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c12511 lot n ◦ 495z001 5  (PromoCell)


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    Structured Review

    PromoCell c12511 lot n ◦ 495z001 5
    C12511 Lot N ◦ 495z001 5, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 121 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/c12511 lot n ◦ 495z001 5/product/PromoCell
    Average 95 stars, based on 121 article reviews
    c12511 lot n ◦ 495z001 5 - by Bioz Stars, 2026-06
    95/100 stars

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    (A) AlphaGenome predicted quantile scores for prioritised CAD variants in vascular <t>smooth</t> <t>muscle</t> <t>cells</t> versus a non-vascular comparator (B cells) across chromatin and transcriptional output tracks. The quantile score represents a standardised rank of the impact of a variant, derived from quantile normalisation of the raw predicted score for each variant. (B) In-silico motif disruption analysis (motifbreakR) for prioritised variants within ABC enhancers, showing reference versus alternate PWM scores, coloured by ΔPWM (alternate − reference). TFs were restricted to those expressed in <t>Human</t> <t>coronary</t> <t>artery</t> VSMCs. (C) Locus-level example at rs9624456:CCTCA>T. Top left: AlphaGenome-predicted genome tracks comparing alternate versus reference alleles at rs9624456. Bottom left: observed genome tracks in Human coronary artery VSMCs following ox-LDL exposure. Top right: Hi-C contact map showing chromatin interactions within the SPECC1L-GUCD1 topologically associating domain (TAD). Bottom right: RNA-seq shows ox-LDL-associated induction of GUCD1 in Human coronary artery VSMCs. (D) CRISPR knockout (KO) experimental design and proliferation readout. Human coronary artery VSMCs were transfected with sgRNA, labelled with CFSE, and exposed to ox-LDL. CFSE histograms and quantification are shown; higher CFSE signal indicates reduced proliferation.
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    Image Search Results


    (A) AlphaGenome predicted quantile scores for prioritised CAD variants in vascular smooth muscle cells versus a non-vascular comparator (B cells) across chromatin and transcriptional output tracks. The quantile score represents a standardised rank of the impact of a variant, derived from quantile normalisation of the raw predicted score for each variant. (B) In-silico motif disruption analysis (motifbreakR) for prioritised variants within ABC enhancers, showing reference versus alternate PWM scores, coloured by ΔPWM (alternate − reference). TFs were restricted to those expressed in Human coronary artery VSMCs. (C) Locus-level example at rs9624456:CCTCA>T. Top left: AlphaGenome-predicted genome tracks comparing alternate versus reference alleles at rs9624456. Bottom left: observed genome tracks in Human coronary artery VSMCs following ox-LDL exposure. Top right: Hi-C contact map showing chromatin interactions within the SPECC1L-GUCD1 topologically associating domain (TAD). Bottom right: RNA-seq shows ox-LDL-associated induction of GUCD1 in Human coronary artery VSMCs. (D) CRISPR knockout (KO) experimental design and proliferation readout. Human coronary artery VSMCs were transfected with sgRNA, labelled with CFSE, and exposed to ox-LDL. CFSE histograms and quantification are shown; higher CFSE signal indicates reduced proliferation.

    Journal: bioRxiv

    Article Title: CAD variants act through ox-LDL-induced enhancer remodelling to alter VSMC gene programmes

    doi: 10.64898/2026.04.21.718843

    Figure Lengend Snippet: (A) AlphaGenome predicted quantile scores for prioritised CAD variants in vascular smooth muscle cells versus a non-vascular comparator (B cells) across chromatin and transcriptional output tracks. The quantile score represents a standardised rank of the impact of a variant, derived from quantile normalisation of the raw predicted score for each variant. (B) In-silico motif disruption analysis (motifbreakR) for prioritised variants within ABC enhancers, showing reference versus alternate PWM scores, coloured by ΔPWM (alternate − reference). TFs were restricted to those expressed in Human coronary artery VSMCs. (C) Locus-level example at rs9624456:CCTCA>T. Top left: AlphaGenome-predicted genome tracks comparing alternate versus reference alleles at rs9624456. Bottom left: observed genome tracks in Human coronary artery VSMCs following ox-LDL exposure. Top right: Hi-C contact map showing chromatin interactions within the SPECC1L-GUCD1 topologically associating domain (TAD). Bottom right: RNA-seq shows ox-LDL-associated induction of GUCD1 in Human coronary artery VSMCs. (D) CRISPR knockout (KO) experimental design and proliferation readout. Human coronary artery VSMCs were transfected with sgRNA, labelled with CFSE, and exposed to ox-LDL. CFSE histograms and quantification are shown; higher CFSE signal indicates reduced proliferation.

    Article Snippet: Primary human coronary artery smooth muscle cells (Human coronary artery VSMCs) were obtained at passage 2 from Promocell (Heidelberg, Germany) and expanded before usage.

    Techniques: Variant Assay, Derivative Assay, In Silico, Disruption, Hi-C, RNA Sequencing, CRISPR, Knock-Out, Transfection

    In vitro biocompatibility and intracellular NO generation characterisation of DSENO materials. (a, b) Cell viability of HUVECs (a) and HCASMCs (b) after 48 h incubation with printed DSENO plates. (c) Quantitative analysis of material‐induced intracellular NO generation. Endogenous NO production in HUVECs was quantified by measuring the mean fluorescence intensity (MFI) of the DAF‐FM probe using high‐resolution confocal laser scanning microscopy (CLSM). (d) CLSM images of HUVECs after 48 h incubation with material candidates, cells stained with DAF‐FM (green) and Hoechst (blue) ( n ≥ 6). Scale bar = 100 µm. Data are normalized to the blank control and represent the average MFI of multiple regions of interest. Error bars indicate standard deviation; statistical significance was determined via one‐way ANOVA ( * p < 0.05).

    Journal: Advanced Materials (Deerfield Beach, Fla.)

    Article Title: Deployable 3D‐Printed Vascular Stent with Surface‐Catalysed Endogenous Nitric Oxide Generation

    doi: 10.1002/adma.202520199

    Figure Lengend Snippet: In vitro biocompatibility and intracellular NO generation characterisation of DSENO materials. (a, b) Cell viability of HUVECs (a) and HCASMCs (b) after 48 h incubation with printed DSENO plates. (c) Quantitative analysis of material‐induced intracellular NO generation. Endogenous NO production in HUVECs was quantified by measuring the mean fluorescence intensity (MFI) of the DAF‐FM probe using high‐resolution confocal laser scanning microscopy (CLSM). (d) CLSM images of HUVECs after 48 h incubation with material candidates, cells stained with DAF‐FM (green) and Hoechst (blue) ( n ≥ 6). Scale bar = 100 µm. Data are normalized to the blank control and represent the average MFI of multiple regions of interest. Error bars indicate standard deviation; statistical significance was determined via one‐way ANOVA ( * p < 0.05).

    Article Snippet: Human coronary artery smooth muscle cells (HCASMCs) from Cell Applications were maintained in human smooth muscle cell growth medium (311–500) and passaged at 70–90% confluency.

    Techniques: In Vitro, Incubation, Fluorescence, Confocal Laser Scanning Microscopy, Staining, Control, Standard Deviation