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    Danaher Inc nanoparticle coating anti histone h2b
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    resource source identifier antibodies anti histone h2b antibody abcam  (Danaher Inc)


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    anti h2b antibody  (Danaher Inc)


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    Danaher Inc anti h2b antibody
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    Proteintech histone h2b anti rabbit antibody
    (A) Steady-state chromatin organization predicted by numerical simulations showing phase separation into compacted heterochromatin domains (red) and loosely packed euchromatin domains (blue) and the formation of heterochromatin-rich LADs at the nuclear periphery. (B) Representative Voronoi density rendering of <t>H2B</t> STORM images, color-coded to indicate density levels (blue for low density and red for high density). (C) Numerical simulations showing the synergistic effects of chromatin-lamin affinity and methylation rates on LADs and inner heterochromatin domain morphology. At low levels of chromatin-lamina affinity, as the methylation level increases, the radius of the discrete LADs increases at a fixed value of the contact angle . The morphology of LADs is determined by both the level of methylation and chromatin-lamin affinity. Low affinity results in the formation of isolated LADs, while at greater levels of affinity LAD spread along the lamina. (D) Kinetic balance determines the steady-state size of interior HC domains. The diffusion of methylate histones from the EC region towards the HC domains and histone methylation drive their growth, counteracted by the opposing kinetics of histone acetylation. (E) The scaling relationship between the size of interior HC domains and the level of methylation. (F) (Left) At the interface of HC-rich LAD, EC-rich environment, and lamina, a balance of interfacial interaction between the two phases of chromatin ( γ he ) and the strength of chromatin-lamina affinities ( γ lh ) gives rise to a stable morphology of LADs, which have a characteristic contact angle with the lamina( θ ). (Right) The formation of LADs in steady state requires a balance between diffusion-driven heterochromatin influx (into the LAD) and acetylation-driven conversion of heterochromatin into euchromatin. (G) Schematics illustrating the morphology of LAD at varying levels of chromatin-lamina affinity. (H) The scaling relationship between the thickness of LAD and chromatin-lamina affinity at a given methylation level. The inset shows the scaling relation at varying methylation levels.
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    1) Product Images from "Revealing the Biophysics of Lamina-Associated Domain Formation by Integrating Theoretical Modeling and High-Resolution Imaging"

    Article Title: Revealing the Biophysics of Lamina-Associated Domain Formation by Integrating Theoretical Modeling and High-Resolution Imaging

    Journal: bioRxiv

    doi: 10.1101/2024.06.24.600310

    (A) Steady-state chromatin organization predicted by numerical simulations showing phase separation into compacted heterochromatin domains (red) and loosely packed euchromatin domains (blue) and the formation of heterochromatin-rich LADs at the nuclear periphery. (B) Representative Voronoi density rendering of H2B STORM images, color-coded to indicate density levels (blue for low density and red for high density). (C) Numerical simulations showing the synergistic effects of chromatin-lamin affinity and methylation rates on LADs and inner heterochromatin domain morphology. At low levels of chromatin-lamina affinity, as the methylation level increases, the radius of the discrete LADs increases at a fixed value of the contact angle . The morphology of LADs is determined by both the level of methylation and chromatin-lamin affinity. Low affinity results in the formation of isolated LADs, while at greater levels of affinity LAD spread along the lamina. (D) Kinetic balance determines the steady-state size of interior HC domains. The diffusion of methylate histones from the EC region towards the HC domains and histone methylation drive their growth, counteracted by the opposing kinetics of histone acetylation. (E) The scaling relationship between the size of interior HC domains and the level of methylation. (F) (Left) At the interface of HC-rich LAD, EC-rich environment, and lamina, a balance of interfacial interaction between the two phases of chromatin ( γ he ) and the strength of chromatin-lamina affinities ( γ lh ) gives rise to a stable morphology of LADs, which have a characteristic contact angle with the lamina( θ ). (Right) The formation of LADs in steady state requires a balance between diffusion-driven heterochromatin influx (into the LAD) and acetylation-driven conversion of heterochromatin into euchromatin. (G) Schematics illustrating the morphology of LAD at varying levels of chromatin-lamina affinity. (H) The scaling relationship between the thickness of LAD and chromatin-lamina affinity at a given methylation level. The inset shows the scaling relation at varying methylation levels.
    Figure Legend Snippet: (A) Steady-state chromatin organization predicted by numerical simulations showing phase separation into compacted heterochromatin domains (red) and loosely packed euchromatin domains (blue) and the formation of heterochromatin-rich LADs at the nuclear periphery. (B) Representative Voronoi density rendering of H2B STORM images, color-coded to indicate density levels (blue for low density and red for high density). (C) Numerical simulations showing the synergistic effects of chromatin-lamin affinity and methylation rates on LADs and inner heterochromatin domain morphology. At low levels of chromatin-lamina affinity, as the methylation level increases, the radius of the discrete LADs increases at a fixed value of the contact angle . The morphology of LADs is determined by both the level of methylation and chromatin-lamin affinity. Low affinity results in the formation of isolated LADs, while at greater levels of affinity LAD spread along the lamina. (D) Kinetic balance determines the steady-state size of interior HC domains. The diffusion of methylate histones from the EC region towards the HC domains and histone methylation drive their growth, counteracted by the opposing kinetics of histone acetylation. (E) The scaling relationship between the size of interior HC domains and the level of methylation. (F) (Left) At the interface of HC-rich LAD, EC-rich environment, and lamina, a balance of interfacial interaction between the two phases of chromatin ( γ he ) and the strength of chromatin-lamina affinities ( γ lh ) gives rise to a stable morphology of LADs, which have a characteristic contact angle with the lamina( θ ). (Right) The formation of LADs in steady state requires a balance between diffusion-driven heterochromatin influx (into the LAD) and acetylation-driven conversion of heterochromatin into euchromatin. (G) Schematics illustrating the morphology of LAD at varying levels of chromatin-lamina affinity. (H) The scaling relationship between the thickness of LAD and chromatin-lamina affinity at a given methylation level. The inset shows the scaling relation at varying methylation levels.

    Techniques Used: Methylation, Isolation, Diffusion-based Assay

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    (A) Steady-state chromatin organization predicted by numerical simulations showing phase separation into compacted heterochromatin domains (red) and loosely packed euchromatin domains (blue) and the formation of heterochromatin-rich LADs at the nuclear periphery. (B) Representative Voronoi density rendering of <t>H2B</t> STORM images, color-coded to indicate density levels (blue for low density and red for high density). (C) Numerical simulations showing the synergistic effects of chromatin-lamin affinity and methylation rates on LADs and inner heterochromatin domain morphology. At low levels of chromatin-lamina affinity, as the methylation level increases, the radius of the discrete LADs increases at a fixed value of the contact angle . The morphology of LADs is determined by both the level of methylation and chromatin-lamin affinity. Low affinity results in the formation of isolated LADs, while at greater levels of affinity LAD spread along the lamina. (D) Kinetic balance determines the steady-state size of interior HC domains. The diffusion of methylate histones from the EC region towards the HC domains and histone methylation drive their growth, counteracted by the opposing kinetics of histone acetylation. (E) The scaling relationship between the size of interior HC domains and the level of methylation. (F) (Left) At the interface of HC-rich LAD, EC-rich environment, and lamina, a balance of interfacial interaction between the two phases of chromatin ( γ he ) and the strength of chromatin-lamina affinities ( γ lh ) gives rise to a stable morphology of LADs, which have a characteristic contact angle with the lamina( θ ). (Right) The formation of LADs in steady state requires a balance between diffusion-driven heterochromatin influx (into the LAD) and acetylation-driven conversion of heterochromatin into euchromatin. (G) Schematics illustrating the morphology of LAD at varying levels of chromatin-lamina affinity. (H) The scaling relationship between the thickness of LAD and chromatin-lamina affinity at a given methylation level. The inset shows the scaling relation at varying methylation levels.
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    (A) Steady-state chromatin organization predicted by numerical simulations showing phase separation into compacted heterochromatin domains (red) and loosely packed euchromatin domains (blue) and the formation of heterochromatin-rich LADs at the nuclear periphery. (B) Representative Voronoi density rendering of H2B STORM images, color-coded to indicate density levels (blue for low density and red for high density). (C) Numerical simulations showing the synergistic effects of chromatin-lamin affinity and methylation rates on LADs and inner heterochromatin domain morphology. At low levels of chromatin-lamina affinity, as the methylation level increases, the radius of the discrete LADs increases at a fixed value of the contact angle . The morphology of LADs is determined by both the level of methylation and chromatin-lamin affinity. Low affinity results in the formation of isolated LADs, while at greater levels of affinity LAD spread along the lamina. (D) Kinetic balance determines the steady-state size of interior HC domains. The diffusion of methylate histones from the EC region towards the HC domains and histone methylation drive their growth, counteracted by the opposing kinetics of histone acetylation. (E) The scaling relationship between the size of interior HC domains and the level of methylation. (F) (Left) At the interface of HC-rich LAD, EC-rich environment, and lamina, a balance of interfacial interaction between the two phases of chromatin ( γ he ) and the strength of chromatin-lamina affinities ( γ lh ) gives rise to a stable morphology of LADs, which have a characteristic contact angle with the lamina( θ ). (Right) The formation of LADs in steady state requires a balance between diffusion-driven heterochromatin influx (into the LAD) and acetylation-driven conversion of heterochromatin into euchromatin. (G) Schematics illustrating the morphology of LAD at varying levels of chromatin-lamina affinity. (H) The scaling relationship between the thickness of LAD and chromatin-lamina affinity at a given methylation level. The inset shows the scaling relation at varying methylation levels.

    Journal: bioRxiv

    Article Title: Revealing the Biophysics of Lamina-Associated Domain Formation by Integrating Theoretical Modeling and High-Resolution Imaging

    doi: 10.1101/2024.06.24.600310

    Figure Lengend Snippet: (A) Steady-state chromatin organization predicted by numerical simulations showing phase separation into compacted heterochromatin domains (red) and loosely packed euchromatin domains (blue) and the formation of heterochromatin-rich LADs at the nuclear periphery. (B) Representative Voronoi density rendering of H2B STORM images, color-coded to indicate density levels (blue for low density and red for high density). (C) Numerical simulations showing the synergistic effects of chromatin-lamin affinity and methylation rates on LADs and inner heterochromatin domain morphology. At low levels of chromatin-lamina affinity, as the methylation level increases, the radius of the discrete LADs increases at a fixed value of the contact angle . The morphology of LADs is determined by both the level of methylation and chromatin-lamin affinity. Low affinity results in the formation of isolated LADs, while at greater levels of affinity LAD spread along the lamina. (D) Kinetic balance determines the steady-state size of interior HC domains. The diffusion of methylate histones from the EC region towards the HC domains and histone methylation drive their growth, counteracted by the opposing kinetics of histone acetylation. (E) The scaling relationship between the size of interior HC domains and the level of methylation. (F) (Left) At the interface of HC-rich LAD, EC-rich environment, and lamina, a balance of interfacial interaction between the two phases of chromatin ( γ he ) and the strength of chromatin-lamina affinities ( γ lh ) gives rise to a stable morphology of LADs, which have a characteristic contact angle with the lamina( θ ). (Right) The formation of LADs in steady state requires a balance between diffusion-driven heterochromatin influx (into the LAD) and acetylation-driven conversion of heterochromatin into euchromatin. (G) Schematics illustrating the morphology of LAD at varying levels of chromatin-lamina affinity. (H) The scaling relationship between the thickness of LAD and chromatin-lamina affinity at a given methylation level. The inset shows the scaling relation at varying methylation levels.

    Article Snippet: Subsequently, the cells were subjected to overnight incubation at 4°C with a 1:50 dilution of histone H2B anti-rabbit antibody (ProteinTech, #15857-1-AP).

    Techniques: Methylation, Isolation, Diffusion-based Assay