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3d surface reconstruction  (Oxford Instruments)


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    Oxford Instruments 3d surface reconstruction
    3d Surface Reconstruction, supplied by Oxford Instruments, used in various techniques. Bioz Stars score: 99/100, based on 44474 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/imaris+3d+surface+reconstruction/Imaris/pm42778718-93-3-9
    Average 99 stars, based on 44474 article reviews
    3d surface reconstruction - by Bioz Stars, 2026-10
    99/100 stars

    Images

    Related Articles

    Microscopy:

    Article Title: Characterization of the structure and control of the blood-nerve barrier identifies avenues for therapeutic delivery.
    Article Snippet: Junctional protein expression was quantified using a Nikon iSIM. .. Imaris 3D surface reconstruction and quantification Images acquired from the Leica SP8 STED microscope were opened on Imaris (V9.1.2 and V9.9.1). .. Imaris 3D surface reconstruction and quantification Images acquired from the Leica SP8 STED microscope were opened on Imaris (V9.1.2 and V9.9.1).

    Quantitation Assay:

    Article Title: Microgliopathy as a primary mediator of neuronal death in models of Friedreich's Ataxia.
    Article Snippet: .. Ratio is total lipids (590) 1082 /peroxidized lipids (510). e) Confocal images of γH2AX (left) with quantitation of γH2AX+ 1083 puncta/cell using IMARIS 3D surface reconstruction. ..

    Article Title: Microgliopathy as a primary mediator of neuronal death in models of Friedreich’s Ataxia
    Article Snippet: .. Ratio is total lipids (590 nm)/peroxidized lipids (510 nm). e Confocal images of γH2AX (left) with quantitation of γH2AX + puncta/cell using IMARIS 3D surface reconstruction. ..

    Marker:

    Article Title: A quantitative analysis of bestrophin 1 cellular localization in mouse cerebral cortex
    Article Snippet: .. BEST + cells were then processed to quantify the colocalization with the BEST1 signal using Imaris 3D surface reconstruction of BEST1 and cellular marker volume (Figure ). ..

    Article Title: A quantitative analysis of bestrophin 1 cellular localization in mouse cerebral cortex.
    Article Snippet: .. These analyses were carried out in cortical layers 2/3, which have the highest number of glutamatergic and GABAergic synapses.26 BEST+ cells were then processed to quantify the colocalization with the BEST1 signal using Imaris 3D surface reconstruction of BEST1 and cellular marker volume20 (Figure 2). ..



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    MtDNA release mediated by mPTP promotes ferroptosis. (A) Relative cytosolic mtDNA amounts <t>in</t> <t>RSL3‐treated</t> NCI‐H1299 WT and CypD‐KO cells. The relative ratios of ND1 mtDNA, 18S nuclear DNA (left panel), and actin (right panel) are shown. (B) Relative amounts of Ox‐mtDNA in cytosols of RSL3‐primed WT or CypD‐KO NCI‐H1299 cells. (C) Representative <t>3D</t> reconstruction images showing mitochondria (red, MitoTracker) and mitochondrial DNA (green, PicoGreen) in cells treated with DMSO or RSL3. Super‐resolution images were acquired using structured illumination microscopy (SIM). Mitochondria structures were labeled in red, and mtDNA signals were labeled in green (left panels). The mtDNA signals that were in contact with the mitochondrial surface were labeled in light pink, while those not in contact with the mitochondrial surface were in green (right panels, shown in the overlap images). Scale bar was 2 µm. (D) Quantification of cytosolic mtDNA (mtDNA in cytosol) in indicated groups. (E, F) ANT2 (E) and FEN1 (F) were knocked down by specific siRNA in NCI‐H1299 cells, followed by RSL3 treatment for 6 h to detect relative cytosolic mtDNA. (G) Western Blot analysis of FEN1 knockdown cells. (H) FEN1 was knocked down by specific siRNA in NCI‐H1299 cells, followed by indicated doses of erastin for 24 h to detect cell death. (I) NCI‐H1299 cells were transfected with siRNA specifically against FEN1 for 48 h, then subjected to 5 µ m erastin for 18 h. Lipid peroxidation was measured with C11‐BODIPY staining by flow cytometry. (J) Quantitative analysis of the fold change of lipid oxidation ratio in (I). The statistical significance between different groups (A, D, E, and F) was analyzed by One‐way ANOVA (Prism; GraphPad). Two‐Way ANOVA was used for (B and J).
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    MtDNA release mediated by mPTP promotes ferroptosis. (A) Relative cytosolic mtDNA amounts <t>in</t> <t>RSL3‐treated</t> NCI‐H1299 WT and CypD‐KO cells. The relative ratios of ND1 mtDNA, 18S nuclear DNA (left panel), and actin (right panel) are shown. (B) Relative amounts of Ox‐mtDNA in cytosols of RSL3‐primed WT or CypD‐KO NCI‐H1299 cells. (C) Representative <t>3D</t> reconstruction images showing mitochondria (red, MitoTracker) and mitochondrial DNA (green, PicoGreen) in cells treated with DMSO or RSL3. Super‐resolution images were acquired using structured illumination microscopy (SIM). Mitochondria structures were labeled in red, and mtDNA signals were labeled in green (left panels). The mtDNA signals that were in contact with the mitochondrial surface were labeled in light pink, while those not in contact with the mitochondrial surface were in green (right panels, shown in the overlap images). Scale bar was 2 µm. (D) Quantification of cytosolic mtDNA (mtDNA in cytosol) in indicated groups. (E, F) ANT2 (E) and FEN1 (F) were knocked down by specific siRNA in NCI‐H1299 cells, followed by RSL3 treatment for 6 h to detect relative cytosolic mtDNA. (G) Western Blot analysis of FEN1 knockdown cells. (H) FEN1 was knocked down by specific siRNA in NCI‐H1299 cells, followed by indicated doses of erastin for 24 h to detect cell death. (I) NCI‐H1299 cells were transfected with siRNA specifically against FEN1 for 48 h, then subjected to 5 µ m erastin for 18 h. Lipid peroxidation was measured with C11‐BODIPY staining by flow cytometry. (J) Quantitative analysis of the fold change of lipid oxidation ratio in (I). The statistical significance between different groups (A, D, E, and F) was analyzed by One‐way ANOVA (Prism; GraphPad). Two‐Way ANOVA was used for (B and J).
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    Oxford Instruments imaris 3d surface reconstruction
    MtDNA release mediated by mPTP promotes ferroptosis. (A) Relative cytosolic mtDNA amounts <t>in</t> <t>RSL3‐treated</t> NCI‐H1299 WT and CypD‐KO cells. The relative ratios of ND1 mtDNA, 18S nuclear DNA (left panel), and actin (right panel) are shown. (B) Relative amounts of Ox‐mtDNA in cytosols of RSL3‐primed WT or CypD‐KO NCI‐H1299 cells. (C) Representative <t>3D</t> reconstruction images showing mitochondria (red, MitoTracker) and mitochondrial DNA (green, PicoGreen) in cells treated with DMSO or RSL3. Super‐resolution images were acquired using structured illumination microscopy (SIM). Mitochondria structures were labeled in red, and mtDNA signals were labeled in green (left panels). The mtDNA signals that were in contact with the mitochondrial surface were labeled in light pink, while those not in contact with the mitochondrial surface were in green (right panels, shown in the overlap images). Scale bar was 2 µm. (D) Quantification of cytosolic mtDNA (mtDNA in cytosol) in indicated groups. (E, F) ANT2 (E) and FEN1 (F) were knocked down by specific siRNA in NCI‐H1299 cells, followed by RSL3 treatment for 6 h to detect relative cytosolic mtDNA. (G) Western Blot analysis of FEN1 knockdown cells. (H) FEN1 was knocked down by specific siRNA in NCI‐H1299 cells, followed by indicated doses of erastin for 24 h to detect cell death. (I) NCI‐H1299 cells were transfected with siRNA specifically against FEN1 for 48 h, then subjected to 5 µ m erastin for 18 h. Lipid peroxidation was measured with C11‐BODIPY staining by flow cytometry. (J) Quantitative analysis of the fold change of lipid oxidation ratio in (I). The statistical significance between different groups (A, D, E, and F) was analyzed by One‐way ANOVA (Prism; GraphPad). Two‐Way ANOVA was used for (B and J).
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    Image Search Results


    MtDNA release mediated by mPTP promotes ferroptosis. (A) Relative cytosolic mtDNA amounts in RSL3‐treated NCI‐H1299 WT and CypD‐KO cells. The relative ratios of ND1 mtDNA, 18S nuclear DNA (left panel), and actin (right panel) are shown. (B) Relative amounts of Ox‐mtDNA in cytosols of RSL3‐primed WT or CypD‐KO NCI‐H1299 cells. (C) Representative 3D reconstruction images showing mitochondria (red, MitoTracker) and mitochondrial DNA (green, PicoGreen) in cells treated with DMSO or RSL3. Super‐resolution images were acquired using structured illumination microscopy (SIM). Mitochondria structures were labeled in red, and mtDNA signals were labeled in green (left panels). The mtDNA signals that were in contact with the mitochondrial surface were labeled in light pink, while those not in contact with the mitochondrial surface were in green (right panels, shown in the overlap images). Scale bar was 2 µm. (D) Quantification of cytosolic mtDNA (mtDNA in cytosol) in indicated groups. (E, F) ANT2 (E) and FEN1 (F) were knocked down by specific siRNA in NCI‐H1299 cells, followed by RSL3 treatment for 6 h to detect relative cytosolic mtDNA. (G) Western Blot analysis of FEN1 knockdown cells. (H) FEN1 was knocked down by specific siRNA in NCI‐H1299 cells, followed by indicated doses of erastin for 24 h to detect cell death. (I) NCI‐H1299 cells were transfected with siRNA specifically against FEN1 for 48 h, then subjected to 5 µ m erastin for 18 h. Lipid peroxidation was measured with C11‐BODIPY staining by flow cytometry. (J) Quantitative analysis of the fold change of lipid oxidation ratio in (I). The statistical significance between different groups (A, D, E, and F) was analyzed by One‐way ANOVA (Prism; GraphPad). Two‐Way ANOVA was used for (B and J).

    Journal: Advanced Science

    Article Title: CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis

    doi: 10.1002/advs.202502239

    Figure Lengend Snippet: MtDNA release mediated by mPTP promotes ferroptosis. (A) Relative cytosolic mtDNA amounts in RSL3‐treated NCI‐H1299 WT and CypD‐KO cells. The relative ratios of ND1 mtDNA, 18S nuclear DNA (left panel), and actin (right panel) are shown. (B) Relative amounts of Ox‐mtDNA in cytosols of RSL3‐primed WT or CypD‐KO NCI‐H1299 cells. (C) Representative 3D reconstruction images showing mitochondria (red, MitoTracker) and mitochondrial DNA (green, PicoGreen) in cells treated with DMSO or RSL3. Super‐resolution images were acquired using structured illumination microscopy (SIM). Mitochondria structures were labeled in red, and mtDNA signals were labeled in green (left panels). The mtDNA signals that were in contact with the mitochondrial surface were labeled in light pink, while those not in contact with the mitochondrial surface were in green (right panels, shown in the overlap images). Scale bar was 2 µm. (D) Quantification of cytosolic mtDNA (mtDNA in cytosol) in indicated groups. (E, F) ANT2 (E) and FEN1 (F) were knocked down by specific siRNA in NCI‐H1299 cells, followed by RSL3 treatment for 6 h to detect relative cytosolic mtDNA. (G) Western Blot analysis of FEN1 knockdown cells. (H) FEN1 was knocked down by specific siRNA in NCI‐H1299 cells, followed by indicated doses of erastin for 24 h to detect cell death. (I) NCI‐H1299 cells were transfected with siRNA specifically against FEN1 for 48 h, then subjected to 5 µ m erastin for 18 h. Lipid peroxidation was measured with C11‐BODIPY staining by flow cytometry. (J) Quantitative analysis of the fold change of lipid oxidation ratio in (I). The statistical significance between different groups (A, D, E, and F) was analyzed by One‐way ANOVA (Prism; GraphPad). Two‐Way ANOVA was used for (B and J).

    Article Snippet: 3D surface reconstructions were generated with Imaris software, revealing that, upon RSL3 treatment, mtDNA signals were redistributed from mitochondria into the cytoplasm (Figure ).

    Techniques: Microscopy, Labeling, Western Blot, Knockdown, Transfection, Staining, Flow Cytometry