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Image Search Results
Journal: Regenerative Biomaterials
Article Title: Improved the biocompatibility of cancellous bone with compound physicochemical decellularization process
doi: 10.1093/rb/rbaa024
Figure Lengend Snippet: Number of MSCs cultured on scaffolds after 1, 3, 5 and 7 days, which show the proliferation of MSCs on scaffolds. (* P < 0.05 vs DCB# P < 0.05 vs MC1). cells seeded on CB were not detected, the number of cells significantly larger on the DCB and MC1 than that on MC2.
Article Snippet:
Techniques: Cell Culture
Journal: Regenerative Biomaterials
Article Title: Improved the biocompatibility of cancellous bone with compound physicochemical decellularization process
doi: 10.1093/rb/rbaa024
Figure Lengend Snippet: SEM Images show the MSCs cultured on fresh CB, DCB and MC1 after 7 days. ( a , b) Fresh CB, ( c , d) DCB, and ( e , f) MC1, ×500 and ×1000 magnification. No cell adhesion was found in CB group. Cells grew well in DCB and MC1 group.
Article Snippet:
Techniques: Cell Culture
Journal: ACS biomaterials science & engineering
Article Title: Automated Addressable Microfluidic Device for Minimally Disruptive Manipulation of Cells and Fluids within Living Cultures.
doi: 10.1021/acsbiomaterials.9b01969
Figure Lengend Snippet: Figure 9. Minimally-disruptive additive cell manipulations within the Culture Chamber of the device. (A) Fluorescence panorama showing MSCs (green) seeded in a square pattern, with NIH/3T3s (red) in its center. Pane size is ~4.5 x 4.5 mm. (B) Bright field microscopy image showing the ability to trap and manipulate a single cell (red arrow) at a time.
Article Snippet: Mouse Bone Marrow-Derived
Techniques: Fluorescence, Microscopy
Journal: bioRxiv
Article Title: A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform
doi: 10.1101/2025.08.01.667725
Figure Lengend Snippet: A. Bar graph depicting human transcription factors grouped by family; those selected for HA-tagged expression and genomic studies in hMSCs are indicated. B. Heatmap displaying the z-score normalized RPKM occupancies of HA-tagged TFs (as shown on top in colored boxes), SMARCA4, and DNA accessibility (ATAC-Seq) at all merged SMARCA4 and ATAC-Seq sites across all samples. Z-scores were calculated for each experiment individually prior to grouping of columns by cell lines for data visualization. Unguided hierarchical clustering was performed on using z-score normalized values for HA-TF CUT&RUN, which identified 18 distinct clusters as shown on the right. C. Representative site showing TF-dependent mSWI/SNF localization and accessibility at the CCRL2 locus. RPKM-normalized enrichment of HA-tagged PU.1, SMARCA4, H3K27ac, DNA accessibility (ATAC-Seq) and gene expression (RNA-Seq) are shown. D. GLMnet motif enrichment analysis was performed to identify top TF motifs underlying SMARCA4 peaks that displaying gain of SMARCA4 enrichment (in red) and loss of enrichment (in blue) upon TF overexpression. E. Scatterplots displaying the correlation between change in SMARCA4 occupancy (x-axis) and DNA accessibility measured by ATAC-Seq (Y-axis) in MSCs expressing PU.1 compared to empty vector. Color key indicates PU.1 RPKM enrichment (top panel), number of PU.1-motifs (middle panel) and number of AP.1 motifs (lower panel). F. Bar chart displaying Pearson correlation coefficients (r) for the correlation between changes in SMARCA4 occupancies and HA-tagged transcription factor occupancies in hMSC cell lines expressing the TF indicated on X-axis. PU.1 and GATA3 were top-ranked TFs for their ability to guide SMARCA4 (mSWI/SNF complexes) to de novo TF motif-enriched target sites on chromatin.
Article Snippet: Human ASC52telo,
Techniques: Expressing, Gene Expression, RNA Sequencing, Over Expression, Plasmid Preparation
Journal: bioRxiv
Article Title: A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform
doi: 10.1101/2025.08.01.667725
Figure Lengend Snippet: A. Schematic for in vitro incubation experiments using endogenous, fully-assembled human cBAF complexes and full-length human PU.1. Domains within PU.1 are indicated. B. SMARCA4 pulldown experiments performed with 2.5 µg of purified cBAF incubated with 10-fold molar excess of PU.1 wild-type or PU.1 deltAD (delaa1-160). C. (Top) schematic for HA-tagged PU.1 variants introduced into human MSCs for PU.1 and SMARCA4 ChIP-seq experiments; (Bottom) heatmaps depicting PU.1 and SMARCA4 occupancy across all merged SMARCA4 sites in empty vector, and PU.1 WT, delDBD, and delTAD variant conditions. PU.1-specific target sites are indicated. D. Schematic for mass-spec-based GEE protein footprinting experiments performed with endogenous human cBAF complexes and full-length PU.1. E. cBAF peptides displaying GEE-labeling changes were mapped onto the 3D structure of NCP-bound cBAF, with SMARCD1 modeled with AlphaFold2 and superimposed on PDB:6LTJ. F. Bar charts across mSWI/SNF SMARCD and SMARCC subunits depicting %GEE labeling change upon incubation with NCP (top) or PU.1 (bottom). G. (Top), schematic depicting mSWI/SNF complexes with a stable and independently assembled core upon removal of the ATPase subunits; (bottom) Expression of HA-tagged PU.1 or GATA3 TFs in SMARCA4/SMARCA2 dual-deficient HEK-293T cells results in mSWI/SNF complex interactions. H. Heatmaps depicting occupancy of mSWI/SNF complexes (SMARCC1, SMARCA4) with and without expression of HA-tagged TFs PU.1 and GATA3. I. HOMER motif analyses performed on SMARCA4 sites gained in the setting of TF overexpression.
Article Snippet: Human ASC52telo,
Techniques: In Vitro, Incubation, Purification, ChIP-sequencing, Plasmid Preparation, Variant Assay, Mass Spectrometry, Protein Footprinting, Labeling, Expressing, Over Expression
Journal: The Journal of Pathology
Article Title: Genomic profiling identifies genes and pathways dysregulated by HEY1–NCOA2 fusion and shines a light on mesenchymal chondrosarcoma tumorigenesis
doi: 10.1002/path.5899
Figure Lengend Snippet: Schematic diagrams of HEY1, NCOA2, and HEY1–NCOA2 chimeric proteins and their intracellular localization, as well as the induced expression of FLAG‐tagged HEY1, NCOA2, and HEY1–NCOA2 in the iPSC‐MSCs cell models. (A) Schematic diagrams of HEY1, NCOA2, and HEY1–NCOA2 proteins. Dashed lines represent exon–exon borders. Only coding exons are presented. (B) The mEGFP‐HEY1 , mEGFP‐NCOA2 , and mEGFP‐HEY1–NCOA2 constructs as well as the empty vector were introduced into iPSC MSC cells transiently and photographed at 24 h. The first row shows the direct EGFP fluorescence, the second row shows Hoechst staining of DNA, and the third row shows the merged image indicating the intracellular localization. Bars, 20 μm. (C) Immunoblot using anti‐Flag antibody showed the induced expression of FLAG‐tagged HEY1–NCOA2, HEY1, and NCOA2 in stably transduced iPSC‐MSCs.
Article Snippet: The human cell lines HEK293T (CRL3216) and
Techniques: Expressing, Construct, Plasmid Preparation, Fluorescence, Staining, Western Blot, Stable Transfection
Journal: The Journal of Pathology
Article Title: Genomic profiling identifies genes and pathways dysregulated by HEY1–NCOA2 fusion and shines a light on mesenchymal chondrosarcoma tumorigenesis
doi: 10.1002/path.5899
Figure Lengend Snippet: Gene expression profile associated with HEY1–NCOA2. (A) Heatmap showing row‐normalized expression level of genes differentially regulated by HEY1‐NCOA2 in comparison to wildtype HEY1 [MSC‐HEY1‐NCOA2(+) versus MSC‐HEY1(+)]. (B) GSEA Enrichment plot of the expression of genes that were identified as downregulated by HEY1 in MSC‐HEY1(+) versus MSC‐HEY1 ctrl . The gene rank was based on the log2(fold‐change) of the expression of genes in MSC‐HEY1‐NCOA2(+) versus MSC‐HEY1‐NCOA2 ctrl . (C) GSEA enrichment plot for the expression of genes of which their promoters had binding peaks of both HEY1 and HEY1–NCOA2. The gene rank was based on the log2(fold‐change) of the gene expression in MSC‐HEY1‐NCOA2(+) versus MSC‐HEY1(+). (D) Boxplots visualizing the enrichment of the 674 HEY1–NCOA2 direct‐target‐and‐transactivating genes identified using the iPSC‐MSCs cell models in sarcoma tumor samples. The enrichment was visualized across patients' samples from a total of eight sarcoma entities. GSEA, Gene Set Enrichment Analysis; NES, Normalized Enrichment Score; FDR, False Discovery Rate; MCS, Mesenchymal Chondrosarcoma; GIST, Gastrointestinal Stromal tumor; RHB, Rhabdomyosarcoma; IFS, Infantile Fibrosarcoma; ASPS, Alveolar Soft Part Sarcoma; SS, Synovial Sarcoma; DSRCT, Desmoplastic Small Round Cell Tumors; EWS, Ewing's Sarcoma.
Article Snippet: The human cell lines HEK293T (CRL3216) and
Techniques: Gene Expression, Expressing, Comparison, Binding Assay
Journal: The Journal of Pathology
Article Title: Genomic profiling identifies genes and pathways dysregulated by HEY1–NCOA2 fusion and shines a light on mesenchymal chondrosarcoma tumorigenesis
doi: 10.1002/path.5899
Figure Lengend Snippet: HEY1–NCOA2 target gene expression validation. (A) RT‐qPCR validation of genes regulation by inducible HEY1, NCOA2, or HEY1–NCOA2 expression in iPSC MSC. The graph represents the fold change between the induced and uninduced condition. (B) Immunoblotting was performed to further confirm the expression of BCL2, CCND1, and HES1 after HEY1–NCOA2 induction in stably transduced iPSC‐MSCs. GAPDH was used as a loading control.
Article Snippet: The human cell lines HEK293T (CRL3216) and
Techniques: Targeted Gene Expression, Biomarker Discovery, Quantitative RT-PCR, Expressing, Western Blot, Stable Transfection, Control
Journal: The Journal of Pathology
Article Title: Genomic profiling identifies genes and pathways dysregulated by HEY1–NCOA2 fusion and shines a light on mesenchymal chondrosarcoma tumorigenesis
doi: 10.1002/path.5899
Figure Lengend Snippet: HEY1‐NCOA2 significantly increases cell proliferation in iPSC‐MSC. (A) 1 × 10 5 of FACS sorted GFP+ iPSC‐MSCs were seeded with or without doxycycline (50 ng/ml). Cell numbers were counted on days 6 and 12; the graph shows the mean ± SD ( n = 3). (B) GFP+ iPSC‐MSCs were cultured with or without doxycycline (50 ng/ml) for 7 days and labeled with 10 μM of EdU for 3 h. Cells were then harvested, fixed, and stained with fluorescent dye 647 picolyl azide. EdU was detected by flow cytometry and the percentage of cells in S‐phase was analyzed using FlowJo software. The graph shows the mean ± SD ( n = 2). (C) FACS‐sorted GFP+ iPSC‐MSCs were cultured as in panel A except without addition of rh‐FGF basic and rh‐IGF‐1 to the culture medium. Cell numbers were counted on day 7; the graph shows the mean ± SD ( n = 3).
Article Snippet: The human cell lines HEK293T (CRL3216) and
Techniques: Cell Culture, Labeling, Staining, Flow Cytometry, Software
Journal: Stem Cell Research & Therapy
Article Title: Empagliflozin-pretreated BMSC exosomes attenuate myocardial ischemia-reperfusion injury by enhancing atad3a/pink1-dependent mitophagy
doi: 10.1186/s13287-025-04715-6
Figure Lengend Snippet: EMPA Enhanced Exosome Biogenesis in BMSCs. A , B Exosome particle and protein concentration. C EMPA upregulated key exosome biogenesis regulators: Alix, nSMase2, RAB27a
Article Snippet:
Techniques: Protein Concentration