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fitc anti mouse cd41 antibody  (Elabscience Biotechnology)


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    Elabscience Biotechnology fitc anti mouse cd41 antibody
    Fitc Anti Mouse Cd41 Antibody, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fitc+anti+mouse+cd41+antibody/10__1016_slash_j__cej__2026__175417-180-5-12?v=Elabscience+Biotechnology
    Average 94 stars, based on 3 article reviews
    fitc anti mouse cd41 antibody - by Bioz Stars, 2026-08
    94/100 stars

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    Fisher Scientific rat anti mouse cd41 fitc conjugated antibodies
    ( A ) Whole blood cells from freshly drawn citrated human blood were precipitated and washed to deplete fibrinogen, and DPAL was added to cell suspensions at 6 x 10 11 particles/mL, followed by stimulation with thrombin (Thr) and/or convulxin (CVX) in the presence of 2 mM CaCl 2 as indicated. Platelets were identified in a flow cytometer by forward and side scatter, and counterstaining with AlexaFluor ® 488- or AlexaFluor ® 647-conjugated <t>anti-CD41</t> antibodies. (i) Liposome binding was assessed by Cy3 fluorescencein CD41+ platelets, and are shown as percent Cy3-positive (DPAL+) platelets ± S.E.M. (ii) PS exposure was assessed with Annexin V-FITC (AXV) in separate tubes containing aliquots from the treated samples from (i), shown as mean fluorescence intensities (MFI) ± S.E.M. p < 0.01 for all samples compared to unstimulated. ( B ) (i) Platelets as in (A) were stimulated with thrombin with or without 10 μL AXV added as indicated, and DPAL binding is shown as fold change from unstimulated ± S.E.M. (ii) AXV MFI from the samples in (i) are shown ± S.E.M. ( C ) Washed platelets from WT or Ano6 KO mice were suspended in Tyrode’s buffer in the presence of DPAL at 6 x 10 11 particles/mL, stimulated with 0.1 U/mL thrombin as indicated, and assessed for (i) liposome binding as in (B), using FITC-conjugated anti-Cd41 antibodies to identify murine platelets, or (ii) AXV MFI, shown ± S.E.M. ( D ) Human platelets treated as in (A) were counterstained with FITC-conjugated PAC-1; FITC-PAC-1 MFI are shown ± S.E.M. n.s., no significant differences between groups. (E) Aggregation of human platelets suspended in buffer at 2x10 8 platelets/mL, following stimulation with thrombin at the indicated concentrations was measured in the absence (control, CTL) or presence of DPAL added as in (D). Representative of 4 independent experiments. ( F ) Dilute prothrombin time in pooled normal plasma with added rabbit brain tissue thromboplastin, in the presence or absence of DPAL as indicated, and shown as mean ± S.E.M.
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    Bio-Rad mwreg30 mca2245f cd80 fitc
    ( A ) Whole blood cells from freshly drawn citrated human blood were precipitated and washed to deplete fibrinogen, and DPAL was added to cell suspensions at 6 x 10 11 particles/mL, followed by stimulation with thrombin (Thr) and/or convulxin (CVX) in the presence of 2 mM CaCl 2 as indicated. Platelets were identified in a flow cytometer by forward and side scatter, and counterstaining with AlexaFluor ® 488- or AlexaFluor ® 647-conjugated <t>anti-CD41</t> antibodies. (i) Liposome binding was assessed by Cy3 fluorescencein CD41+ platelets, and are shown as percent Cy3-positive (DPAL+) platelets ± S.E.M. (ii) PS exposure was assessed with Annexin V-FITC (AXV) in separate tubes containing aliquots from the treated samples from (i), shown as mean fluorescence intensities (MFI) ± S.E.M. p < 0.01 for all samples compared to unstimulated. ( B ) (i) Platelets as in (A) were stimulated with thrombin with or without 10 μL AXV added as indicated, and DPAL binding is shown as fold change from unstimulated ± S.E.M. (ii) AXV MFI from the samples in (i) are shown ± S.E.M. ( C ) Washed platelets from WT or Ano6 KO mice were suspended in Tyrode’s buffer in the presence of DPAL at 6 x 10 11 particles/mL, stimulated with 0.1 U/mL thrombin as indicated, and assessed for (i) liposome binding as in (B), using FITC-conjugated anti-Cd41 antibodies to identify murine platelets, or (ii) AXV MFI, shown ± S.E.M. ( D ) Human platelets treated as in (A) were counterstained with FITC-conjugated PAC-1; FITC-PAC-1 MFI are shown ± S.E.M. n.s., no significant differences between groups. (E) Aggregation of human platelets suspended in buffer at 2x10 8 platelets/mL, following stimulation with thrombin at the indicated concentrations was measured in the absence (control, CTL) or presence of DPAL added as in (D). Representative of 4 independent experiments. ( F ) Dilute prothrombin time in pooled normal plasma with added rabbit brain tissue thromboplastin, in the presence or absence of DPAL as indicated, and shown as mean ± S.E.M.
    Mwreg30 Mca2245f Cd80 Fitc, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ( A ) Whole blood cells from freshly drawn citrated human blood were precipitated and washed to deplete fibrinogen, and DPAL was added to cell suspensions at 6 x 10 11 particles/mL, followed by stimulation with thrombin (Thr) and/or convulxin (CVX) in the presence of 2 mM CaCl 2 as indicated. Platelets were identified in a flow cytometer by forward and side scatter, and counterstaining with AlexaFluor ® 488- or AlexaFluor ® 647-conjugated <t>anti-CD41</t> antibodies. (i) Liposome binding was assessed by Cy3 fluorescencein CD41+ platelets, and are shown as percent Cy3-positive (DPAL+) platelets ± S.E.M. (ii) PS exposure was assessed with Annexin V-FITC (AXV) in separate tubes containing aliquots from the treated samples from (i), shown as mean fluorescence intensities (MFI) ± S.E.M. p < 0.01 for all samples compared to unstimulated. ( B ) (i) Platelets as in (A) were stimulated with thrombin with or without 10 μL AXV added as indicated, and DPAL binding is shown as fold change from unstimulated ± S.E.M. (ii) AXV MFI from the samples in (i) are shown ± S.E.M. ( C ) Washed platelets from WT or Ano6 KO mice were suspended in Tyrode’s buffer in the presence of DPAL at 6 x 10 11 particles/mL, stimulated with 0.1 U/mL thrombin as indicated, and assessed for (i) liposome binding as in (B), using FITC-conjugated anti-Cd41 antibodies to identify murine platelets, or (ii) AXV MFI, shown ± S.E.M. ( D ) Human platelets treated as in (A) were counterstained with FITC-conjugated PAC-1; FITC-PAC-1 MFI are shown ± S.E.M. n.s., no significant differences between groups. (E) Aggregation of human platelets suspended in buffer at 2x10 8 platelets/mL, following stimulation with thrombin at the indicated concentrations was measured in the absence (control, CTL) or presence of DPAL added as in (D). Representative of 4 independent experiments. ( F ) Dilute prothrombin time in pooled normal plasma with added rabbit brain tissue thromboplastin, in the presence or absence of DPAL as indicated, and shown as mean ± S.E.M.
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    Elabscience Biotechnology fitc cd41
    Miltefosine promotes MK differentiation and maturation in K562 and HEL cells (A) Flow cytometric analyses of proportion of <t>CD41</t> + CD42b + cells in K562 and HEL cells treated with miltefosine (10, 20, and 40 μM) or PMA (0.8 nM) for 5 days. (B) Flow cytometric analyses of proportion of CD41 + CD61 + cells of each group. (C) DNA ploidy of each group. (D) Quantification of the percentage of CD41 + CD42b + cells in K562. n = 3. (E) Quantification of the percentage of CD41 + CD42b + cells in HEL. n = 3. (F) Quantification of the percentage of CD41 + CD61 + cells in K562. n = 3. (G) Quantification of the percentage of CD41 + CD61 + cells in HEL. n = 3. (H) Quantification of the DNA ploidy in K562. n = 3. (I) Quantification of the DNA ploidy in HEL. n = 3. Statistical significance in (D–I) was calculated using a one-way analysis of variance (ANOVA) test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, vs. control group. Error bars represent mean ± SD.
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    Image Search Results


    ( A ) Whole blood cells from freshly drawn citrated human blood were precipitated and washed to deplete fibrinogen, and DPAL was added to cell suspensions at 6 x 10 11 particles/mL, followed by stimulation with thrombin (Thr) and/or convulxin (CVX) in the presence of 2 mM CaCl 2 as indicated. Platelets were identified in a flow cytometer by forward and side scatter, and counterstaining with AlexaFluor ® 488- or AlexaFluor ® 647-conjugated anti-CD41 antibodies. (i) Liposome binding was assessed by Cy3 fluorescencein CD41+ platelets, and are shown as percent Cy3-positive (DPAL+) platelets ± S.E.M. (ii) PS exposure was assessed with Annexin V-FITC (AXV) in separate tubes containing aliquots from the treated samples from (i), shown as mean fluorescence intensities (MFI) ± S.E.M. p < 0.01 for all samples compared to unstimulated. ( B ) (i) Platelets as in (A) were stimulated with thrombin with or without 10 μL AXV added as indicated, and DPAL binding is shown as fold change from unstimulated ± S.E.M. (ii) AXV MFI from the samples in (i) are shown ± S.E.M. ( C ) Washed platelets from WT or Ano6 KO mice were suspended in Tyrode’s buffer in the presence of DPAL at 6 x 10 11 particles/mL, stimulated with 0.1 U/mL thrombin as indicated, and assessed for (i) liposome binding as in (B), using FITC-conjugated anti-Cd41 antibodies to identify murine platelets, or (ii) AXV MFI, shown ± S.E.M. ( D ) Human platelets treated as in (A) were counterstained with FITC-conjugated PAC-1; FITC-PAC-1 MFI are shown ± S.E.M. n.s., no significant differences between groups. (E) Aggregation of human platelets suspended in buffer at 2x10 8 platelets/mL, following stimulation with thrombin at the indicated concentrations was measured in the absence (control, CTL) or presence of DPAL added as in (D). Representative of 4 independent experiments. ( F ) Dilute prothrombin time in pooled normal plasma with added rabbit brain tissue thromboplastin, in the presence or absence of DPAL as indicated, and shown as mean ± S.E.M.

    Journal: Journal of thrombosis and haemostasis : JTH

    Article Title: Phosphatidylserine-blocking nanoparticles inhibit thrombosis without increased bleeding in mice

    doi: 10.1016/j.jtha.2024.10.007

    Figure Lengend Snippet: ( A ) Whole blood cells from freshly drawn citrated human blood were precipitated and washed to deplete fibrinogen, and DPAL was added to cell suspensions at 6 x 10 11 particles/mL, followed by stimulation with thrombin (Thr) and/or convulxin (CVX) in the presence of 2 mM CaCl 2 as indicated. Platelets were identified in a flow cytometer by forward and side scatter, and counterstaining with AlexaFluor ® 488- or AlexaFluor ® 647-conjugated anti-CD41 antibodies. (i) Liposome binding was assessed by Cy3 fluorescencein CD41+ platelets, and are shown as percent Cy3-positive (DPAL+) platelets ± S.E.M. (ii) PS exposure was assessed with Annexin V-FITC (AXV) in separate tubes containing aliquots from the treated samples from (i), shown as mean fluorescence intensities (MFI) ± S.E.M. p < 0.01 for all samples compared to unstimulated. ( B ) (i) Platelets as in (A) were stimulated with thrombin with or without 10 μL AXV added as indicated, and DPAL binding is shown as fold change from unstimulated ± S.E.M. (ii) AXV MFI from the samples in (i) are shown ± S.E.M. ( C ) Washed platelets from WT or Ano6 KO mice were suspended in Tyrode’s buffer in the presence of DPAL at 6 x 10 11 particles/mL, stimulated with 0.1 U/mL thrombin as indicated, and assessed for (i) liposome binding as in (B), using FITC-conjugated anti-Cd41 antibodies to identify murine platelets, or (ii) AXV MFI, shown ± S.E.M. ( D ) Human platelets treated as in (A) were counterstained with FITC-conjugated PAC-1; FITC-PAC-1 MFI are shown ± S.E.M. n.s., no significant differences between groups. (E) Aggregation of human platelets suspended in buffer at 2x10 8 platelets/mL, following stimulation with thrombin at the indicated concentrations was measured in the absence (control, CTL) or presence of DPAL added as in (D). Representative of 4 independent experiments. ( F ) Dilute prothrombin time in pooled normal plasma with added rabbit brain tissue thromboplastin, in the presence or absence of DPAL as indicated, and shown as mean ± S.E.M.

    Article Snippet: Rat-anti-mouse Cd41 FITC-conjugated antibodies and dry chemicals were from Fisher Scientific (Pittsburgh, PA, USA).

    Techniques: Binding Assay, Flow Cytometry, Fluorescence, Control, Clinical Proteomics

    Journal: iScience

    Article Title: Targeting CCR5 with miltefosine as a therapeutic strategy for thrombocytopenia

    doi: 10.1016/j.isci.2025.112379

    Figure Lengend Snippet:

    Article Snippet: FITC Anti-Mouse CD41 Antibody , Elabscience , Cat# E-AB-F1183C.

    Techniques: Recombinant, Lysis, CCK-8 Assay, Staining, Membrane, Western Blot, Software

    Miltefosine promotes MK differentiation and maturation in K562 and HEL cells (A) Flow cytometric analyses of proportion of CD41 + CD42b + cells in K562 and HEL cells treated with miltefosine (10, 20, and 40 μM) or PMA (0.8 nM) for 5 days. (B) Flow cytometric analyses of proportion of CD41 + CD61 + cells of each group. (C) DNA ploidy of each group. (D) Quantification of the percentage of CD41 + CD42b + cells in K562. n = 3. (E) Quantification of the percentage of CD41 + CD42b + cells in HEL. n = 3. (F) Quantification of the percentage of CD41 + CD61 + cells in K562. n = 3. (G) Quantification of the percentage of CD41 + CD61 + cells in HEL. n = 3. (H) Quantification of the DNA ploidy in K562. n = 3. (I) Quantification of the DNA ploidy in HEL. n = 3. Statistical significance in (D–I) was calculated using a one-way analysis of variance (ANOVA) test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, vs. control group. Error bars represent mean ± SD.

    Journal: iScience

    Article Title: Targeting CCR5 with miltefosine as a therapeutic strategy for thrombocytopenia

    doi: 10.1016/j.isci.2025.112379

    Figure Lengend Snippet: Miltefosine promotes MK differentiation and maturation in K562 and HEL cells (A) Flow cytometric analyses of proportion of CD41 + CD42b + cells in K562 and HEL cells treated with miltefosine (10, 20, and 40 μM) or PMA (0.8 nM) for 5 days. (B) Flow cytometric analyses of proportion of CD41 + CD61 + cells of each group. (C) DNA ploidy of each group. (D) Quantification of the percentage of CD41 + CD42b + cells in K562. n = 3. (E) Quantification of the percentage of CD41 + CD42b + cells in HEL. n = 3. (F) Quantification of the percentage of CD41 + CD61 + cells in K562. n = 3. (G) Quantification of the percentage of CD41 + CD61 + cells in HEL. n = 3. (H) Quantification of the DNA ploidy in K562. n = 3. (I) Quantification of the DNA ploidy in HEL. n = 3. Statistical significance in (D–I) was calculated using a one-way analysis of variance (ANOVA) test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, vs. control group. Error bars represent mean ± SD.

    Article Snippet: Samples were incubated with the following antibodies: PE-CD117 (c-Kit, Thermo Fisher Scientific, Waltham, MA, USA), FITC-CD41 (Elabscience, Wuhan, China), APC-CD42d (Thermo Fisher Scientific, Waltham, MA, USA), APC-61 (Thermo Fisher Scientific, Waltham, MA, USA), or PI (Beyotime, Shanghai, China).

    Techniques: Control

    Miltefosine stimulates hematopoietic recovery in RIT mice (A) H&E staining of BM from control, model, TPO (3000 U/kg), and miltefosine (10, 20, and 40 mg/kg)-treated groups on day 10. Scale bar: 50 μM. (B) Quantification of MK counts in BM across groups. n = 3. (C) Immunohistochemical analysis for CD41 in BM. Scale bar, 50 μM. (D) Quantification of CD41-positive MKs in BM. n = 3. (E) H&E staining of spleen in each group. Scale bar, 50 μM. (F) Quantification of MK counts in spleen across groups. n = 3. (G and H) Flow cytometric analysis and quantification of c-Kit + CD41 + cells in BM. n = 3. (I and J) Flow cytometric analysis and quantification of CD41 + CD42d + cells in BM. n = 3. (K and L) Flow cytometric analysis and quantification of CD41 + CD42d + cells in spleen. n = 3. (M and N) Flow cytometric analysis and quantification of CD41 + CD61 + cells in BM. n = 3. (O and P) Flow cytometric analysis and quantification of CD41 + CD61 + cells in spleen. n = 3. (Q and R) Flow cytometric analysis and quantification of DNA ploidy in BM. n = 3. (S and T) Flow cytometric analysis and quantification of DNA ploidy in spleen. n = 3. Statistical significance in (B,D,F,H,J,L,N,P,R,T) was calculated using a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, vs. model group. Error bars represent mean ± SD.

    Journal: iScience

    Article Title: Targeting CCR5 with miltefosine as a therapeutic strategy for thrombocytopenia

    doi: 10.1016/j.isci.2025.112379

    Figure Lengend Snippet: Miltefosine stimulates hematopoietic recovery in RIT mice (A) H&E staining of BM from control, model, TPO (3000 U/kg), and miltefosine (10, 20, and 40 mg/kg)-treated groups on day 10. Scale bar: 50 μM. (B) Quantification of MK counts in BM across groups. n = 3. (C) Immunohistochemical analysis for CD41 in BM. Scale bar, 50 μM. (D) Quantification of CD41-positive MKs in BM. n = 3. (E) H&E staining of spleen in each group. Scale bar, 50 μM. (F) Quantification of MK counts in spleen across groups. n = 3. (G and H) Flow cytometric analysis and quantification of c-Kit + CD41 + cells in BM. n = 3. (I and J) Flow cytometric analysis and quantification of CD41 + CD42d + cells in BM. n = 3. (K and L) Flow cytometric analysis and quantification of CD41 + CD42d + cells in spleen. n = 3. (M and N) Flow cytometric analysis and quantification of CD41 + CD61 + cells in BM. n = 3. (O and P) Flow cytometric analysis and quantification of CD41 + CD61 + cells in spleen. n = 3. (Q and R) Flow cytometric analysis and quantification of DNA ploidy in BM. n = 3. (S and T) Flow cytometric analysis and quantification of DNA ploidy in spleen. n = 3. Statistical significance in (B,D,F,H,J,L,N,P,R,T) was calculated using a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, vs. model group. Error bars represent mean ± SD.

    Article Snippet: Samples were incubated with the following antibodies: PE-CD117 (c-Kit, Thermo Fisher Scientific, Waltham, MA, USA), FITC-CD41 (Elabscience, Wuhan, China), APC-CD42d (Thermo Fisher Scientific, Waltham, MA, USA), APC-61 (Thermo Fisher Scientific, Waltham, MA, USA), or PI (Beyotime, Shanghai, China).

    Techniques: Staining, Control, Immunohistochemical staining

    CCR5, MAPK, and JAK2/STAT3 signaling pathways mediate miltefosine-induced MK differentiation (A) Representative bright-field images of K562 cells treated with miltefosine (40 μM), maraviroc (1 μM), SCH772984 (1 μM), or ruxolitinib (0.5 μM) for 5 days. Scale bar: 100 μM. (B) Giemsa staining of K562 cells after indicated treatments. Scale bar: 20 μM. (C and D) Flow cytometric analysis and quantification of CD41 + CD42b + cells after indicated treatments. n = 3. Statistical significance was calculated using a one-way ANOVA test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, vs. control group. ### p < 0.001, vs. miltefosine-treated group. Error bars represent mean ± SD.

    Journal: iScience

    Article Title: Targeting CCR5 with miltefosine as a therapeutic strategy for thrombocytopenia

    doi: 10.1016/j.isci.2025.112379

    Figure Lengend Snippet: CCR5, MAPK, and JAK2/STAT3 signaling pathways mediate miltefosine-induced MK differentiation (A) Representative bright-field images of K562 cells treated with miltefosine (40 μM), maraviroc (1 μM), SCH772984 (1 μM), or ruxolitinib (0.5 μM) for 5 days. Scale bar: 100 μM. (B) Giemsa staining of K562 cells after indicated treatments. Scale bar: 20 μM. (C and D) Flow cytometric analysis and quantification of CD41 + CD42b + cells after indicated treatments. n = 3. Statistical significance was calculated using a one-way ANOVA test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, vs. control group. ### p < 0.001, vs. miltefosine-treated group. Error bars represent mean ± SD.

    Article Snippet: Samples were incubated with the following antibodies: PE-CD117 (c-Kit, Thermo Fisher Scientific, Waltham, MA, USA), FITC-CD41 (Elabscience, Wuhan, China), APC-CD42d (Thermo Fisher Scientific, Waltham, MA, USA), APC-61 (Thermo Fisher Scientific, Waltham, MA, USA), or PI (Beyotime, Shanghai, China).

    Techniques: Protein-Protein interactions, Staining, Control

    Journal: iScience

    Article Title: Targeting CCR5 with miltefosine as a therapeutic strategy for thrombocytopenia

    doi: 10.1016/j.isci.2025.112379

    Figure Lengend Snippet:

    Article Snippet: Samples were incubated with the following antibodies: PE-CD117 (c-Kit, Thermo Fisher Scientific, Waltham, MA, USA), FITC-CD41 (Elabscience, Wuhan, China), APC-CD42d (Thermo Fisher Scientific, Waltham, MA, USA), APC-61 (Thermo Fisher Scientific, Waltham, MA, USA), or PI (Beyotime, Shanghai, China).

    Techniques: Recombinant, Lysis, CCK-8 Assay, Staining, Membrane, Western Blot, Software