dapi d9542 Search Results


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Vector Laboratories vectashield antifade mounting medium with dapi
(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with <t>DAPI,</t> Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.
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(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with <t>DAPI,</t> Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.
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(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with <t>DAPI,</t> Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.
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(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with <t>DAPI,</t> Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.
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(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with <t>DAPI,</t> Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.
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Becton Dickinson cd4-pe cat id 347327
(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with <t>DAPI,</t> Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.
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Merck KGaA 4′,6-diamidino-2-phenylindole dapi
(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with <t>DAPI,</t> Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.
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Fisher Scientific subcellular localization
(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with <t>DAPI,</t> Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.
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Merck & Co nuclear stain dapi
(A) Schematic representation of an OrganoPlate® 3-lane tissue chip formed by two channels for cell seeding and a middle channel for gel loading. (B) Brightfield image and (C) confocal projection of HUVECs (red) seeded on top channel and HDLECs (green) seeded in bottom channel. Images taken after 24 h of culture under flow conditions. (D) Representative confocal max projection of HDLECs cultured in flow for 14 days in OrganoPlate® and treated for 24 h with DENV-2 NS1 (NS1) or control medium (untreated=Unt). Nuclei stained with <t>DAPI.</t> Merged images shows VE-cadherin (green) and F-actin (red) and DAPI (blue). Scale bar = 30 µm.
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Thermo Fisher 4 6 diamidino 2 phenylindole dihydrochloride
(A) Schematic representation of an OrganoPlate® 3-lane tissue chip formed by two channels for cell seeding and a middle channel for gel loading. (B) Brightfield image and (C) confocal projection of HUVECs (red) seeded on top channel and HDLECs (green) seeded in bottom channel. Images taken after 24 h of culture under flow conditions. (D) Representative confocal max projection of HDLECs cultured in flow for 14 days in OrganoPlate® and treated for 24 h with DENV-2 NS1 (NS1) or control medium (untreated=Unt). Nuclei stained with <t>DAPI.</t> Merged images shows VE-cadherin (green) and F-actin (red) and DAPI (blue). Scale bar = 30 µm.
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(A) Schematic representation of an OrganoPlate® 3-lane tissue chip formed by two channels for cell seeding and a middle channel for gel loading. (B) Brightfield image and (C) confocal projection of HUVECs (red) seeded on top channel and HDLECs (green) seeded in bottom channel. Images taken after 24 h of culture under flow conditions. (D) Representative confocal max projection of HDLECs cultured in flow for 14 days in OrganoPlate® and treated for 24 h with DENV-2 NS1 (NS1) or control medium (untreated=Unt). Nuclei stained with <t>DAPI.</t> Merged images shows VE-cadherin (green) and F-actin (red) and DAPI (blue). Scale bar = 30 µm.
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Image Search Results


(a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with DAPI, Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.

Journal: bioRxiv

Article Title: cGAS-mediated IFN-I signaling contributes to disease progression in drug-refractory epilepsy

doi: 10.64898/2026.01.30.702860

Figure Lengend Snippet: (a) Schematic showing the experiment design of the EV isolation and ICH in Dravet mice. (b) Confocal image of the brain section stained with DAPI, Iba1, and double-strain DNA (dsDNA), displaying sampling windows in hippocampus CA1. Bar = 1000 ⎧m. (c) 100x images from Scn1a +/+ and Scn1a +/- mouse showing immuno-fluorescence signals of DAPI, Iba1, and dsDNA in hippocampus CA1 single microglia cells. Bar=10 ⎧m. (d) Analysis of total dsDNA puncta in the cytoplasma of single hippocampal microglia cells and comparison between the two groups. N=79 cells ( Scn1a +/+ ), 101 cells ( Scn1a +/- ). N = 4 mice per group. Mixed-effects model ANOVA (F(1,6)= 9.742). (e) NanoFCM showed significant changes in size-based distribution in of hippocampal tissue EVs. N = 4 mice per group, two-way ANOVA (F (2, 18) = 78.95), Sidak’s multiple comparisons test. (f) Experimental scheme for the in vitro identification of the endogenous neuronal ligand for cGAS activation in primary microglia. (g) Acute PTZ-induced spontaneous epileptic activity in primary neurons. Up: representative fluorescence images of neurons expressing GCaMP8f (up). Scale bar: 50 μm. Down: calcium times course of each cell from above image showed spontaneous epileptic events after treated with 10 mM PTZ. (h) Representative western blot image for pTBK1, TBK1, and β-actin in primary Cgas+/+ and Cgas-/- microglia treated with untreated neuronal CM, HT-DNA, and PTZ-treated neuronal CM. (i) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Cgas+/+ : untreated CM, n=6, PTZ-treated CM, n=6. Cgas-/- : untreated CM, n=4, PTZ-treated CM, n=5. Two-way ANOVA with uncorrected Fisher’s LSD. (j) Experimental scheme for the in vitro identification of the endogenous neuronal ligand in PTZ-treated primary microglia (up). Representative western blot image for pTBK1, TBK1, and β-actin in primary wt microglia treated with control (ctrl) and PTZ (bottom). (k) Quantification of the ratio of pTBK1 to total TBK1 protein level. Each dot represents one well from two biologically independent experiments. Ctrl , n=7, PTZ, n=9. Welch’s t test.

Article Snippet: The following day, sections were washed thoroughly and incubated in appropriate secondary antibodies (1:500; Invitrogen) for 1 h. Sections were washed, mounted on slides using Vectashield antifade mounting medium with DAPI (Vector Laboratories, H-1200; or Sigma, D9542), and imaged.

Techniques: Isolation, Staining, Sampling, Fluorescence, Comparison, In Vitro, Activation Assay, Activity Assay, Expressing, Western Blot, Control

(A) Schematic representation of an OrganoPlate® 3-lane tissue chip formed by two channels for cell seeding and a middle channel for gel loading. (B) Brightfield image and (C) confocal projection of HUVECs (red) seeded on top channel and HDLECs (green) seeded in bottom channel. Images taken after 24 h of culture under flow conditions. (D) Representative confocal max projection of HDLECs cultured in flow for 14 days in OrganoPlate® and treated for 24 h with DENV-2 NS1 (NS1) or control medium (untreated=Unt). Nuclei stained with DAPI. Merged images shows VE-cadherin (green) and F-actin (red) and DAPI (blue). Scale bar = 30 µm.

Journal: bioRxiv

Article Title: Lymphatic vessel dysfunction contributes to severe dengue pathogenesis

doi: 10.64898/2026.03.27.714698

Figure Lengend Snippet: (A) Schematic representation of an OrganoPlate® 3-lane tissue chip formed by two channels for cell seeding and a middle channel for gel loading. (B) Brightfield image and (C) confocal projection of HUVECs (red) seeded on top channel and HDLECs (green) seeded in bottom channel. Images taken after 24 h of culture under flow conditions. (D) Representative confocal max projection of HDLECs cultured in flow for 14 days in OrganoPlate® and treated for 24 h with DENV-2 NS1 (NS1) or control medium (untreated=Unt). Nuclei stained with DAPI. Merged images shows VE-cadherin (green) and F-actin (red) and DAPI (blue). Scale bar = 30 µm.

Article Snippet: The slides were then incubated with the nuclear stain DAPI (cat# D9542, Merck) at 1:1000 dilution for 10 min and mounted onto glass slides using mounting medium (InvitrogenTM Fluoromount-GTM Mounting Medium-00495802).

Techniques: Cell Culture, Control, Staining