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counterstaining with dapi  (Beyotime)


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    Structured Review

    Beyotime counterstaining with dapi
    Counterstaining With Dapi, supplied by Beyotime, used in various techniques. Bioz Stars score: 99/100, based on 32584 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/counterstaining+with+dapi/DAPI/pm41981465-107-32-35
    Average 99 stars, based on 32584 article reviews
    counterstaining with dapi - by Bioz Stars, 2026-10
    99/100 stars

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    Related Articles

    Staining:

    Article Title: Chemo-metallo nanodrivers for spatiotemporally controlled in situ vaccination
    Article Snippet: .. Cell staining and viability assays were performed using a LIVE/DEAD kit (calcein AM/propidium iodide), an annexin V–FITC/PI apoptosis detection kit, MTT reagent, Alexa Fluor 488–conjugated secondary antibody, and DAPI (Beyotime Biotechnology, Shanghai, China). .. The JC-1 MitoMP Detection Kit was obtained from Dojindo Molecular Technologies Inc. (Kumamoto, Japan).

    Article Title: CD52+ cells are associated with faster short-term neutrophil recovery in mobilized hematopoietic stem cell transplant.
    Article Snippet: .. Cells were stained with CD52 primary antibody (Bioss, #bs-34117R) at 4 oC for overnight, and subsequently incubated for 2 hours at 37 oC with the Alexa Flur 488- conjugated anti-rabbit secondary antibody (Invitrogen, #A21206) and DAPI (Beyotime Biotechnology, #P0131) were used for depiction of the nuclei. .. Image acquisition was performed using either a confocal ultra-spectral microscope (Zeiss, LSM900).

    Article Title: DEAD-box RNA helicase 21 interacts with the nucleocapsid protein and inhibits porcine deltacoronavirus infection through upregulation of interferon responses.
    Article Snippet: The cells were then incubated with primary antibodies for 1 h, followed by washing with PBS and incubation with Alexa Fluor 488- and 594-conjugated secondary antibodies (Thermo Fisher Scientific) for 1 h at 37°C in the dark. .. Afterward, the cells were stained with DAPI (Cat. No. C1005, Beyotime), mounted with glycerin, and observed under a confocal microscope (Olympus). ..

    MTT Assay:

    Article Title: Chemo-metallo nanodrivers for spatiotemporally controlled in situ vaccination
    Article Snippet: .. Cell staining and viability assays were performed using a LIVE/DEAD kit (calcein AM/propidium iodide), an annexin V–FITC/PI apoptosis detection kit, MTT reagent, Alexa Fluor 488–conjugated secondary antibody, and DAPI (Beyotime Biotechnology, Shanghai, China). .. The JC-1 MitoMP Detection Kit was obtained from Dojindo Molecular Technologies Inc. (Kumamoto, Japan).

    Incubation:

    Article Title: CD52+ cells are associated with faster short-term neutrophil recovery in mobilized hematopoietic stem cell transplant.
    Article Snippet: .. Cells were stained with CD52 primary antibody (Bioss, #bs-34117R) at 4 oC for overnight, and subsequently incubated for 2 hours at 37 oC with the Alexa Flur 488- conjugated anti-rabbit secondary antibody (Invitrogen, #A21206) and DAPI (Beyotime Biotechnology, #P0131) were used for depiction of the nuclei. .. Image acquisition was performed using either a confocal ultra-spectral microscope (Zeiss, LSM900).

    Article Title: Glucocorticoid-induced METTL3 promotes SONFH by enhancing MEG3 m6A methylation and subsequent ABL2 upregulation.
    Article Snippet: Background: Steroid-induced osteonecrosis of the femoral head (SONFH) is a refractory orthopedic disease.. While N6-methyladenosine (m6A) modification is implicated in bone metabolism, its specific role and mechanism in SONFH pathogenesis require further elucidation.. Methods: Bioinformatics analysis identified key m6A-related genes.

    TUNEL Assay:

    Article Title: Glucocorticoid-induced METTL3 promotes SONFH by enhancing MEG3 m6A methylation and subsequent ABL2 upregulation.
    Article Snippet: Background: Steroid-induced osteonecrosis of the femoral head (SONFH) is a refractory orthopedic disease.. While N6-methyladenosine (m6A) modification is implicated in bone metabolism, its specific role and mechanism in SONFH pathogenesis require further elucidation.. Methods: Bioinformatics analysis identified key m6A-related genes.

    Confocal:

    Article Title: DEAD-box RNA helicase 21 interacts with the nucleocapsid protein and inhibits porcine deltacoronavirus infection through upregulation of interferon responses.
    Article Snippet: The cells were then incubated with primary antibodies for 1 h, followed by washing with PBS and incubation with Alexa Fluor 488- and 594-conjugated secondary antibodies (Thermo Fisher Scientific) for 1 h at 37°C in the dark. .. Afterward, the cells were stained with DAPI (Cat. No. C1005, Beyotime), mounted with glycerin, and observed under a confocal microscope (Olympus). ..

    Microscopy:

    Article Title: DEAD-box RNA helicase 21 interacts with the nucleocapsid protein and inhibits porcine deltacoronavirus infection through upregulation of interferon responses.
    Article Snippet: The cells were then incubated with primary antibodies for 1 h, followed by washing with PBS and incubation with Alexa Fluor 488- and 594-conjugated secondary antibodies (Thermo Fisher Scientific) for 1 h at 37°C in the dark. .. Afterward, the cells were stained with DAPI (Cat. No. C1005, Beyotime), mounted with glycerin, and observed under a confocal microscope (Olympus). ..



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    Age-dependent impairment in myelin phagocytosis and lipid droplet clearance in vitro and in vivo (Ai-ii) In vitro myelin phagocytosis assay with primary peritoneal macrophages from young (1-month-old) and aged (12-month-old) mice. (Ai) Representative immunofluorescence cytochemistry images (myelin basic protein (MBP, green), Iba1 (red), and <t>DAPI</t> (blue) of macrophages from young and aged mice incubated with myelin debris for 2, 4, 16, or 24 h. Scale bar: 20μm. (Aii) Quantification of macrophages containing phagocytosed myelin (% of MBP-positive Iba1- macrophages) at early (2–4 h) and late (16–24 h) time points. (Bi-iii) Delayed metabolism of phagocytosed myelin by aged macrophages. (Bi) Experimental scheme showing removal of myelin from culture medium after 16 h, and assessment of intracellular myelin metabolism by accumulation of Oil-Red-O (ORO) lipid droplets at 24 and 48 h. As an experimental control, representative images of MBP (green), Iba1 (red), and DAPI (blue) (Scale bar: 20μm) in young and aged macrophages showing comparable levels of phagocytosed MBP-immunoreactive myelin in young and aged macrophages at 16 h, and absence of MBP-immunoreactive myelin at 24 h and 48 h, (Bii) ORO and hematoxylin staining of young and aged macrophages showing ORO+ lipid droplet accumulation (red, arrowheads). (Biii) Quantification of ORO+ lipid–containing macrophages following myelin incubation and withdrawal, demonstrating impaired lipid clearance in aged compared to young macrophages. Scale bar: 3μm. (Ci-iii) In vivo accumulation of ORO+ lipid droplets in young (2-month-old) and old (24-month-old) mice during cuprizone-induced demyelination. (Ci) Representative ORO-stained coronal brain sections from young and aged mice after 4 (CPZ4), 6 (CPZ6) and 8 (CPZ8) weeks of continuous cuprizone feeding, and CPZ6 followed by 4 weeks of recovery after cuprizone withdrawal (CPZ6+4). Scale bar: 10μm. Quantification of ORO+ lipid droplets in, (Cii) the corpus callosum (CC) and (Ciii) dorsal fornix (DF) between young and aged mice at CPZ0, CPZ4, CPZ6, CPZ6+4 and CPZ8. (n = 5 mice/group; Mean ± SEM, p<0.05, *p<0.01, **p<0.001, ***p<0.0001).
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    (a) Actin (green) and <t>DAPI</t> (blue) stain of tendon derived cells seeded on tissue culture plate (TCP) monolayer controls, healthy mimetic models and diseased mimetic models ( n = 3). Scale bar: 100 μm. (b) Nuclear aspect ratio (NAR) was quantified using ImageJ by converting microscopic image to grayscale and measuring major and minor axes of individual nuclei. A higher major‐to‐minor ratio indicates increased cellular elongations. (c) Cells on the healthy model showed greater elongation than both the monolayer control and diseased model by day 3, while the diseased model also exceeded the monolayer control. By day 5, elongation remained elevated only in the healthy model relative to the diseased, and by day 7, the healthy group exhibited significantly greater elongation than all other models. No significant differences were observed by day 10. Significance was defined as p < 0.05 (*), p < 0.01 (**), p < 0.001 (***), p < 0.0001 (****), ns = not significant.
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    Beyotime counterstaining with dapi
    (a) Actin (green) and <t>DAPI</t> (blue) stain of tendon derived cells seeded on tissue culture plate (TCP) monolayer controls, healthy mimetic models and diseased mimetic models ( n = 3). Scale bar: 100 μm. (b) Nuclear aspect ratio (NAR) was quantified using ImageJ by converting microscopic image to grayscale and measuring major and minor axes of individual nuclei. A higher major‐to‐minor ratio indicates increased cellular elongations. (c) Cells on the healthy model showed greater elongation than both the monolayer control and diseased model by day 3, while the diseased model also exceeded the monolayer control. By day 5, elongation remained elevated only in the healthy model relative to the diseased, and by day 7, the healthy group exhibited significantly greater elongation than all other models. No significant differences were observed by day 10. Significance was defined as p < 0.05 (*), p < 0.01 (**), p < 0.001 (***), p < 0.0001 (****), ns = not significant.
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    (a) Actin (green) and <t>DAPI</t> (blue) stain of tendon derived cells seeded on tissue culture plate (TCP) monolayer controls, healthy mimetic models and diseased mimetic models ( n = 3). Scale bar: 100 μm. (b) Nuclear aspect ratio (NAR) was quantified using ImageJ by converting microscopic image to grayscale and measuring major and minor axes of individual nuclei. A higher major‐to‐minor ratio indicates increased cellular elongations. (c) Cells on the healthy model showed greater elongation than both the monolayer control and diseased model by day 3, while the diseased model also exceeded the monolayer control. By day 5, elongation remained elevated only in the healthy model relative to the diseased, and by day 7, the healthy group exhibited significantly greater elongation than all other models. No significant differences were observed by day 10. Significance was defined as p < 0.05 (*), p < 0.01 (**), p < 0.001 (***), p < 0.0001 (****), ns = not significant.
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    Image Search Results


    Age-dependent impairment in myelin phagocytosis and lipid droplet clearance in vitro and in vivo (Ai-ii) In vitro myelin phagocytosis assay with primary peritoneal macrophages from young (1-month-old) and aged (12-month-old) mice. (Ai) Representative immunofluorescence cytochemistry images (myelin basic protein (MBP, green), Iba1 (red), and DAPI (blue) of macrophages from young and aged mice incubated with myelin debris for 2, 4, 16, or 24 h. Scale bar: 20μm. (Aii) Quantification of macrophages containing phagocytosed myelin (% of MBP-positive Iba1- macrophages) at early (2–4 h) and late (16–24 h) time points. (Bi-iii) Delayed metabolism of phagocytosed myelin by aged macrophages. (Bi) Experimental scheme showing removal of myelin from culture medium after 16 h, and assessment of intracellular myelin metabolism by accumulation of Oil-Red-O (ORO) lipid droplets at 24 and 48 h. As an experimental control, representative images of MBP (green), Iba1 (red), and DAPI (blue) (Scale bar: 20μm) in young and aged macrophages showing comparable levels of phagocytosed MBP-immunoreactive myelin in young and aged macrophages at 16 h, and absence of MBP-immunoreactive myelin at 24 h and 48 h, (Bii) ORO and hematoxylin staining of young and aged macrophages showing ORO+ lipid droplet accumulation (red, arrowheads). (Biii) Quantification of ORO+ lipid–containing macrophages following myelin incubation and withdrawal, demonstrating impaired lipid clearance in aged compared to young macrophages. Scale bar: 3μm. (Ci-iii) In vivo accumulation of ORO+ lipid droplets in young (2-month-old) and old (24-month-old) mice during cuprizone-induced demyelination. (Ci) Representative ORO-stained coronal brain sections from young and aged mice after 4 (CPZ4), 6 (CPZ6) and 8 (CPZ8) weeks of continuous cuprizone feeding, and CPZ6 followed by 4 weeks of recovery after cuprizone withdrawal (CPZ6+4). Scale bar: 10μm. Quantification of ORO+ lipid droplets in, (Cii) the corpus callosum (CC) and (Ciii) dorsal fornix (DF) between young and aged mice at CPZ0, CPZ4, CPZ6, CPZ6+4 and CPZ8. (n = 5 mice/group; Mean ± SEM, p<0.05, *p<0.01, **p<0.001, ***p<0.0001).

    Journal: bioRxiv

    Article Title: Age-related loss of brain demyelinating and remyelinating potential is overcome by microglia renewal

    doi: 10.64898/2026.06.15.732390

    Figure Lengend Snippet: Age-dependent impairment in myelin phagocytosis and lipid droplet clearance in vitro and in vivo (Ai-ii) In vitro myelin phagocytosis assay with primary peritoneal macrophages from young (1-month-old) and aged (12-month-old) mice. (Ai) Representative immunofluorescence cytochemistry images (myelin basic protein (MBP, green), Iba1 (red), and DAPI (blue) of macrophages from young and aged mice incubated with myelin debris for 2, 4, 16, or 24 h. Scale bar: 20μm. (Aii) Quantification of macrophages containing phagocytosed myelin (% of MBP-positive Iba1- macrophages) at early (2–4 h) and late (16–24 h) time points. (Bi-iii) Delayed metabolism of phagocytosed myelin by aged macrophages. (Bi) Experimental scheme showing removal of myelin from culture medium after 16 h, and assessment of intracellular myelin metabolism by accumulation of Oil-Red-O (ORO) lipid droplets at 24 and 48 h. As an experimental control, representative images of MBP (green), Iba1 (red), and DAPI (blue) (Scale bar: 20μm) in young and aged macrophages showing comparable levels of phagocytosed MBP-immunoreactive myelin in young and aged macrophages at 16 h, and absence of MBP-immunoreactive myelin at 24 h and 48 h, (Bii) ORO and hematoxylin staining of young and aged macrophages showing ORO+ lipid droplet accumulation (red, arrowheads). (Biii) Quantification of ORO+ lipid–containing macrophages following myelin incubation and withdrawal, demonstrating impaired lipid clearance in aged compared to young macrophages. Scale bar: 3μm. (Ci-iii) In vivo accumulation of ORO+ lipid droplets in young (2-month-old) and old (24-month-old) mice during cuprizone-induced demyelination. (Ci) Representative ORO-stained coronal brain sections from young and aged mice after 4 (CPZ4), 6 (CPZ6) and 8 (CPZ8) weeks of continuous cuprizone feeding, and CPZ6 followed by 4 weeks of recovery after cuprizone withdrawal (CPZ6+4). Scale bar: 10μm. Quantification of ORO+ lipid droplets in, (Cii) the corpus callosum (CC) and (Ciii) dorsal fornix (DF) between young and aged mice at CPZ0, CPZ4, CPZ6, CPZ6+4 and CPZ8. (n = 5 mice/group; Mean ± SEM, p<0.05, *p<0.01, **p<0.001, ***p<0.0001).

    Article Snippet: This was followed by a three-probe amplification steps (AMP1-AMP3), fluorophore conjugation (Opal 570) and DAPI counterstaining (ACD, CA).

    Techniques: In Vitro, In Vivo, Phagocytosis Assay, Immunofluorescence, Incubation, Control, Staining

    (a) Actin (green) and DAPI (blue) stain of tendon derived cells seeded on tissue culture plate (TCP) monolayer controls, healthy mimetic models and diseased mimetic models ( n = 3). Scale bar: 100 μm. (b) Nuclear aspect ratio (NAR) was quantified using ImageJ by converting microscopic image to grayscale and measuring major and minor axes of individual nuclei. A higher major‐to‐minor ratio indicates increased cellular elongations. (c) Cells on the healthy model showed greater elongation than both the monolayer control and diseased model by day 3, while the diseased model also exceeded the monolayer control. By day 5, elongation remained elevated only in the healthy model relative to the diseased, and by day 7, the healthy group exhibited significantly greater elongation than all other models. No significant differences were observed by day 10. Significance was defined as p < 0.05 (*), p < 0.01 (**), p < 0.001 (***), p < 0.0001 (****), ns = not significant.

    Journal: Bioengineering & Translational Medicine

    Article Title: Extracellular matrix microarchitecture modulates cellular behavior and extracellular vesicle phenotypes in biomimetic tendon models

    doi: 10.1002/btm2.70134

    Figure Lengend Snippet: (a) Actin (green) and DAPI (blue) stain of tendon derived cells seeded on tissue culture plate (TCP) monolayer controls, healthy mimetic models and diseased mimetic models ( n = 3). Scale bar: 100 μm. (b) Nuclear aspect ratio (NAR) was quantified using ImageJ by converting microscopic image to grayscale and measuring major and minor axes of individual nuclei. A higher major‐to‐minor ratio indicates increased cellular elongations. (c) Cells on the healthy model showed greater elongation than both the monolayer control and diseased model by day 3, while the diseased model also exceeded the monolayer control. By day 5, elongation remained elevated only in the healthy model relative to the diseased, and by day 7, the healthy group exhibited significantly greater elongation than all other models. No significant differences were observed by day 10. Significance was defined as p < 0.05 (*), p < 0.01 (**), p < 0.001 (***), p < 0.0001 (****), ns = not significant.

    Article Snippet: Cellular morphology was assessed via actin staining (Invitrogen, Cat. No. A12379) and nuclear counterstaining with DAPI (Fisher Scientific, Cat. No. H‐1200‐10) ( n = 3).

    Techniques: Staining, Derivative Assay, Control