagonists (300 nM candesartan for AT1R or 1 μM PD123319 for AT2R) and subsequently treated with selective agonists (100 nM angiotensin II for AT1R and/or 300 nM CGP-42112A for AT2R). Values are the mean ± S.E.M. of 5 independent experiments performed in triplicates. One-way ANOVA followed by Bonferroni’s multiple comparison post-hoc test were used for statistical analysis. Signaling output was the dependent variable and the different treatments were the independent variables. (&p < 0.05 versus CGP-42112A treatment; *p < 0.05, **p < 0.01, ***p < 0.001 versus forskolin treatment in cAMP determinations or versus vehicle treatment (basal) in pERK determinations)

Techniques Used: Phospho-proteomics, Comparison

Fig. 3 Functional characterization of AT1R-AT2R heteromer in HEK-293T cells. HEK-293T cells were transfected with cDNAs for AT1R (1 μg) and/or AT2R (1 μg). Cells were pretreated (15 min) with selective receptor antagonists (300 nM candesartan for AT1R or 1 μM PD123319 for AT2R receptors) and subsequently treated with selective agonists (100 nM angiotensin II for AT1R and 300 nM CGP-42112A for AT2R receptors). a–c ERK1/2 phosphorylation was analyzed using an AlphaScreen®SureFire® kit (Perkin Elmer). Values are the mean ± S.E.M. of 5 independent experiments performed in duplicates. One-way ANOVA followed by Bonferroni’s multiple comparison post-hoc test were used for statistical analysis. Signaling output was the dependent variable and the different treatments were the independent variables (*p < 0.05, **p < 0.01, ***p < 0.001; versus vehicle treatment (basal)). d–f DMR tracings represent the picometer-shifts of reflected light wavelength over time. Values are the mean ± S.E.M. 8 independent experiments performed in triplicates

Figure Legend Snippet: Fig. 3 Functional characterization of AT1R-AT2R heteromer in HEK-293T cells. HEK-293T cells were transfected with cDNAs for AT1R (1 μg) and/or AT2R (1 μg). Cells were pretreated (15 min) with selective receptor antagonists (300 nM candesartan for AT1R or 1 μM PD123319 for AT2R receptors) and subsequently treated with selective agonists (100 nM angiotensin II for AT1R and 300 nM CGP-42112A for AT2R receptors). a–c ERK1/2 phosphorylation was analyzed using an AlphaScreen®SureFire® kit (Perkin Elmer). Values are the mean ± S.E.M. of 5 independent experiments performed in duplicates. One-way ANOVA followed by Bonferroni’s multiple comparison post-hoc test were used for statistical analysis. Signaling output was the dependent variable and the different treatments were the independent variables (*p < 0.05, **p < 0.01, ***p < 0.001; versus vehicle treatment (basal)). d–f DMR tracings represent the picometer-shifts of reflected light wavelength over time. Values are the mean ± S.E.M. 8 independent experiments performed in triplicates

Techniques Used: Functional Assay, Transfection, Phospho-proteomics, Amplified Luminescent Proximity Homogenous Assay, Comparison

Fig. 5 AT1R-AT2R heteromer functionality in microglial primary cultures treated with LPS and IFN-γ. a–c Expression of AT1R/AT2R heteromers in primary microglial cultures were determined by PLA, which was performed using specific primary antibodies against AT1 and AT2 receptors (confocal microscopy images (stacks of 3 consecutive planes) show heteroreceptor complexes as red clusters and Hoechst-stained nuclei (blue)). Scale bar: 20 μm. d Bar graph showing the percentage of red dots/cell respect non-treated cells; mean ± S.E.M of counts in 5–7 different fields (n = 5; **p < 0.01; Student’s t test versus the control condition). e, f Microglial cultures were incubated for 48 h in the absence (left) or in the presence (right) of 1 μM LPS and 200 U/mL IFN-γ. Microglial cells were pretreated (15 min) with selective receptor antagonists (300 nM candesartan for AT1R or 1 μM PD123319 for AT2R receptors) and subsequently with the specific agonists (100 nM angiotensin II for AT1R and 300 nM CGP-42112A for AT2R receptors). cAMP (e-f) and ERK1/2 phosphorylation (g-h) were subsequently measured. Values are the mean ± S.E.M. of 5 independent experiments performed in triplicates. One-way ANOVA followed by Bonferroni’s multiple comparison post-hoc test were used for statistical analysis. Signaling output was the dependent variable and the different treatments were the independent variables. (+p < 0.05 versus Ang II treatment in pERK determinations; and *p < 0.05, **p < 0.01, ***p < 0.001; versus forskolin treatment in cAMP measurements or versus vehicle treatment (basal) in pERK measurements)

Figure Legend Snippet: Fig. 5 AT1R-AT2R heteromer functionality in microglial primary cultures treated with LPS and IFN-γ. a–c Expression of AT1R/AT2R heteromers in primary microglial cultures were determined by PLA, which was performed using specific primary antibodies against AT1 and AT2 receptors (confocal microscopy images (stacks of 3 consecutive planes) show heteroreceptor complexes as red clusters and Hoechst-stained nuclei (blue)). Scale bar: 20 μm. d Bar graph showing the percentage of red dots/cell respect non-treated cells; mean ± S.E.M of counts in 5–7 different fields (n = 5; **p < 0.01; Student’s t test versus the control condition). e, f Microglial cultures were incubated for 48 h in the absence (left) or in the presence (right) of 1 μM LPS and 200 U/mL IFN-γ. Microglial cells were pretreated (15 min) with selective receptor antagonists (300 nM candesartan for AT1R or 1 μM PD123319 for AT2R receptors) and subsequently with the specific agonists (100 nM angiotensin II for AT1R and 300 nM CGP-42112A for AT2R receptors). cAMP (e-f) and ERK1/2 phosphorylation (g-h) were subsequently measured. Values are the mean ± S.E.M. of 5 independent experiments performed in triplicates. One-way ANOVA followed by Bonferroni’s multiple comparison post-hoc test were used for statistical analysis. Signaling output was the dependent variable and the different treatments were the independent variables. (+p < 0.05 versus Ang II treatment in pERK determinations; and *p < 0.05, **p < 0.01, ***p < 0.001; versus forskolin treatment in cAMP measurements or versus vehicle treatment (basal) in pERK measurements)

Techniques Used: Expressing, Confocal Microscopy, Staining, Control, Incubation, Phospho-proteomics, Comparison

Fig. 6 AT1R-AT2R heteromer expression in brain striatal sections of Parkinson’s disease (PD) rat model. a–d PLA assays in striatal sections from the 6-OH-dopamine PD rat model, non-lesioned (a), lesioned (b), and lesioned plus chronically treated with L-DOPA and either lacking (c) or displaying (d) dyskinesias. Confocal microscopy images (stacks of 3 consecutive planes) show heteroreceptor complexes as red clusters and Hoechst-stained nuclei (blue). Scale bar: 20 μm. e Bar graph showing the percentage of red dots/cell. Data are the mean S.E.M . of counts in 9–12 different fields per animal (n = 4 per group). One-way ANOVA followed by Bonferroni’s post-hoc multiple comparison tests were used to compare the red dots/cell values. The number of clusters (r) was the dependent variable and the four animal groups treatments were independent variables (***p < 0.001; versus lesioned condition, ++p < 0.01; versus L-DOPA non-dyskinesia condition)

Figure Legend Snippet: Fig. 6 AT1R-AT2R heteromer expression in brain striatal sections of Parkinson’s disease (PD) rat model. a–d PLA assays in striatal sections from the 6-OH-dopamine PD rat model, non-lesioned (a), lesioned (b), and lesioned plus chronically treated with L-DOPA and either lacking (c) or displaying (d) dyskinesias. Confocal microscopy images (stacks of 3 consecutive planes) show heteroreceptor complexes as red clusters and Hoechst-stained nuclei (blue). Scale bar: 20 μm. e Bar graph showing the percentage of red dots/cell. Data are the mean S.E.M . of counts in 9–12 different fields per animal (n = 4 per group). One-way ANOVA followed by Bonferroni’s post-hoc multiple comparison tests were used to compare the red dots/cell values. The number of clusters (r) was the dependent variable and the four animal groups treatments were independent variables (***p < 0.001; versus lesioned condition, ++p < 0.01; versus L-DOPA non-dyskinesia condition)

Techniques Used: Expressing, Confocal Microscopy, Staining, Comparison

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Article Title: Angiotensin II type 1 receptor signaling promotes bladder cancer progression and its inhibition by Losartan.
Article Snippet: .. Briefly, after the overnight incubation at 4 °C with anti-AGTR1 antibody (1:400; sc515884; Santa Cruz Biotechnology, California, USA), the sections were washed with phosphate-buffered saline (PBS) containing 0.05% Tween-20. .. They were then incubated for 1 h at room temperature with anti-mouse HRP polymer (Vector Laboratories, California, USA), followed by a 30- min incubation with the VECTASTAIN Elite ABC kit (Vector Laboratories).

Article Title: Exogenous hydrogen sulfide inhibits the progression of vascular dysfunction and hypertension mediated by the renin-angiotensin system in chronic kidney disease.
Article Snippet: .. After 235 three washes with fresh PBST, membranes were sectioned according to the molecular 236 weight of the target proteins and incubated overnight at 4 °C in blocking buffer containing 237 the respective primary antibodies: AT1 (mouse, 1:1000; sc-515884), AT2 (mouse, 1:1000; 238 sc-518054), Mas (mouse, 1:1000; sc-390453), CBS (mouse, 1:500; sc-133154), and CSE 239 (mouse, 1:1000; sc-365381) from Santa Cruz Biotechnology (Dallas, TX, USA), as well as 240 3-MST (rabbit, 1:1000; HPA001240) from Sigma-Aldrich (St. Louis, MO, USA). ..

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mouse monoclonal anti at1r antibody (Santa Cruz Biotechnology)

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1) Product Images from "Angiotensin AT 1 and AT 2 receptor heteromer expression in the hemilesioned rat model of Parkinson's disease that increases with levodopa-induced dyskinesia."

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