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mouse anti human p selectin  (R&D Systems)


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    Structured Review

    R&D Systems mouse anti human p selectin
    Prothrombotic effects of STEC-HUS serum are dependent on WPB exocytosis from endothelial <t>cells.</t> <t>P-selectin</t> (A) and vWF (B) expression on unstimulated HMEC-1 exposed to serum from patients with acute STEC-HUS (n = 5 for P-selectin experiments; n = 6 for vWF experiments), in the presence or in the absence of different complement inhibitors (sCR1, 150 µg/mL; factor B inhibitor, iptacopan,10 µM; eculizumab 100 µg/mL) or to a pool of control sera (normal human serum, NHS), run in parallel. Results are shown as pixel 2 /high-power field (HPF) of stained surface area. Data are mean ± SD. Circles represent single patients’ data. The addition of either sCR1, or iptacopan or eculizumab to patient’s serum significantly decrease both P-selectin and vWF expression induced by patient’s serum alone. *P < 0.05 vs STEC-HUS serum alone (ANOVA, followed by Tukey’s multiple comparisons test for data of P-selectin expression and by Holm-Šídák’s multiple comparisons test for data of vWF expression). (C) Endothelial surface area covered by thrombi on ADP-activated HMEC-1 exposed to serum from STEC-HUS patients collected during the acute phase of the disease and then perfused with whole blood. Before the experiments, HMEC-1 were left for 16 hours with medium added or not with the RalA inhibitor BQU57 (10 µM). Data are expressed as mean ± SD of percentages of serum-induced thrombus formation in respect to a pool of control sera (normal human serum, NHS), run in parallel in each experiment and set as 100% (n = 3 independent experiments). Circles indicate single patients’ data. Horizontal dashed lines indicate upper and lower limits of the normal range . *P < 0.05 (paired Student’s t test). (D) Representative confocal microscopy images (original magnification X200) of experiments of thrombus formation (green staining) relative to <xref ref-type=Figure 6C . Scale bar: 100 µm. " width="250" height="auto" />
    Mouse Anti Human P Selectin, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+human+p+selectin/Human+E-Selectin%2FP-Selectin+(CD62E%2FP)+APC-conjugated+Antibody/pmc13021478-120-97-100
    Average 94 stars, based on 5 article reviews
    mouse anti human p selectin - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "Molecular determinants of STEC-HUS: from complement activation to microvascular thrombosis"

    Article Title: Molecular determinants of STEC-HUS: from complement activation to microvascular thrombosis

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2026.1749811

    Prothrombotic effects of STEC-HUS serum are dependent on WPB exocytosis from endothelial cells. P-selectin (A) and vWF (B) expression on unstimulated HMEC-1 exposed to serum from patients with acute STEC-HUS (n = 5 for P-selectin experiments; n = 6 for vWF experiments), in the presence or in the absence of different complement inhibitors (sCR1, 150 µg/mL; factor B inhibitor, iptacopan,10 µM; eculizumab 100 µg/mL) or to a pool of control sera (normal human serum, NHS), run in parallel. Results are shown as pixel 2 /high-power field (HPF) of stained surface area. Data are mean ± SD. Circles represent single patients’ data. The addition of either sCR1, or iptacopan or eculizumab to patient’s serum significantly decrease both P-selectin and vWF expression induced by patient’s serum alone. *P < 0.05 vs STEC-HUS serum alone (ANOVA, followed by Tukey’s multiple comparisons test for data of P-selectin expression and by Holm-Šídák’s multiple comparisons test for data of vWF expression). (C) Endothelial surface area covered by thrombi on ADP-activated HMEC-1 exposed to serum from STEC-HUS patients collected during the acute phase of the disease and then perfused with whole blood. Before the experiments, HMEC-1 were left for 16 hours with medium added or not with the RalA inhibitor BQU57 (10 µM). Data are expressed as mean ± SD of percentages of serum-induced thrombus formation in respect to a pool of control sera (normal human serum, NHS), run in parallel in each experiment and set as 100% (n = 3 independent experiments). Circles indicate single patients’ data. Horizontal dashed lines indicate upper and lower limits of the normal range . *P < 0.05 (paired Student’s t test). (D) Representative confocal microscopy images (original magnification X200) of experiments of thrombus formation (green staining) relative to <xref ref-type=Figure 6C . Scale bar: 100 µm. " title="... serum are dependent on WPB exocytosis from endothelial cells. P-selectin (A) and vWF (B) expression on unstimulated ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Prothrombotic effects of STEC-HUS serum are dependent on WPB exocytosis from endothelial cells. P-selectin (A) and vWF (B) expression on unstimulated HMEC-1 exposed to serum from patients with acute STEC-HUS (n = 5 for P-selectin experiments; n = 6 for vWF experiments), in the presence or in the absence of different complement inhibitors (sCR1, 150 µg/mL; factor B inhibitor, iptacopan,10 µM; eculizumab 100 µg/mL) or to a pool of control sera (normal human serum, NHS), run in parallel. Results are shown as pixel 2 /high-power field (HPF) of stained surface area. Data are mean ± SD. Circles represent single patients’ data. The addition of either sCR1, or iptacopan or eculizumab to patient’s serum significantly decrease both P-selectin and vWF expression induced by patient’s serum alone. *P < 0.05 vs STEC-HUS serum alone (ANOVA, followed by Tukey’s multiple comparisons test for data of P-selectin expression and by Holm-Šídák’s multiple comparisons test for data of vWF expression). (C) Endothelial surface area covered by thrombi on ADP-activated HMEC-1 exposed to serum from STEC-HUS patients collected during the acute phase of the disease and then perfused with whole blood. Before the experiments, HMEC-1 were left for 16 hours with medium added or not with the RalA inhibitor BQU57 (10 µM). Data are expressed as mean ± SD of percentages of serum-induced thrombus formation in respect to a pool of control sera (normal human serum, NHS), run in parallel in each experiment and set as 100% (n = 3 independent experiments). Circles indicate single patients’ data. Horizontal dashed lines indicate upper and lower limits of the normal range . *P < 0.05 (paired Student’s t test). (D) Representative confocal microscopy images (original magnification X200) of experiments of thrombus formation (green staining) relative to Figure 6C . Scale bar: 100 µm.

    Techniques Used: Expressing, Control, Staining, Confocal Microscopy

    Related Articles

    Staining:

    Article Title: Alternative pathway activation of complement by Shiga toxin promotes exuberant C3a formation that triggers microvascular thrombosis.
    Article Snippet: .. HMEC-1 at the end of the perfusions were fixed in 3% paraformaldehyde and stained with the following Abs: FITC-conjugated anti-human C3c (11.3 mg/ml; Dako), anti-human C5b-9 (27.6 mg/ml; Calbiochem) followed by FITC-conjugated secondary Ab (13.6 mg/ml; Jackson Immunoresearch Laboratories), anti-human P-selectin (20 mg/ml, R&D Systems) followed by Cy3-conjugated secondary Ab (13.6 mg/ml; Jackson Immunoresearch Laboratories), and anti-human TM (1:50; R&D Systems) followed by Cy3conjugated secondary Ab. ..

    Immunofluorescence:

    Article Title: Ultraviolet B light-exposed human platelets mediate acute lung injury in a two-event mouse model of transfusion.
    Article Snippet: BACKGROUND: Ultraviolet B (UVB) light has been used alone on platelet (PLT) transfusion products to prevent alloimmunization or with chemical sensitizers to reduce pathogens.. Such processing can damage PLTs and potentiate their storage lesion.. Transfusion-related acute lung injury (ALI) has occurred in patients whose underlying condition led to an inflamed endothelium and who were transfused with products that contained either HLA or HNA antibodies or biologic modifiers such as lipids or antigens from stored cells.

    Avidin-Biotin Assay:

    Article Title: Ultraviolet B light-exposed human platelets mediate acute lung injury in a two-event mouse model of transfusion.
    Article Snippet: BACKGROUND: Ultraviolet B (UVB) light has been used alone on platelet (PLT) transfusion products to prevent alloimmunization or with chemical sensitizers to reduce pathogens.. Such processing can damage PLTs and potentiate their storage lesion.. Transfusion-related acute lung injury (ALI) has occurred in patients whose underlying condition led to an inflamed endothelium and who were transfused with products that contained either HLA or HNA antibodies or biologic modifiers such as lipids or antigens from stored cells.

    Incubation:

    Article Title: Synergistic action of beta-glucan and platelets on interleukin-8 production by human peripheral blood leukocytes.
    Article Snippet: Color development was stopped with 1 N phosphoric acid and the optimal density at 450 nm was measured using a microplate reader (Corona Electric Co., Ltd.). .. Flow Cytometric Analysis of P-Selectin Expressed on Human Platelets Stimulated with SPG Platelets were prepared as described above and incubated with SPG at 37 °C for 2 h. After incubation, platelets were washed three times with PBS, and fluorescein isothiocyanate (FITC)-conjugated anti-human P-selectin (R & D System) was added. .. Expression of P-selectin on human platelets was measured using FACS Calibur (Becton-Dickinson).

    Article Title: CD63 is an essential cofactor to leukocyte recruitment by endothelial P-selectin.
    Article Snippet: 1Medical Research Council (MRC) Laboratory for Molecular Cell Biology, 2MRC Cell Biology Unit, and 3Department of Cell and Developmental Biology, University College London (UCL), London, United Kingdom; 4Department of Cardiovascular Science, Faculty of Medicine, Dentistry and Health, The University of Sheffield, Sheffield, United Kingdom; and 5Biochemisches Institut, Christian-Albrechts-Universität Kiel, Kiel, Germany

    Article Title: Hypertonic Saline Solution Reduces Microcirculatory Dysfunction and Inflammation in a Rat Model of Brain Death
    Article Snippet: .. The sections were incubated for 1 h at 37oC with the following primary antibodies: anti-human P-selectin (1:40; CD62P; R&D Systems, Minneapolis, MN, USA), anti-eNOS (1:100; Abcam, Cambridge, MA, USA), or anti-endothelin-1 (1:100; Abcam). ..

    other:

    Article Title: Early Platelet Dysfunction in Sepsis: An ICU Pilot Study
    Article Snippet: Measurement of soluble P-selectin and soluble CD40 ligand in serum was per-formed using the anti-human P-selectin (R&D System, Inc., Minneapolis, MN, USA) and human CD40L/TNFSF5 (R&D System, Inc., Minneapolis, MN, USA) immunoassay kits ac-cording to the manufacturer’s instructions.

    Blocking Assay:

    Article Title: CD63 is an essential cofactor to leukocyte recruitment by endothelial P-selectin.
    Article Snippet: 1Medical Research Council (MRC) Laboratory for Molecular Cell Biology, 2MRC Cell Biology Unit, and 3Department of Cell and Developmental Biology, University College London (UCL), London, United Kingdom; 4Department of Cardiovascular Science, Faculty of Medicine, Dentistry and Health, The University of Sheffield, Sheffield, United Kingdom; and 5Biochemisches Institut, Christian-Albrechts-Universität Kiel, Kiel, Germany

    Concentration Assay:

    Article Title: CD63 is an essential cofactor to leukocyte recruitment by endothelial P-selectin.
    Article Snippet: 1Medical Research Council (MRC) Laboratory for Molecular Cell Biology, 2MRC Cell Biology Unit, and 3Department of Cell and Developmental Biology, University College London (UCL), London, United Kingdom; 4Department of Cardiovascular Science, Faculty of Medicine, Dentistry and Health, The University of Sheffield, Sheffield, United Kingdom; and 5Biochemisches Institut, Christian-Albrechts-Universität Kiel, Kiel, Germany



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    Prothrombotic effects of STEC-HUS serum are dependent on WPB exocytosis from endothelial <t>cells.</t> <t>P-selectin</t> (A) and vWF (B) expression on unstimulated HMEC-1 exposed to serum from patients with acute STEC-HUS (n = 5 for P-selectin experiments; n = 6 for vWF experiments), in the presence or in the absence of different complement inhibitors (sCR1, 150 µg/mL; factor B inhibitor, iptacopan,10 µM; eculizumab 100 µg/mL) or to a pool of control sera (normal human serum, NHS), run in parallel. Results are shown as pixel 2 /high-power field (HPF) of stained surface area. Data are mean ± SD. Circles represent single patients’ data. The addition of either sCR1, or iptacopan or eculizumab to patient’s serum significantly decrease both P-selectin and vWF expression induced by patient’s serum alone. *P < 0.05 vs STEC-HUS serum alone (ANOVA, followed by Tukey’s multiple comparisons test for data of P-selectin expression and by Holm-Šídák’s multiple comparisons test for data of vWF expression). (C) Endothelial surface area covered by thrombi on ADP-activated HMEC-1 exposed to serum from STEC-HUS patients collected during the acute phase of the disease and then perfused with whole blood. Before the experiments, HMEC-1 were left for 16 hours with medium added or not with the RalA inhibitor BQU57 (10 µM). Data are expressed as mean ± SD of percentages of serum-induced thrombus formation in respect to a pool of control sera (normal human serum, NHS), run in parallel in each experiment and set as 100% (n = 3 independent experiments). Circles indicate single patients’ data. Horizontal dashed lines indicate upper and lower limits of the normal range . *P < 0.05 (paired Student’s t test). (D) Representative confocal microscopy images (original magnification X200) of experiments of thrombus formation (green staining) relative to <xref ref-type=Figure 6C . Scale bar: 100 µm. " width="250" height="auto" />
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    Image Search Results


    Prothrombotic effects of STEC-HUS serum are dependent on WPB exocytosis from endothelial cells. P-selectin (A) and vWF (B) expression on unstimulated HMEC-1 exposed to serum from patients with acute STEC-HUS (n = 5 for P-selectin experiments; n = 6 for vWF experiments), in the presence or in the absence of different complement inhibitors (sCR1, 150 µg/mL; factor B inhibitor, iptacopan,10 µM; eculizumab 100 µg/mL) or to a pool of control sera (normal human serum, NHS), run in parallel. Results are shown as pixel 2 /high-power field (HPF) of stained surface area. Data are mean ± SD. Circles represent single patients’ data. The addition of either sCR1, or iptacopan or eculizumab to patient’s serum significantly decrease both P-selectin and vWF expression induced by patient’s serum alone. *P < 0.05 vs STEC-HUS serum alone (ANOVA, followed by Tukey’s multiple comparisons test for data of P-selectin expression and by Holm-Šídák’s multiple comparisons test for data of vWF expression). (C) Endothelial surface area covered by thrombi on ADP-activated HMEC-1 exposed to serum from STEC-HUS patients collected during the acute phase of the disease and then perfused with whole blood. Before the experiments, HMEC-1 were left for 16 hours with medium added or not with the RalA inhibitor BQU57 (10 µM). Data are expressed as mean ± SD of percentages of serum-induced thrombus formation in respect to a pool of control sera (normal human serum, NHS), run in parallel in each experiment and set as 100% (n = 3 independent experiments). Circles indicate single patients’ data. Horizontal dashed lines indicate upper and lower limits of the normal range . *P < 0.05 (paired Student’s t test). (D) Representative confocal microscopy images (original magnification X200) of experiments of thrombus formation (green staining) relative to <xref ref-type=Figure 6C . Scale bar: 100 µm. " width="100%" height="100%">

    Journal: Frontiers in Immunology

    Article Title: Molecular determinants of STEC-HUS: from complement activation to microvascular thrombosis

    doi: 10.3389/fimmu.2026.1749811

    Figure Lengend Snippet: Prothrombotic effects of STEC-HUS serum are dependent on WPB exocytosis from endothelial cells. P-selectin (A) and vWF (B) expression on unstimulated HMEC-1 exposed to serum from patients with acute STEC-HUS (n = 5 for P-selectin experiments; n = 6 for vWF experiments), in the presence or in the absence of different complement inhibitors (sCR1, 150 µg/mL; factor B inhibitor, iptacopan,10 µM; eculizumab 100 µg/mL) or to a pool of control sera (normal human serum, NHS), run in parallel. Results are shown as pixel 2 /high-power field (HPF) of stained surface area. Data are mean ± SD. Circles represent single patients’ data. The addition of either sCR1, or iptacopan or eculizumab to patient’s serum significantly decrease both P-selectin and vWF expression induced by patient’s serum alone. *P < 0.05 vs STEC-HUS serum alone (ANOVA, followed by Tukey’s multiple comparisons test for data of P-selectin expression and by Holm-Šídák’s multiple comparisons test for data of vWF expression). (C) Endothelial surface area covered by thrombi on ADP-activated HMEC-1 exposed to serum from STEC-HUS patients collected during the acute phase of the disease and then perfused with whole blood. Before the experiments, HMEC-1 were left for 16 hours with medium added or not with the RalA inhibitor BQU57 (10 µM). Data are expressed as mean ± SD of percentages of serum-induced thrombus formation in respect to a pool of control sera (normal human serum, NHS), run in parallel in each experiment and set as 100% (n = 3 independent experiments). Circles indicate single patients’ data. Horizontal dashed lines indicate upper and lower limits of the normal range . *P < 0.05 (paired Student’s t test). (D) Representative confocal microscopy images (original magnification X200) of experiments of thrombus formation (green staining) relative to Figure 6C . Scale bar: 100 µm.

    Article Snippet: Cells were washed again and treated with the following specific antibodies: FITC-conjugated rabbit anti-human C3c-complement (Dako, that recognizes C3c, part of C3 and C3b, 1:300 final dilution in Dapi 1 μg/mL); or rabbit anti-human complement C5b-9 complex (Calbiochem, 1:200 final dilution in PBS1X) followed by FITC-conjugated secondary antibody (Jackson ImmunoResearch Laboratories, 1:50 final dilution in 1 μg/mL Dapi); or goat anti-human C4 (Abcam, 1:100 final dilution in PBS1X) followed by Cy3-conjugated secondary antibody (Jackson ImmunoResearch Laboratories, 1:200 final dilution in Dapi 1 μg/mL); or FITC-conjugated anti-human IgG (Sigma Aldrich, 1:32 final dilution in 1 μg/mL Dapi); or mouse anti-human P-selectin (R&D System, 20 μg/mL final concentration in PBS1X), followed by Cy3-conjugated secondary antibody (Jackson ImmunoResearch Laboratories, 1:60 final dilution in 1 μg/mL Dapi); or rabbit anti-human vWF (Dako, 10 μg/mL final concentration in PBS1X), followed by Cy3-conjugated secondary antibody (Jackson ImmunoResearch Laboratories, 1:50 final dilution in 1 μg/mL Dapi).

    Techniques: Expressing, Control, Staining, Confocal Microscopy

    ( A – C ): P-selectin expression on unstimulated ( A ), ADP-stimulated ( B ), and TRAP-stimulated ( C ) platelets of patients with sepsis and septic shock compared to healthy controls at T0, T1, and T2. Results are expressed as a % of P-selectin-positive platelets, identified as CD42 B-positive events. ( A ) T0 vs. CTRL: p bonf = 0.0006; T1 vs. CTRL: p bonf = 0.0006; T2 vs. CTRL: p bonf = 0.12; ( B ) T0 vs. CTRL: p bonf = 0.026; T1 vs. CTRL: p bonf = 0.056; T2 vs. CTRL: p bonf = 0.037; ( C ) n.s.= not significant. Bonferroni correction was applied for all pairwise comparisons; p -values (p bonf ) are reported. Sample size: n = 10 at T0 and T2, n = 9 at T1. * p < 0.05, ** p < 0.005. ns = no significance.

    Journal: Pathogens

    Article Title: Early Platelet Dysfunction in Sepsis: An ICU Pilot Study

    doi: 10.3390/pathogens15020196

    Figure Lengend Snippet: ( A – C ): P-selectin expression on unstimulated ( A ), ADP-stimulated ( B ), and TRAP-stimulated ( C ) platelets of patients with sepsis and septic shock compared to healthy controls at T0, T1, and T2. Results are expressed as a % of P-selectin-positive platelets, identified as CD42 B-positive events. ( A ) T0 vs. CTRL: p bonf = 0.0006; T1 vs. CTRL: p bonf = 0.0006; T2 vs. CTRL: p bonf = 0.12; ( B ) T0 vs. CTRL: p bonf = 0.026; T1 vs. CTRL: p bonf = 0.056; T2 vs. CTRL: p bonf = 0.037; ( C ) n.s.= not significant. Bonferroni correction was applied for all pairwise comparisons; p -values (p bonf ) are reported. Sample size: n = 10 at T0 and T2, n = 9 at T1. * p < 0.05, ** p < 0.005. ns = no significance.

    Article Snippet: Measurement of soluble P-selectin and soluble CD40 ligand in serum was per-formed using the anti-human P-selectin (R&D System, Inc., Minneapolis, MN, USA) and human CD40L/TNFSF5 (R&D System, Inc., Minneapolis, MN, USA) immunoassay kits ac-cording to the manufacturer’s instructions.

    Techniques: Expressing

    ( A , B ): Patient soluble CD40L ( A ) and soluble P-selectin ( B ) plasma levels at times T0, T1, and T2 compared to controls. ( A ) T0 vs. CTRL: p bonf = 0.05; T1 vs. CTRL: p bonf = 0.04; T2 vs. CTRL: p bonf = 0.018. Bonferroni correction was applied for all pairwise comparisons; p -values (p bonf ) are re-ported. Sample size: n = 10 at T0 and T2, n = 9 at T1. * p < 0.05. ns = no significance.

    Journal: Pathogens

    Article Title: Early Platelet Dysfunction in Sepsis: An ICU Pilot Study

    doi: 10.3390/pathogens15020196

    Figure Lengend Snippet: ( A , B ): Patient soluble CD40L ( A ) and soluble P-selectin ( B ) plasma levels at times T0, T1, and T2 compared to controls. ( A ) T0 vs. CTRL: p bonf = 0.05; T1 vs. CTRL: p bonf = 0.04; T2 vs. CTRL: p bonf = 0.018. Bonferroni correction was applied for all pairwise comparisons; p -values (p bonf ) are re-ported. Sample size: n = 10 at T0 and T2, n = 9 at T1. * p < 0.05. ns = no significance.

    Article Snippet: Measurement of soluble P-selectin and soluble CD40 ligand in serum was per-formed using the anti-human P-selectin (R&D System, Inc., Minneapolis, MN, USA) and human CD40L/TNFSF5 (R&D System, Inc., Minneapolis, MN, USA) immunoassay kits ac-cording to the manufacturer’s instructions.

    Techniques: Clinical Proteomics

    EV surface marker changes after RIC treatment: The expression of the EV-markers CD62 and MCP-1 is plotted showing the Log 2 fold changes compared to the baseline sample of each patient. The p-value is shown for both the significant changes within RIC group (red) and compared with the miRNA expression changes over time in Sham group (grey). ( a ) CD62 shows an upregulation in RIC treated patients compared to Sham. ( b ) MCP-1 showed no significant changes in between the different timepoints

    Journal: BMC Neuroscience

    Article Title: Exploring extracellular vesicle surface markers and microRNA regulation following remote ischemic conditioning in patients with stroke; a randomized-controlled pilot study

    doi: 10.1186/s12868-025-00993-1

    Figure Lengend Snippet: EV surface marker changes after RIC treatment: The expression of the EV-markers CD62 and MCP-1 is plotted showing the Log 2 fold changes compared to the baseline sample of each patient. The p-value is shown for both the significant changes within RIC group (red) and compared with the miRNA expression changes over time in Sham group (grey). ( a ) CD62 shows an upregulation in RIC treated patients compared to Sham. ( b ) MCP-1 showed no significant changes in between the different timepoints

    Article Snippet: CD62 E/P , R & D Systems , BBA1 , BBIG-E(13D5).

    Techniques: Marker, Expressing

    Correlation analysis of significant miRNA measurements (hsa-miR-19b-3p, hsa-miR-30d-5p, hsa-miR-374a-5p, hsa-miR-20a/20b-5p, hsa-miR-24-3p) and CD62/P-selectin. The histograms on the diagonal show the distribution of each variable. The lower triangular panels depict scatter plots with fitted lines, illustrating the linear relationships between pairs of variables. The upper triangular panels display the correlation coefficients, with significance levels indicated by asterisks (* p < 0.05, ** p < 0.01, *** p < 0.001)

    Journal: BMC Neuroscience

    Article Title: Exploring extracellular vesicle surface markers and microRNA regulation following remote ischemic conditioning in patients with stroke; a randomized-controlled pilot study

    doi: 10.1186/s12868-025-00993-1

    Figure Lengend Snippet: Correlation analysis of significant miRNA measurements (hsa-miR-19b-3p, hsa-miR-30d-5p, hsa-miR-374a-5p, hsa-miR-20a/20b-5p, hsa-miR-24-3p) and CD62/P-selectin. The histograms on the diagonal show the distribution of each variable. The lower triangular panels depict scatter plots with fitted lines, illustrating the linear relationships between pairs of variables. The upper triangular panels display the correlation coefficients, with significance levels indicated by asterisks (* p < 0.05, ** p < 0.01, *** p < 0.001)

    Article Snippet: CD62 E/P , R & D Systems , BBA1 , BBIG-E(13D5).

    Techniques:

    LFM A13 inhibits P-selectin exposure. Platelets were pretreated with 10 µM of TQ and or LFMA13 for 10 minutes then were co-cultured with MDA-MB-231 cells for 24 hours. Proteins were analyzed by SDS/PAGE and subsequent Western blotting with a specific P-selectin antibody (CTB201) as described in Materials and Methods section. Histograms represent protein expression level and are presented as a percentage of control (untreated resting cells) and expressed as mean ± SEM of 6 separate experiments. *** P < .001 compared to control (non-treated platelets).

    Journal: Integrative Cancer Therapies

    Article Title: Thymoquinone’s Role in Suppressing Platelet-Mediated Migration and Epithelial to Mesenchymal Transition in MDA-MB231 Cells: Mechanistic Involvement of Btk Signaling

    doi: 10.1177/15347354251378060

    Figure Lengend Snippet: LFM A13 inhibits P-selectin exposure. Platelets were pretreated with 10 µM of TQ and or LFMA13 for 10 minutes then were co-cultured with MDA-MB-231 cells for 24 hours. Proteins were analyzed by SDS/PAGE and subsequent Western blotting with a specific P-selectin antibody (CTB201) as described in Materials and Methods section. Histograms represent protein expression level and are presented as a percentage of control (untreated resting cells) and expressed as mean ± SEM of 6 separate experiments. *** P < .001 compared to control (non-treated platelets).

    Article Snippet: Greening et al, then the membrane fraction was electrophoretically separated in SDS-PAGE 10%, transferred, and revealed for membrane P-selectin using anti-human P-selectin antibody (Santa Cruz Biotechnology Cat #sc-8419, RRID:AB_627151).

    Techniques: Cell Culture, SDS Page, Western Blot, Expressing, Control