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ndst3  (Novus Biologicals)


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    Novus Biologicals ndst3
    Identification of regenerating factor as a regulator of therapeutic genes for Parkinson's disease therapy. A) Conceptual diagram outlining the basis of an epigenetic regulator. B) Comparative gene expression heatmap of substantia nigra (SN) in wild type control versus 6‐OHDA‐induced Parkinson's disease (PD) mouse model. C) Heatmap showing gene expression profiles in the caudate and putamen regions of healthy individuals (HI) and a cohort of human PD patients. BG: Basal Ganglia. D) Immunofluorescence images showing TUJ1‐ and MAP2‐positive cells under each condition. Scale bar = 50 µm. E) Immunochemistry and Sholl analysis of TH‐labeled neurons. Left panel: morphology of individual neurons. Right panel: Sholl analysis showing the number of neurite intersections as a function of distance from the soma. Scale bar = 100 µm. The data are presented as mean ± SEM ( n = 5 – 6 cells per group). F) Representative traces of action potentials evoked by depolarizing current injections under each condition (sham, 6‐OHDA, <t>6‐OHDA+NDST3).</t> G) Dot plot showing the top 14 GO Biological Process terms from enrichment analyses: 6‐OHDA versus Sham (left side) and 6‐OHDA+NDST3 versus 6‐OHDA (right side). H) Pearson correlation matrix of transcriptomic among samples.
    Ndst3, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/single-cell+spatial+transcriptomics+data/pmc12970244-400-25-26?v=Novus+Biologicals
    Average 93 stars, based on 2 article reviews
    ndst3 - by Bioz Stars, 2026-08
    93/100 stars

    Images

    1) Product Images from "NDST3‐Induced Epigenetic Reprogramming Reverses Neurodegeneration in Parkinson's Disease"

    Article Title: NDST3‐Induced Epigenetic Reprogramming Reverses Neurodegeneration in Parkinson's Disease

    Journal: Advanced Science

    doi: 10.1002/advs.202507323

    Identification of regenerating factor as a regulator of therapeutic genes for Parkinson's disease therapy. A) Conceptual diagram outlining the basis of an epigenetic regulator. B) Comparative gene expression heatmap of substantia nigra (SN) in wild type control versus 6‐OHDA‐induced Parkinson's disease (PD) mouse model. C) Heatmap showing gene expression profiles in the caudate and putamen regions of healthy individuals (HI) and a cohort of human PD patients. BG: Basal Ganglia. D) Immunofluorescence images showing TUJ1‐ and MAP2‐positive cells under each condition. Scale bar = 50 µm. E) Immunochemistry and Sholl analysis of TH‐labeled neurons. Left panel: morphology of individual neurons. Right panel: Sholl analysis showing the number of neurite intersections as a function of distance from the soma. Scale bar = 100 µm. The data are presented as mean ± SEM ( n = 5 – 6 cells per group). F) Representative traces of action potentials evoked by depolarizing current injections under each condition (sham, 6‐OHDA, 6‐OHDA+NDST3). G) Dot plot showing the top 14 GO Biological Process terms from enrichment analyses: 6‐OHDA versus Sham (left side) and 6‐OHDA+NDST3 versus 6‐OHDA (right side). H) Pearson correlation matrix of transcriptomic among samples.
    Figure Legend Snippet: Identification of regenerating factor as a regulator of therapeutic genes for Parkinson's disease therapy. A) Conceptual diagram outlining the basis of an epigenetic regulator. B) Comparative gene expression heatmap of substantia nigra (SN) in wild type control versus 6‐OHDA‐induced Parkinson's disease (PD) mouse model. C) Heatmap showing gene expression profiles in the caudate and putamen regions of healthy individuals (HI) and a cohort of human PD patients. BG: Basal Ganglia. D) Immunofluorescence images showing TUJ1‐ and MAP2‐positive cells under each condition. Scale bar = 50 µm. E) Immunochemistry and Sholl analysis of TH‐labeled neurons. Left panel: morphology of individual neurons. Right panel: Sholl analysis showing the number of neurite intersections as a function of distance from the soma. Scale bar = 100 µm. The data are presented as mean ± SEM ( n = 5 – 6 cells per group). F) Representative traces of action potentials evoked by depolarizing current injections under each condition (sham, 6‐OHDA, 6‐OHDA+NDST3). G) Dot plot showing the top 14 GO Biological Process terms from enrichment analyses: 6‐OHDA versus Sham (left side) and 6‐OHDA+NDST3 versus 6‐OHDA (right side). H) Pearson correlation matrix of transcriptomic among samples.

    Techniques Used: Gene Expression, Control, Immunofluorescence, Labeling

    Therapeutic efficacy of NDST3 and retrograde tracing with CTB in mice. A) Schematic diagram of in vivo experimental design involving CTB injection in the PD mouse model. B) Representative immunofluorescence images of CTB, TH, and NDST3 expression in the SN of Sham, 6‐OHDA‐induced PD mice, and NDST3‐treated PD mice. Scale bar = 50 µm and 10 µm (Magnified image). C) Quantification of CTB‐, TH‐, and NDST3‐positive cells shown in Figure . Data are presented as mean ± SEM ( n = 6 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns = not significant. D) Immunofluorescence images showing GIRK2‐ and TH‐positive cells in the Sham, 6‐OHDA‐induced PD mice, and NDST3‐treated PD mice. Scale bar = 50 µm and 10 µm (Magnified image). E) 3D Z‐stack analysis (IMARIS) of TH‐positive neurons obtained via confocal microscopy. F) DAB‐DAT staining in the SN.
    Figure Legend Snippet: Therapeutic efficacy of NDST3 and retrograde tracing with CTB in mice. A) Schematic diagram of in vivo experimental design involving CTB injection in the PD mouse model. B) Representative immunofluorescence images of CTB, TH, and NDST3 expression in the SN of Sham, 6‐OHDA‐induced PD mice, and NDST3‐treated PD mice. Scale bar = 50 µm and 10 µm (Magnified image). C) Quantification of CTB‐, TH‐, and NDST3‐positive cells shown in Figure . Data are presented as mean ± SEM ( n = 6 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns = not significant. D) Immunofluorescence images showing GIRK2‐ and TH‐positive cells in the Sham, 6‐OHDA‐induced PD mice, and NDST3‐treated PD mice. Scale bar = 50 µm and 10 µm (Magnified image). E) 3D Z‐stack analysis (IMARIS) of TH‐positive neurons obtained via confocal microscopy. F) DAB‐DAT staining in the SN.

    Techniques Used: Drug discovery, Retrograde Tracing, In Vivo, Injection, Immunofluorescence, Expressing, Confocal Microscopy, Staining

    Efficacy and electrophysiological properties of NDST3 in chemical‐induced PD model. A) Representative traces of spontaneous firing currents recorded from DA neurons of the SNpc in brain slices from each group. B) Cumulative fractions curves showing shortened inter‐event intervals, indicating a higher frequency of spontaneous firing in the 6‐OHDA + NDST3 group compared to the 6‐OHDA group. The inner bar graph showed mean inter‐event intervals in the ipsilateral of SNpc of each group. Data are presented as mean ± SEM ( n = 6 – 8 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. *** p < 0.001. C) Quantification of DA neuronal firing rates in the ipsilateral SNpc of each group. The data are presented as mean ± SEM ( n = 6–8 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. * p < 0.05, and ** p < 0.01. D) Representative in vivo recording traces from the SNpc of live animals in each condition. E) Instantaneous firing frequencies during the recorded period. ( n = 4–6 independent animals per group; repeated measures) Two‐way ANOVA with Tukey's multiple comparisons test, * p < 0.05. F) Comparison of action potential waveforms among DA neurons across conditions. G) Representative image of DAB‐TH staining in ST and SN. Scale bar = 1 mm. H) Immunofluorescence images showing GIRK2‐ and TH‐positive cells in the Sham, MPTP‐induced PD mice, NDST3‐treated PD mice, and NDST3 only‐treated mice. Scale bar = 50 µm and 10 µm (Magnified image). I) Error count during the challenging beam traversal test for each experimental condition. The data are presented as mean ± SEM. ( n = 7 – 8 independent animals per group) Two‐way ANOVA with Tukey's multiple comparisons test. **** p < 0.0001. J) Errors per step during the challenging beam traversal test across conditions. The data are presented as mean ± SEM ( n = 7 – 8 independent animal per group). One‐way ANOVA with Tukey's multiple comparisons test. **** p < 0.0001. K) Fall latency in the wire‐hanging test. The data are presented as mean ± SEM ( n = 7–8 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. *** p < 0.001 and **** p < 0.0001. L) Time to orient downward (T‐turn) and M) time to descend to the base (T‐total). The data are presented as mean ± SEM ( n = 7–8 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. * p < 0.05, *** p < 0.001 and **** p < 0.0001.
    Figure Legend Snippet: Efficacy and electrophysiological properties of NDST3 in chemical‐induced PD model. A) Representative traces of spontaneous firing currents recorded from DA neurons of the SNpc in brain slices from each group. B) Cumulative fractions curves showing shortened inter‐event intervals, indicating a higher frequency of spontaneous firing in the 6‐OHDA + NDST3 group compared to the 6‐OHDA group. The inner bar graph showed mean inter‐event intervals in the ipsilateral of SNpc of each group. Data are presented as mean ± SEM ( n = 6 – 8 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. *** p < 0.001. C) Quantification of DA neuronal firing rates in the ipsilateral SNpc of each group. The data are presented as mean ± SEM ( n = 6–8 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. * p < 0.05, and ** p < 0.01. D) Representative in vivo recording traces from the SNpc of live animals in each condition. E) Instantaneous firing frequencies during the recorded period. ( n = 4–6 independent animals per group; repeated measures) Two‐way ANOVA with Tukey's multiple comparisons test, * p < 0.05. F) Comparison of action potential waveforms among DA neurons across conditions. G) Representative image of DAB‐TH staining in ST and SN. Scale bar = 1 mm. H) Immunofluorescence images showing GIRK2‐ and TH‐positive cells in the Sham, MPTP‐induced PD mice, NDST3‐treated PD mice, and NDST3 only‐treated mice. Scale bar = 50 µm and 10 µm (Magnified image). I) Error count during the challenging beam traversal test for each experimental condition. The data are presented as mean ± SEM. ( n = 7 – 8 independent animals per group) Two‐way ANOVA with Tukey's multiple comparisons test. **** p < 0.0001. J) Errors per step during the challenging beam traversal test across conditions. The data are presented as mean ± SEM ( n = 7 – 8 independent animal per group). One‐way ANOVA with Tukey's multiple comparisons test. **** p < 0.0001. K) Fall latency in the wire‐hanging test. The data are presented as mean ± SEM ( n = 7–8 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. *** p < 0.001 and **** p < 0.0001. L) Time to orient downward (T‐turn) and M) time to descend to the base (T‐total). The data are presented as mean ± SEM ( n = 7–8 independent animals per group). One‐way ANOVA with Tukey's multiple comparisons test. * p < 0.05, *** p < 0.001 and **** p < 0.0001.

    Techniques Used: In Vivo, Comparison, Staining, Immunofluorescence

    Molecular mechanisms of NDST3 in the PD model. A) One‐way hierarchical clustering heatmap based on Z‐score of normalized expression value for 5629 genes selected with fold change ≥ 2 and raw p ‐value < 0.05. B) Principal component analysis (PCA) analysis of RNA‐seq data to visualize sample‐to‐sample variation. C) Volcano plot showing differentially expressed genes between 6‐OHDA and Sham group; Down‐regulated genes marked in blue. D) Volcano plot showing differentially expressed genes between 6‐OHDA+NDST3 and 6‐OHDA; Up‐regulated genes marked in red. E) Dot plot of top 14 GO cellular component terms from GO enrichment analyses: 6‐OHDA+NDST3 versus 6‐OHDA. Heatmap showing gene expression patterns in F) pre‐synaptic neurons, G) post‐synaptic neurons, and H) glia compartments. I) UMAP visualizing cluster identity. J) UMAP representation comparing cellular composition in 6‐OHDA and 6‐OHDA+NDST3. K) Branched trajectory analysis illustrating cell state transitions in a 2D state‐space, where each dot represents a single cell, color‐coded by group identity.
    Figure Legend Snippet: Molecular mechanisms of NDST3 in the PD model. A) One‐way hierarchical clustering heatmap based on Z‐score of normalized expression value for 5629 genes selected with fold change ≥ 2 and raw p ‐value < 0.05. B) Principal component analysis (PCA) analysis of RNA‐seq data to visualize sample‐to‐sample variation. C) Volcano plot showing differentially expressed genes between 6‐OHDA and Sham group; Down‐regulated genes marked in blue. D) Volcano plot showing differentially expressed genes between 6‐OHDA+NDST3 and 6‐OHDA; Up‐regulated genes marked in red. E) Dot plot of top 14 GO cellular component terms from GO enrichment analyses: 6‐OHDA+NDST3 versus 6‐OHDA. Heatmap showing gene expression patterns in F) pre‐synaptic neurons, G) post‐synaptic neurons, and H) glia compartments. I) UMAP visualizing cluster identity. J) UMAP representation comparing cellular composition in 6‐OHDA and 6‐OHDA+NDST3. K) Branched trajectory analysis illustrating cell state transitions in a 2D state‐space, where each dot represents a single cell, color‐coded by group identity.

    Techniques Used: Expressing, RNA Sequencing, Gene Expression, Single Cell

    Comprehensive analysis of spatial transcriptomics and epigenetic modulation following NDST3 treatment in a PD model. A) Heatmap showing gene expression patterns in each cluster. ** p < 0.01, and **** p < 0.0001. B) Gene concept network plot displaying genes enriched in catabolic, metabolic, and wound healing GO categories. The top 30 most differentially expressed genes comparing 6‐OHDA versus Sham and 6‐OHDA+NDST3 versus 6‐OHDA. Node color intensity represents the log2 fold‐change of gene expression. C) Cell‐cell communication network plot illustrating interactions among three distinct cell clusters in 6‐OHDA‐induced PD model (left panel) and NDST3‐treated PD model (right panel), based on ligand–receptor pair probabilities using the CellChat database. Line thickness indicates proportionality to the number of interactions. D) Spatial localization of dopamine‐related markers. E) Spatial mapping of dopaminergic lineage markers identified via scRNA‐Seq. F) Heatmap visualization of CUT&RUN and ATAC‐Seq signal intensity ±2 kb around the TSS. G) Immunofluorescence images showing H3K27ac and TH‐positive cells in the Sham, 6‐OHDA‐induced PD mice, and NDST3‐treated PD mice. Scale bar = 50 µm. H) Venn diagram illustrating overlapping genes among DEGs from RNA‐Seq, scRNA‐Seq Cluster 9, CUT&RUN peak, and ATAC‐Seq peak. Average signal plot of I) CUT&RUN and J) ATAC‐seq signals at over‐enriched TSS regions of the Ncoa7 gene. K) Structure of NDST3‐NCOA7‐H3K27ac complex. Blue – NDST3, Green – NCOA7, and Red – H3K27ac. The yellow boundary represents the interaction region.
    Figure Legend Snippet: Comprehensive analysis of spatial transcriptomics and epigenetic modulation following NDST3 treatment in a PD model. A) Heatmap showing gene expression patterns in each cluster. ** p < 0.01, and **** p < 0.0001. B) Gene concept network plot displaying genes enriched in catabolic, metabolic, and wound healing GO categories. The top 30 most differentially expressed genes comparing 6‐OHDA versus Sham and 6‐OHDA+NDST3 versus 6‐OHDA. Node color intensity represents the log2 fold‐change of gene expression. C) Cell‐cell communication network plot illustrating interactions among three distinct cell clusters in 6‐OHDA‐induced PD model (left panel) and NDST3‐treated PD model (right panel), based on ligand–receptor pair probabilities using the CellChat database. Line thickness indicates proportionality to the number of interactions. D) Spatial localization of dopamine‐related markers. E) Spatial mapping of dopaminergic lineage markers identified via scRNA‐Seq. F) Heatmap visualization of CUT&RUN and ATAC‐Seq signal intensity ±2 kb around the TSS. G) Immunofluorescence images showing H3K27ac and TH‐positive cells in the Sham, 6‐OHDA‐induced PD mice, and NDST3‐treated PD mice. Scale bar = 50 µm. H) Venn diagram illustrating overlapping genes among DEGs from RNA‐Seq, scRNA‐Seq Cluster 9, CUT&RUN peak, and ATAC‐Seq peak. Average signal plot of I) CUT&RUN and J) ATAC‐seq signals at over‐enriched TSS regions of the Ncoa7 gene. K) Structure of NDST3‐NCOA7‐H3K27ac complex. Blue – NDST3, Green – NCOA7, and Red – H3K27ac. The yellow boundary represents the interaction region.

    Techniques Used: Spatial Transcriptomics, Gene Expression, Immunofluorescence, RNA Sequencing



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    Image Search Results


    (a) Simplified cross-section of the human epidermis, highlighting squamous cells, melanocytes and basal cells. Coloured regions represent cSCC (green), which originates from squamous cells, melanoma (orange), which originates from melanocytes, and BCC (blue), which originates from basal cells. Two orange melanocytes are shown in the dermal region as occurs in invasive melanoma; other cells in the lower dermis layer are not depicted. (b) Overview of sample design and technologies used to generate data for this project. ROI - region of interest; FOV - field of view; S - cSCC; B - BCC; M - melanoma; HC - healthy (cancer patient); HNC - healthy (non-cancer patient donor). Technologies included are single cell RNA sequencing for fresh samples, single nuclei sequencing for formalin-fixed samples, Visium, Xenium, CosMX, GeoMX DSP for whole transcriptome, GeoMX DSP for proteins, Polaris, RNAscope, the proximal ligation assay, spatial glycomics and CODEX.

    Journal: bioRxiv

    Article Title: Integrating 12 Spatial and Single Cell Technologies to Characterise Tumour Neighbourhoods and Cellular Interactions in three Skin Cancer Types

    doi: 10.1101/2025.07.25.666708

    Figure Lengend Snippet: (a) Simplified cross-section of the human epidermis, highlighting squamous cells, melanocytes and basal cells. Coloured regions represent cSCC (green), which originates from squamous cells, melanoma (orange), which originates from melanocytes, and BCC (blue), which originates from basal cells. Two orange melanocytes are shown in the dermal region as occurs in invasive melanoma; other cells in the lower dermis layer are not depicted. (b) Overview of sample design and technologies used to generate data for this project. ROI - region of interest; FOV - field of view; S - cSCC; B - BCC; M - melanoma; HC - healthy (cancer patient); HNC - healthy (non-cancer patient donor). Technologies included are single cell RNA sequencing for fresh samples, single nuclei sequencing for formalin-fixed samples, Visium, Xenium, CosMX, GeoMX DSP for whole transcriptome, GeoMX DSP for proteins, Polaris, RNAscope, the proximal ligation assay, spatial glycomics and CODEX.

    Article Snippet: Cells expressing the two genes are visualized on single-cell level resolution spatial data from STOmics and Curio-Seeker (Takara Bio, USA) melanoma samples and appear to be in spatial proximity ( ).

    Techniques: RNA Sequencing, Sequencing, RNAscope, Ligation

    (a) Gene specificity score (GSS) and association of spatial spots with skin cancer heritability. GSS score for each gene in a spot/cell represents the enrichment of the gene as a top rank most abundant gene in the spot/cell and its neighbour spots/cells in an anatomical region, a spatial domain, or a cell type. The p-value shows the spatial heritability enrichment significance of a spot with a trait based on SNPs mapped to the genes with high GSS scores (one-sided Z-test for stratified coefficient different to 0). The p-value is more significant if the SNPs that are mapped to the high GSS genes explain a higher proportion of heritability for the trait. (b) Cell types with the highest enrichment of heritability explained by SNPs tagged to GSS genes of cells in a cell type. The white asterisks indicate the most enriched cell-type for heritability of cutaneous melanoma, cSCC and BCC traits. (c) gsMAP significance spatial heritability enrichment is shown at single-cell resolution across the tissue (upper tissue plots) or per annotated skin regions (lower violin plots) from the cosMx data of the sample mel48974. (d) LR pairs with significant association with SNP heritability explained by the corresponding cell types. The rectangles show cases where both L and R genes had PCC >0.3 between GSS of the gene and the gsMAP P-values (the significance level for the LD stratified coefficients for the spot bigger than 0). The results suggest which LR pairs are related with the heritability of a cell type pairs. (e) GSS of two LR pairs showing specificity of the L and R genes to tissue regions at the immune-rich dermal layers and the epidermis of the skin. (f) Manhattan plot showing top significant GWAS SNPs co-localizing with genes in melanocytes (red) and T cells (blue) that had the highest Pearson correlation between GSS and the gsMAP trait association P-value or associated with SNPs with genome-wide significance. The Y-axis shows the -log(P-value) from GWAS analysis.

    Journal: bioRxiv

    Article Title: Integrating 12 Spatial and Single Cell Technologies to Characterise Tumour Neighbourhoods and Cellular Interactions in three Skin Cancer Types

    doi: 10.1101/2025.07.25.666708

    Figure Lengend Snippet: (a) Gene specificity score (GSS) and association of spatial spots with skin cancer heritability. GSS score for each gene in a spot/cell represents the enrichment of the gene as a top rank most abundant gene in the spot/cell and its neighbour spots/cells in an anatomical region, a spatial domain, or a cell type. The p-value shows the spatial heritability enrichment significance of a spot with a trait based on SNPs mapped to the genes with high GSS scores (one-sided Z-test for stratified coefficient different to 0). The p-value is more significant if the SNPs that are mapped to the high GSS genes explain a higher proportion of heritability for the trait. (b) Cell types with the highest enrichment of heritability explained by SNPs tagged to GSS genes of cells in a cell type. The white asterisks indicate the most enriched cell-type for heritability of cutaneous melanoma, cSCC and BCC traits. (c) gsMAP significance spatial heritability enrichment is shown at single-cell resolution across the tissue (upper tissue plots) or per annotated skin regions (lower violin plots) from the cosMx data of the sample mel48974. (d) LR pairs with significant association with SNP heritability explained by the corresponding cell types. The rectangles show cases where both L and R genes had PCC >0.3 between GSS of the gene and the gsMAP P-values (the significance level for the LD stratified coefficients for the spot bigger than 0). The results suggest which LR pairs are related with the heritability of a cell type pairs. (e) GSS of two LR pairs showing specificity of the L and R genes to tissue regions at the immune-rich dermal layers and the epidermis of the skin. (f) Manhattan plot showing top significant GWAS SNPs co-localizing with genes in melanocytes (red) and T cells (blue) that had the highest Pearson correlation between GSS and the gsMAP trait association P-value or associated with SNPs with genome-wide significance. The Y-axis shows the -log(P-value) from GWAS analysis.

    Article Snippet: Cells expressing the two genes are visualized on single-cell level resolution spatial data from STOmics and Curio-Seeker (Takara Bio, USA) melanoma samples and appear to be in spatial proximity ( ).

    Techniques: Genome Wide

    Journal: Cell

    Article Title: Spatiotemporal analysis of human intestinal development at single-cell resolution

    doi: 10.1016/j.cell.2020.12.016

    Figure Lengend Snippet:

    Article Snippet: STAR-FINDer Single Cell and Spatial Transcriptomics Data Portal , This study , https://simmonslab.shinyapps.io/FetalAtlasDataPortal.

    Techniques: Conjugation Assay, Recombinant, Saline, Modification, Plasmid Preparation, Gene Expression, RNAscope, Generated, Software