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rat brain microvascular endothelial cells rbmvec  (Cell Applications Inc)


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    Cell Applications Inc rat brain microvascular endothelial cells rbmvec
    (A) UMAP plot showing the cellular distribution of Angulin-1/LSR expression across identified clusters. Expression values were log-transformed using the log1p() function to normalize data and account for zero values. Points are jittered and colored according to cell type annotation. Dot plot summarizing the proportion and average expression of Angulin-1/LSR across cell clusters. Dot size represents the percentage of cells expressing the gene, while color intensity reflects the mean expression level per cluster. (B) Representative immunoblots showing Angulin-1/LSR protein levels in <t>RBMVECs</t> over a 24-hour period under untreated conditions. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Data represent the mean ± SEM from three independent biological replicates ( n = 3). Statistical comparisons were made across all time points (1, 2, 4, 8, and 24 hours). * p < 0.05, ** p < 0.001, **** p < 0.00001 indicate significant differences relative to other time points.
    Rat Brain Microvascular Endothelial Cells Rbmvec, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 93/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 31 article reviews
    rat brain microvascular endothelial cells rbmvec - by Bioz Stars, 2026-06
    93/100 stars

    Images

    1) Product Images from "Angulin-1/LSR inhibition transiently disrupts the blood-tumor barrier to enhance doxil permeability and impair malignant glioma progression"

    Article Title: Angulin-1/LSR inhibition transiently disrupts the blood-tumor barrier to enhance doxil permeability and impair malignant glioma progression

    Journal: bioRxiv

    doi: 10.1101/2025.07.31.667901

    (A) UMAP plot showing the cellular distribution of Angulin-1/LSR expression across identified clusters. Expression values were log-transformed using the log1p() function to normalize data and account for zero values. Points are jittered and colored according to cell type annotation. Dot plot summarizing the proportion and average expression of Angulin-1/LSR across cell clusters. Dot size represents the percentage of cells expressing the gene, while color intensity reflects the mean expression level per cluster. (B) Representative immunoblots showing Angulin-1/LSR protein levels in RBMVECs over a 24-hour period under untreated conditions. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Data represent the mean ± SEM from three independent biological replicates ( n = 3). Statistical comparisons were made across all time points (1, 2, 4, 8, and 24 hours). * p < 0.05, ** p < 0.001, **** p < 0.00001 indicate significant differences relative to other time points.
    Figure Legend Snippet: (A) UMAP plot showing the cellular distribution of Angulin-1/LSR expression across identified clusters. Expression values were log-transformed using the log1p() function to normalize data and account for zero values. Points are jittered and colored according to cell type annotation. Dot plot summarizing the proportion and average expression of Angulin-1/LSR across cell clusters. Dot size represents the percentage of cells expressing the gene, while color intensity reflects the mean expression level per cluster. (B) Representative immunoblots showing Angulin-1/LSR protein levels in RBMVECs over a 24-hour period under untreated conditions. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Data represent the mean ± SEM from three independent biological replicates ( n = 3). Statistical comparisons were made across all time points (1, 2, 4, 8, and 24 hours). * p < 0.05, ** p < 0.001, **** p < 0.00001 indicate significant differences relative to other time points.

    Techniques Used: Expressing, Transformation Assay, Western Blot, Membrane, Control

    Cells were treated with Angubindin-1 at increasing concentrations (75–600 µg/mL) for 24 hours, followed by co-immunoprecipitation using 6 µg/mL anti-LSR antibody to evaluate Angulin-1/LSR interactions. (A, B) Representative immunoblots of 3X-FLAG-Angubindin-1 and Angulin-1/LSR in RBMVEC and LN-229 cells, respectively. Densitometric quantification of Angulin-1/LSR interactions, normalized to the HA-tagged negative control (NC) loading control. Angubindin-1 elicited a dose-dependent effect on Angulin-1/LSR expression: increased expression was observed in RBMVEC, while a dose-dependent decrease was seen in LN-229 glioma cells. All experiments were conducted in triplicate ( n = 3) across three independent biological replicates. Data are presented as mean ± SEM. Statistical comparisons between negative control (vehicle control) and Angubindin-1-treated groups were analyzed using one-way ANOVA followed by Dunnett’s post hoc test. ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Figure Legend Snippet: Cells were treated with Angubindin-1 at increasing concentrations (75–600 µg/mL) for 24 hours, followed by co-immunoprecipitation using 6 µg/mL anti-LSR antibody to evaluate Angulin-1/LSR interactions. (A, B) Representative immunoblots of 3X-FLAG-Angubindin-1 and Angulin-1/LSR in RBMVEC and LN-229 cells, respectively. Densitometric quantification of Angulin-1/LSR interactions, normalized to the HA-tagged negative control (NC) loading control. Angubindin-1 elicited a dose-dependent effect on Angulin-1/LSR expression: increased expression was observed in RBMVEC, while a dose-dependent decrease was seen in LN-229 glioma cells. All experiments were conducted in triplicate ( n = 3) across three independent biological replicates. Data are presented as mean ± SEM. Statistical comparisons between negative control (vehicle control) and Angubindin-1-treated groups were analyzed using one-way ANOVA followed by Dunnett’s post hoc test. ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Techniques Used: Immunoprecipitation, Western Blot, Negative Control, Control, Expressing



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    (A) UMAP plot showing the cellular distribution of Angulin-1/LSR expression across identified clusters. Expression values were log-transformed using the log1p() function to normalize data and account for zero values. Points are jittered and colored according to cell type annotation. Dot plot summarizing the proportion and average expression of Angulin-1/LSR across cell clusters. Dot size represents the percentage of cells expressing the gene, while color intensity reflects the mean expression level per cluster. (B) Representative immunoblots showing Angulin-1/LSR protein levels in <t>RBMVECs</t> over a 24-hour period under untreated conditions. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Data represent the mean ± SEM from three independent biological replicates ( n = 3). Statistical comparisons were made across all time points (1, 2, 4, 8, and 24 hours). * p < 0.05, ** p < 0.001, **** p < 0.00001 indicate significant differences relative to other time points.
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    Image Search Results


    (A) UMAP plot showing the cellular distribution of Angulin-1/LSR expression across identified clusters. Expression values were log-transformed using the log1p() function to normalize data and account for zero values. Points are jittered and colored according to cell type annotation. Dot plot summarizing the proportion and average expression of Angulin-1/LSR across cell clusters. Dot size represents the percentage of cells expressing the gene, while color intensity reflects the mean expression level per cluster. (B) Representative immunoblots showing Angulin-1/LSR protein levels in RBMVECs over a 24-hour period under untreated conditions. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Data represent the mean ± SEM from three independent biological replicates ( n = 3). Statistical comparisons were made across all time points (1, 2, 4, 8, and 24 hours). * p < 0.05, ** p < 0.001, **** p < 0.00001 indicate significant differences relative to other time points.

    Journal: bioRxiv

    Article Title: Angulin-1/LSR inhibition transiently disrupts the blood-tumor barrier to enhance doxil permeability and impair malignant glioma progression

    doi: 10.1101/2025.07.31.667901

    Figure Lengend Snippet: (A) UMAP plot showing the cellular distribution of Angulin-1/LSR expression across identified clusters. Expression values were log-transformed using the log1p() function to normalize data and account for zero values. Points are jittered and colored according to cell type annotation. Dot plot summarizing the proportion and average expression of Angulin-1/LSR across cell clusters. Dot size represents the percentage of cells expressing the gene, while color intensity reflects the mean expression level per cluster. (B) Representative immunoblots showing Angulin-1/LSR protein levels in RBMVECs over a 24-hour period under untreated conditions. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Quantification of Angulin-1/LSR expression by densitometry, normalized to the AIF, MEK1/2, or Histone H3 membrane loading control. Data represent the mean ± SEM from three independent biological replicates ( n = 3). Statistical comparisons were made across all time points (1, 2, 4, 8, and 24 hours). * p < 0.05, ** p < 0.001, **** p < 0.00001 indicate significant differences relative to other time points.

    Article Snippet: Rat brain microvascular endothelial cells (RBMVEC) were obtained from Cell Applications (Cell Applications, San Diego, CA, USA) and cultured following the manufacturer’s protocol.

    Techniques: Expressing, Transformation Assay, Western Blot, Membrane, Control

    Cells were treated with Angubindin-1 at increasing concentrations (75–600 µg/mL) for 24 hours, followed by co-immunoprecipitation using 6 µg/mL anti-LSR antibody to evaluate Angulin-1/LSR interactions. (A, B) Representative immunoblots of 3X-FLAG-Angubindin-1 and Angulin-1/LSR in RBMVEC and LN-229 cells, respectively. Densitometric quantification of Angulin-1/LSR interactions, normalized to the HA-tagged negative control (NC) loading control. Angubindin-1 elicited a dose-dependent effect on Angulin-1/LSR expression: increased expression was observed in RBMVEC, while a dose-dependent decrease was seen in LN-229 glioma cells. All experiments were conducted in triplicate ( n = 3) across three independent biological replicates. Data are presented as mean ± SEM. Statistical comparisons between negative control (vehicle control) and Angubindin-1-treated groups were analyzed using one-way ANOVA followed by Dunnett’s post hoc test. ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: bioRxiv

    Article Title: Angulin-1/LSR inhibition transiently disrupts the blood-tumor barrier to enhance doxil permeability and impair malignant glioma progression

    doi: 10.1101/2025.07.31.667901

    Figure Lengend Snippet: Cells were treated with Angubindin-1 at increasing concentrations (75–600 µg/mL) for 24 hours, followed by co-immunoprecipitation using 6 µg/mL anti-LSR antibody to evaluate Angulin-1/LSR interactions. (A, B) Representative immunoblots of 3X-FLAG-Angubindin-1 and Angulin-1/LSR in RBMVEC and LN-229 cells, respectively. Densitometric quantification of Angulin-1/LSR interactions, normalized to the HA-tagged negative control (NC) loading control. Angubindin-1 elicited a dose-dependent effect on Angulin-1/LSR expression: increased expression was observed in RBMVEC, while a dose-dependent decrease was seen in LN-229 glioma cells. All experiments were conducted in triplicate ( n = 3) across three independent biological replicates. Data are presented as mean ± SEM. Statistical comparisons between negative control (vehicle control) and Angubindin-1-treated groups were analyzed using one-way ANOVA followed by Dunnett’s post hoc test. ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Rat brain microvascular endothelial cells (RBMVEC) were obtained from Cell Applications (Cell Applications, San Diego, CA, USA) and cultured following the manufacturer’s protocol.

    Techniques: Immunoprecipitation, Western Blot, Negative Control, Control, Expressing

    Depiction of the sequence of experiments performed. ( a ) Phase contrast image of confluent Sprague-Dawley rat brain microvascular endothelial cells were seeded on ( b ) transwell inserts for measurement of Trans-Epithelial/Endothelial Electrical Resistance (TEER). The cells were also cultured on ( c ) chambered cell chambered cell culture slides, which were subsequently processed for immunofluorescence imaging following staining with specific primary antibodies against ZO-1 and claudin-5. See main text for details. Modified from Biorender

    Journal: Journal of Neurovirology

    Article Title: Effects of cigarette smoke and HIV-1 factors on blood-brain barrier integrity and permeability in an in vitro model

    doi: 10.1007/s13365-025-01295-2

    Figure Lengend Snippet: Depiction of the sequence of experiments performed. ( a ) Phase contrast image of confluent Sprague-Dawley rat brain microvascular endothelial cells were seeded on ( b ) transwell inserts for measurement of Trans-Epithelial/Endothelial Electrical Resistance (TEER). The cells were also cultured on ( c ) chambered cell chambered cell culture slides, which were subsequently processed for immunofluorescence imaging following staining with specific primary antibodies against ZO-1 and claudin-5. See main text for details. Modified from Biorender

    Article Snippet: Fig. 1 Depiction of the sequence of experiments performed. ( a ) Phase contrast image of confluent Sprague-Dawley rat brain microvascular endothelial cells were seeded on ( b ) transwell inserts for measurement of Trans-Epithelial/Endothelial Electrical Resistance (TEER).

    Techniques: Sequencing, Cell Culture, Immunofluorescence, Imaging, Staining, Modification