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Fisher Scientific red fluorescence dye
Red Fluorescence Dye, supplied by Fisher Scientific, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 86 stars, based on 1 article reviews
red fluorescence dye - by Bioz Stars, 2026-07
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Co-inhibition of PRMT5 and CHK1 increases DSB accumulation and induces apoptotic cell death in PDAC cells. L3.6 PL cells were treated with 200 nM EPZ015938 and 1.95–2.34 nM prexasertib, alone or in combination. (A,B) Neutral comet assay detecting DSBs in L3.6 PL cells after 48-h treatment. Representative fields are shown (×4 magnification; scale bar = 100 µm). Violin plots depict the distribution of tail moments across treatments. (n = 4; ***p ≤ 0.005, and ****p ≤ 0.001; log-transformed one-way ANOVA with Tukey’s post hoc ). (C,D) BrdU proliferation measuring DNA synthesis following 72-h drug exposure and 1-h BrdU pulse. ASH2L was used as a nuclear marker to detect the total number of cells. Representative images (×60 magnification; scale bar = 40 µm) and quantification of change in BrdU-positive nuclei are shown as mean ± SEM. (n = 4; ***p ≤ 0.005 and ****p ≤ 0.0001; Kruskal–Wallis H-test with Dunn’s post hoc ). (E) Live-cell cell death assays using IncuCyte SX5 imaging. Cells were treated for 96 h in the presence of Caspase 3/7 green, <t>Annexin</t> <t>V</t> red, and CytoTox NIR dyes, and fluorescence was quantified over time. Caspase 3/7, Annexin V, and total cell death levels after 96 h are shown as mean ± SEM. (n = 3; *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.005, and ****p ≤ 0.001; one-way ANOVA with Tukey’s post hoc ).
Annexin V Red Fluorescent Dye, supplied by Sartorius AG, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Shanghai Titan Scientific red fluorescent cell membrane dye did
Neutralization of merozoites. A Purification of infected erythrocytes using the Percoll separation solution, displaying infected (black arrow) and normal (red arrow) erythrocytes. B Confocal <t>fluorescent</t> images of merozoites (blue), PECm-Allicin@LM (red), and their colocalization (purple). Scale bar = 50 μm. C Representative scatter plots of Hoechst 33342/CFDA-SE for the invasion test of merozoites and normal erythrocytes after drug treatment. D Intrusion rate (the percentage of cells in the Q2 area in each group relative to that in the Q2 area in the Model group). Data are presented as mean ± SEM ( n = 3), * P < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Neutralization of merozoites. A Purification of infected erythrocytes using the Percoll separation solution, displaying infected (black arrow) and normal (red arrow) erythrocytes. B Confocal <t>fluorescent</t> images of merozoites (blue), PECm-Allicin@LM (red), and their colocalization (purple). Scale bar = 50 μm. C Representative scatter plots of Hoechst 33342/CFDA-SE for the invasion test of merozoites and normal erythrocytes after drug treatment. D Intrusion rate (the percentage of cells in the Q2 area in each group relative to that in the Q2 area in the Model group). Data are presented as mean ± SEM ( n = 3), * P < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fisher Scientific red fluorescence dye
Neutralization of merozoites. A Purification of infected erythrocytes using the Percoll separation solution, displaying infected (black arrow) and normal (red arrow) erythrocytes. B Confocal <t>fluorescent</t> images of merozoites (blue), PECm-Allicin@LM (red), and their colocalization (purple). Scale bar = 50 μm. C Representative scatter plots of Hoechst 33342/CFDA-SE for the invasion test of merozoites and normal erythrocytes after drug treatment. D Intrusion rate (the percentage of cells in the Q2 area in each group relative to that in the Q2 area in the Model group). Data are presented as mean ± SEM ( n = 3), * P < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Red Fluorescence Dye, supplied by Fisher Scientific, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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GFPT2 influenced foam cell formation, macrophage efferocytosis, and pro-inflammatory responses. ( A – B ) Knockdown efficiency of sh-GFPT2 constructs in RAW264.7 cells verified by qRT-PCR and WB. RAW264.7 cells were transfected with sh-NC or sh-GFPT2 and then treated with ox-LDL. ( C – D ) Oil-red-O staining (red) and quantification of lipid accumulation in RAW264.7 macrophages under different treatment conditions across groups. ( E ) Confocal images of Dil-marked ox-LDL (red) uptake in RAW264.7 macrophages across groups. ( F – G ) Efferocytosis assay showing phagocytosis of CFDA SE-labeled apoptotic thymocytes (green) by <t>CMTPX-labeled</t> RAW264.7 macrophages (red). ( H – J ) Flow cytometry and qRT-PCR analysis of scavenger receptor CD36 and efferocytosis mediator MerTK in RAW264.7 macrophages across experimental groups. ( K – L ) ELISA measurements of chemokine MCP-1 and inflammatory cytokine IL-8. ( M–O ) qRT-PCR analysis of chemokine (MCP-1) and inflammatory cytokine (IL-8 and TNF-α). RAW264.7 cells were subjected to the indicated genetic manipulations (sh-NC, sh-GFPT2, OE-NC, or OE-GFPT2) followed by ox-LDL treatment. ( P–Q ) Measurement of mitochondrial ROS level using MitoSOX Red probe. ( R – T ) ELISA quantification of MCP-1, TNF-α, and IL-8 levels. *** p < 0.001, ** p < 0.01, * p < 0.05 vs. sh-NC/ Ctrl/ ox-LDL + sh-NC/ ox-LDL + OE-NC
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GFPT2 influenced foam cell formation, macrophage efferocytosis, and pro-inflammatory responses. ( A – B ) Knockdown efficiency of sh-GFPT2 constructs in RAW264.7 cells verified by qRT-PCR and WB. RAW264.7 cells were transfected with sh-NC or sh-GFPT2 and then treated with ox-LDL. ( C – D ) Oil-red-O staining (red) and quantification of lipid accumulation in RAW264.7 macrophages under different treatment conditions across groups. ( E ) Confocal images of Dil-marked ox-LDL (red) uptake in RAW264.7 macrophages across groups. ( F – G ) Efferocytosis assay showing phagocytosis of CFDA SE-labeled apoptotic thymocytes (green) by <t>CMTPX-labeled</t> RAW264.7 macrophages (red). ( H – J ) Flow cytometry and qRT-PCR analysis of scavenger receptor CD36 and efferocytosis mediator MerTK in RAW264.7 macrophages across experimental groups. ( K – L ) ELISA measurements of chemokine MCP-1 and inflammatory cytokine IL-8. ( M–O ) qRT-PCR analysis of chemokine (MCP-1) and inflammatory cytokine (IL-8 and TNF-α). RAW264.7 cells were subjected to the indicated genetic manipulations (sh-NC, sh-GFPT2, OE-NC, or OE-GFPT2) followed by ox-LDL treatment. ( P–Q ) Measurement of mitochondrial ROS level using MitoSOX Red probe. ( R – T ) ELISA quantification of MCP-1, TNF-α, and IL-8 levels. *** p < 0.001, ** p < 0.01, * p < 0.05 vs. sh-NC/ Ctrl/ ox-LDL + sh-NC/ ox-LDL + OE-NC
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GFPT2 influenced foam cell formation, macrophage efferocytosis, and pro-inflammatory responses. ( A – B ) Knockdown efficiency of sh-GFPT2 constructs in RAW264.7 cells verified by qRT-PCR and WB. RAW264.7 cells were transfected with sh-NC or sh-GFPT2 and then treated with ox-LDL. ( C – D ) Oil-red-O staining (red) and quantification of lipid accumulation in RAW264.7 macrophages under different treatment conditions across groups. ( E ) Confocal images of Dil-marked ox-LDL (red) uptake in RAW264.7 macrophages across groups. ( F – G ) Efferocytosis assay showing phagocytosis of CFDA SE-labeled apoptotic thymocytes (green) by <t>CMTPX-labeled</t> RAW264.7 macrophages (red). ( H – J ) Flow cytometry and qRT-PCR analysis of scavenger receptor CD36 and efferocytosis mediator MerTK in RAW264.7 macrophages across experimental groups. ( K – L ) ELISA measurements of chemokine MCP-1 and inflammatory cytokine IL-8. ( M–O ) qRT-PCR analysis of chemokine (MCP-1) and inflammatory cytokine (IL-8 and TNF-α). RAW264.7 cells were subjected to the indicated genetic manipulations (sh-NC, sh-GFPT2, OE-NC, or OE-GFPT2) followed by ox-LDL treatment. ( P–Q ) Measurement of mitochondrial ROS level using MitoSOX Red probe. ( R – T ) ELISA quantification of MCP-1, TNF-α, and IL-8 levels. *** p < 0.001, ** p < 0.01, * p < 0.05 vs. sh-NC/ Ctrl/ ox-LDL + sh-NC/ ox-LDL + OE-NC
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GFPT2 influenced foam cell formation, macrophage efferocytosis, and pro-inflammatory responses. ( A – B ) Knockdown efficiency of sh-GFPT2 constructs in RAW264.7 cells verified by qRT-PCR and WB. RAW264.7 cells were transfected with sh-NC or sh-GFPT2 and then treated with ox-LDL. ( C – D ) Oil-red-O staining (red) and quantification of lipid accumulation in RAW264.7 macrophages under different treatment conditions across groups. ( E ) Confocal images of Dil-marked ox-LDL (red) uptake in RAW264.7 macrophages across groups. ( F – G ) Efferocytosis assay showing phagocytosis of CFDA SE-labeled apoptotic thymocytes (green) by <t>CMTPX-labeled</t> RAW264.7 macrophages (red). ( H – J ) Flow cytometry and qRT-PCR analysis of scavenger receptor CD36 and efferocytosis mediator MerTK in RAW264.7 macrophages across experimental groups. ( K – L ) ELISA measurements of chemokine MCP-1 and inflammatory cytokine IL-8. ( M–O ) qRT-PCR analysis of chemokine (MCP-1) and inflammatory cytokine (IL-8 and TNF-α). RAW264.7 cells were subjected to the indicated genetic manipulations (sh-NC, sh-GFPT2, OE-NC, or OE-GFPT2) followed by ox-LDL treatment. ( P–Q ) Measurement of mitochondrial ROS level using MitoSOX Red probe. ( R – T ) ELISA quantification of MCP-1, TNF-α, and IL-8 levels. *** p < 0.001, ** p < 0.01, * p < 0.05 vs. sh-NC/ Ctrl/ ox-LDL + sh-NC/ ox-LDL + OE-NC
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Image Search Results


Co-inhibition of PRMT5 and CHK1 increases DSB accumulation and induces apoptotic cell death in PDAC cells. L3.6 PL cells were treated with 200 nM EPZ015938 and 1.95–2.34 nM prexasertib, alone or in combination. (A,B) Neutral comet assay detecting DSBs in L3.6 PL cells after 48-h treatment. Representative fields are shown (×4 magnification; scale bar = 100 µm). Violin plots depict the distribution of tail moments across treatments. (n = 4; ***p ≤ 0.005, and ****p ≤ 0.001; log-transformed one-way ANOVA with Tukey’s post hoc ). (C,D) BrdU proliferation measuring DNA synthesis following 72-h drug exposure and 1-h BrdU pulse. ASH2L was used as a nuclear marker to detect the total number of cells. Representative images (×60 magnification; scale bar = 40 µm) and quantification of change in BrdU-positive nuclei are shown as mean ± SEM. (n = 4; ***p ≤ 0.005 and ****p ≤ 0.0001; Kruskal–Wallis H-test with Dunn’s post hoc ). (E) Live-cell cell death assays using IncuCyte SX5 imaging. Cells were treated for 96 h in the presence of Caspase 3/7 green, Annexin V red, and CytoTox NIR dyes, and fluorescence was quantified over time. Caspase 3/7, Annexin V, and total cell death levels after 96 h are shown as mean ± SEM. (n = 3; *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.005, and ****p ≤ 0.001; one-way ANOVA with Tukey’s post hoc ).

Journal: Frontiers in Cell and Developmental Biology

Article Title: PRMT5 inhibition triggers functional ATM deficiency and sensitizes pancreatic cancer to CHK1 blockade

doi: 10.3389/fcell.2026.1748541

Figure Lengend Snippet: Co-inhibition of PRMT5 and CHK1 increases DSB accumulation and induces apoptotic cell death in PDAC cells. L3.6 PL cells were treated with 200 nM EPZ015938 and 1.95–2.34 nM prexasertib, alone or in combination. (A,B) Neutral comet assay detecting DSBs in L3.6 PL cells after 48-h treatment. Representative fields are shown (×4 magnification; scale bar = 100 µm). Violin plots depict the distribution of tail moments across treatments. (n = 4; ***p ≤ 0.005, and ****p ≤ 0.001; log-transformed one-way ANOVA with Tukey’s post hoc ). (C,D) BrdU proliferation measuring DNA synthesis following 72-h drug exposure and 1-h BrdU pulse. ASH2L was used as a nuclear marker to detect the total number of cells. Representative images (×60 magnification; scale bar = 40 µm) and quantification of change in BrdU-positive nuclei are shown as mean ± SEM. (n = 4; ***p ≤ 0.005 and ****p ≤ 0.0001; Kruskal–Wallis H-test with Dunn’s post hoc ). (E) Live-cell cell death assays using IncuCyte SX5 imaging. Cells were treated for 96 h in the presence of Caspase 3/7 green, Annexin V red, and CytoTox NIR dyes, and fluorescence was quantified over time. Caspase 3/7, Annexin V, and total cell death levels after 96 h are shown as mean ± SEM. (n = 3; *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.005, and ****p ≤ 0.001; one-way ANOVA with Tukey’s post hoc ).

Article Snippet: For live-cell fluorescent apoptosis assays, Caspase 3/7 green fluorescent dye (Sartorius, 4440), Annexin V red fluorescent dye (Sartorius, 4641), and CytoTox dead cell NIR fluorescent dye (Sartorius, 3846) were prepared in culture media according to manufacturer’s instructions.

Techniques: Inhibition, Neutral Comet Assay, Transformation Assay, DNA Synthesis, Marker, Imaging, Fluorescence

Neutralization of merozoites. A Purification of infected erythrocytes using the Percoll separation solution, displaying infected (black arrow) and normal (red arrow) erythrocytes. B Confocal fluorescent images of merozoites (blue), PECm-Allicin@LM (red), and their colocalization (purple). Scale bar = 50 μm. C Representative scatter plots of Hoechst 33342/CFDA-SE for the invasion test of merozoites and normal erythrocytes after drug treatment. D Intrusion rate (the percentage of cells in the Q2 area in each group relative to that in the Q2 area in the Model group). Data are presented as mean ± SEM ( n = 3), * P < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: International Journal of Pharmaceutics: X

Article Title: Allicin-based biomimetic nanoparticles of the erythrocyte membrane for the delivery of lumefantrine to enhance its antimalarial effect

doi: 10.1016/j.ijpx.2026.100487

Figure Lengend Snippet: Neutralization of merozoites. A Purification of infected erythrocytes using the Percoll separation solution, displaying infected (black arrow) and normal (red arrow) erythrocytes. B Confocal fluorescent images of merozoites (blue), PECm-Allicin@LM (red), and their colocalization (purple). Scale bar = 50 μm. C Representative scatter plots of Hoechst 33342/CFDA-SE for the invasion test of merozoites and normal erythrocytes after drug treatment. D Intrusion rate (the percentage of cells in the Q2 area in each group relative to that in the Q2 area in the Model group). Data are presented as mean ± SEM ( n = 3), * P < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The red fluorescent cell membrane dye DiD was purchased from Shanghai Titan Scientific Co., Ltd. (China).

Techniques: Neutralization, Purification, Infection

GFPT2 influenced foam cell formation, macrophage efferocytosis, and pro-inflammatory responses. ( A – B ) Knockdown efficiency of sh-GFPT2 constructs in RAW264.7 cells verified by qRT-PCR and WB. RAW264.7 cells were transfected with sh-NC or sh-GFPT2 and then treated with ox-LDL. ( C – D ) Oil-red-O staining (red) and quantification of lipid accumulation in RAW264.7 macrophages under different treatment conditions across groups. ( E ) Confocal images of Dil-marked ox-LDL (red) uptake in RAW264.7 macrophages across groups. ( F – G ) Efferocytosis assay showing phagocytosis of CFDA SE-labeled apoptotic thymocytes (green) by CMTPX-labeled RAW264.7 macrophages (red). ( H – J ) Flow cytometry and qRT-PCR analysis of scavenger receptor CD36 and efferocytosis mediator MerTK in RAW264.7 macrophages across experimental groups. ( K – L ) ELISA measurements of chemokine MCP-1 and inflammatory cytokine IL-8. ( M–O ) qRT-PCR analysis of chemokine (MCP-1) and inflammatory cytokine (IL-8 and TNF-α). RAW264.7 cells were subjected to the indicated genetic manipulations (sh-NC, sh-GFPT2, OE-NC, or OE-GFPT2) followed by ox-LDL treatment. ( P–Q ) Measurement of mitochondrial ROS level using MitoSOX Red probe. ( R – T ) ELISA quantification of MCP-1, TNF-α, and IL-8 levels. *** p < 0.001, ** p < 0.01, * p < 0.05 vs. sh-NC/ Ctrl/ ox-LDL + sh-NC/ ox-LDL + OE-NC

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: GFPT2 promotes macrophage dysfunction in atherosclerosis via ACADL glycosylation-dependent suppression of ACADL and Arg1

doi: 10.1007/s00018-026-06203-3

Figure Lengend Snippet: GFPT2 influenced foam cell formation, macrophage efferocytosis, and pro-inflammatory responses. ( A – B ) Knockdown efficiency of sh-GFPT2 constructs in RAW264.7 cells verified by qRT-PCR and WB. RAW264.7 cells were transfected with sh-NC or sh-GFPT2 and then treated with ox-LDL. ( C – D ) Oil-red-O staining (red) and quantification of lipid accumulation in RAW264.7 macrophages under different treatment conditions across groups. ( E ) Confocal images of Dil-marked ox-LDL (red) uptake in RAW264.7 macrophages across groups. ( F – G ) Efferocytosis assay showing phagocytosis of CFDA SE-labeled apoptotic thymocytes (green) by CMTPX-labeled RAW264.7 macrophages (red). ( H – J ) Flow cytometry and qRT-PCR analysis of scavenger receptor CD36 and efferocytosis mediator MerTK in RAW264.7 macrophages across experimental groups. ( K – L ) ELISA measurements of chemokine MCP-1 and inflammatory cytokine IL-8. ( M–O ) qRT-PCR analysis of chemokine (MCP-1) and inflammatory cytokine (IL-8 and TNF-α). RAW264.7 cells were subjected to the indicated genetic manipulations (sh-NC, sh-GFPT2, OE-NC, or OE-GFPT2) followed by ox-LDL treatment. ( P–Q ) Measurement of mitochondrial ROS level using MitoSOX Red probe. ( R – T ) ELISA quantification of MCP-1, TNF-α, and IL-8 levels. *** p < 0.001, ** p < 0.01, * p < 0.05 vs. sh-NC/ Ctrl/ ox-LDL + sh-NC/ ox-LDL + OE-NC

Article Snippet: For phagocytosis assays, RAW264.7 or primary peritoneal macrophages were serum-starved for 4 h prior to labeling with 5 μM CMTPX red fluorescent dye (#40717ES50, Yeasen, Shanghai, China; 20 min).

Techniques: Knockdown, Construct, Quantitative RT-PCR, Transfection, Staining, Labeling, Flow Cytometry, Enzyme-linked Immunosorbent Assay