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Federation of European Neuroscience Societies synchrotron small-angle x-ray scattering
Synchrotron Small Angle X Ray Scattering, supplied by Federation of European Neuroscience Societies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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synchrotron small-angle x-ray scattering - by Bioz Stars, 2026-09

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Article Title: Quaternary structure of human, Drosophila melanogaster and Caenorhabditis elegans MFE-2 in solution from synchrotron small-angle X-ray scattering.
Article Snippet: journal homepage: www.FEBSLetters .org Quaternary structure of human, Drosophila melanogaster and Caenorhabditis elegans MFE-2 in solution from synchrotron small-angle X-ray scattering 0014-5793/$36.00 2013 Federation of European Biochemical Societies.

Article Title: Plasmodium falciparum Kelch13 and its artemisinin-resistant mutants assemble as hexamers in solution: a SAXS data-driven modelling study.
Article Snippet: Correspondence S. Bhattacharjee, 3D-FF, Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi 110067, India Tel: +919810125616, +911126738974 E-mails: souvik@jnu.ac.in, sbh174@gmail.com Website: https://www.jnu.ac.in/content/ souvik and F. Ashish, Council of Scientific and Industrial Research-Institute of Microbial Technology, Chandigarh 160036, India Tel: +911722880472/3 E-mail: ashgang@imtech.res.in

Article Title: Identification of a novel 'aggregation-prone'/'amyloidogenic determinant' peptide in the sequence of the highly amyloidogenic human calcitonin.
Article Snippet: 0014-5793/$36.0

Article Title: Structure and inhibition of N-acetylneuraminate lyase from methicillin-resistant Staphylococcus aureus.
Article Snippet: X-ray diffraction data were collected to 8 FEBS Letters (2016) a 2016 Federation of European Biochemical Societies 2.33 A, processed in the space group P212121, and solved by molecular replacement using the monomer of S. aureus N-acetylneuraminate lyase as the search model (PDB entry 4ahp) [15].

Article Title: The flexibility of a homeodomain transcription factor heterodimer and its allosteric regulation by DNA binding.
Article Snippet: doi:10.1111/febs.13801 Transcription factors are known to modify the DNA that they bind.. However, DNA can also serve as an allosteric ligand whose binding modifies the conformation of transcriptional regulators.. Here, we describe how heterodimer PBX1:PREP1, formed by proteins playing major roles in embryonic development and tumorigenesis, undergoes an allosteric transition upon DNA binding.

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Article Title: Polymorphism in disease-related apolipoprotein C-II amyloid fibrils: a structural model for rod-like fibrils.
Article Snippet: 2805The FEBS Journal 285 (2018) 2799–2812 a 2018 Federation of European Biochemical Societies nloaded from https://febs.onlinelibrary.w iley.com /doi/10.1111/febs.14517 by B irm ingham C ity U niversity, W iley O nline L ibrary on [22/05/2024]. .. See the T erm s and C onditions (https://onlinelibrary.w iley.com /term s-and-conditions) on W iley O nline L ibrary for rules of use; O A articles are governed by the applicable C reative C om m ons L icense 2806 The FEBS Journal 285 (2018) 2799–2812 a 2018 Federation of European Biochemical Societies explored, and simulated X-ray diffraction patterns were calculated and compared to the experimental diffraction data (Fig. 9). ..

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Transcriptome screening platform DRUG-seq2 identified chemical compounds for reversing skin fibrosis (A) Schematic of the drug screening process: fibroblasts isolated from pathological scar tissue of patients underwent chemical library treatment, followed by DRUG-seq2 transcriptional profiling. Bioinformatics-driven prioritization yielded lead compounds, with phenotype-reversing hits undergoing further functional validation. (B) Uniform manifold approximation and projection (UMAP) of DRUG-seq2 data from keloid fibroblasts treated with different compounds. (C) Circular heatmap depicting ssGSEA enrichment scores for compound-mediated modulation of fibrosis-associated gene signatures. (D) Bright-field microscopy of keloid fibroblasts treated with DMSO or Rottlerin (0.33, 1, and 3 μM; scale bars, 100 μm), with quantification of cell count. Relative mRNA expression of profibrotic markers ( COL1A1, COL3A1, ACTA2, CTGF ) and the cell proliferation marker MKI67 was determined by RT-qPCR ( n = 3). (E) Western blot analysis of COL1A1 and MMP1 protein expression in keloid fibroblasts exposed to graded concentrations of Rottlerin (0.33, 1, and 3 μM) ( n = 2). (F) RT-qPCR analysis of COL1A1, COL3A1 , and CTGF in keloid fibroblasts from six patients after treatment with Rottlerin at 3 μM ( n = 6). (G) SAR-guided structural optimization of Rottlerin yielding derivatives FR-1 to FR-12. (H) Screening of fibrosis-reversal efficacy among twelve distinct modified compounds (FR-1 to FR-12) at a uniform concentration of 2 μM via RT-qPCR quantification of COL1A1, COL3A1, and ACTA2 ( n = 3). Data are mean ± SD; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO by one-way ANOVA.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: Transcriptome screening platform DRUG-seq2 identified chemical compounds for reversing skin fibrosis (A) Schematic of the drug screening process: fibroblasts isolated from pathological scar tissue of patients underwent chemical library treatment, followed by DRUG-seq2 transcriptional profiling. Bioinformatics-driven prioritization yielded lead compounds, with phenotype-reversing hits undergoing further functional validation. (B) Uniform manifold approximation and projection (UMAP) of DRUG-seq2 data from keloid fibroblasts treated with different compounds. (C) Circular heatmap depicting ssGSEA enrichment scores for compound-mediated modulation of fibrosis-associated gene signatures. (D) Bright-field microscopy of keloid fibroblasts treated with DMSO or Rottlerin (0.33, 1, and 3 μM; scale bars, 100 μm), with quantification of cell count. Relative mRNA expression of profibrotic markers ( COL1A1, COL3A1, ACTA2, CTGF ) and the cell proliferation marker MKI67 was determined by RT-qPCR ( n = 3). (E) Western blot analysis of COL1A1 and MMP1 protein expression in keloid fibroblasts exposed to graded concentrations of Rottlerin (0.33, 1, and 3 μM) ( n = 2). (F) RT-qPCR analysis of COL1A1, COL3A1 , and CTGF in keloid fibroblasts from six patients after treatment with Rottlerin at 3 μM ( n = 6). (G) SAR-guided structural optimization of Rottlerin yielding derivatives FR-1 to FR-12. (H) Screening of fibrosis-reversal efficacy among twelve distinct modified compounds (FR-1 to FR-12) at a uniform concentration of 2 μM via RT-qPCR quantification of COL1A1, COL3A1, and ACTA2 ( n = 3). Data are mean ± SD; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Drug discovery, Isolation, Functional Assay, Biomarker Discovery, Microscopy, Cell Characterization, Expressing, Marker, Quantitative RT-PCR, Western Blot, Modification, Concentration Assay

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: Modified compound FR-1 retains fibrosis-reversal efficacy (A) Bright-field microscopy of keloid fibroblasts treated with DMSO or FR-1 (0.33, 1, and 3 μM; scale bars, 100 μm), with quantification of cell count. Relative mRNA expression of profibrotic markers ( COL1A1, COL3A1, ACTA2, CTGF ) and the cell proliferation marker MKI67 was determined by RT-qPCR ( n = 3). (B) Western blot analysis of COL1A1 and MMP1 protein expression in keloid fibroblasts exposed to graded concentrations of FR-1 (0.33, 1, and 3 μM) ( n = 2). (C) RT-qPCR analysis of COL1A1, COL3A1, ACTA2 , and CTGF in keloid fibroblasts from six patients after treatment with FR-1 at 3 μM ( n = 6). (D) Clustered heatmap analysis of fibrosis-related genes based on bulk RNA-seq. (E and F) Top 10 significantly downregulated GO terms in (E) Rottlerin- and (F) FR-1-treated groups relative to DMSO controls. (G) Enriched biological processes comparing FR-1 versus Rottlerin treatment. (H) Kinase inhibition profile of Rottlerin and FR-1. Data are mean ± SD, n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Modification, Microscopy, Cell Characterization, Expressing, Marker, Quantitative RT-PCR, Western Blot, RNA Sequencing, Inhibition

FR-1 attenuates established scars and preserves hair follicles in a murine linear excisional wound model (A) Schematic and timeline of the murine linear excisional wound model (1.5 × 0.2 cm wounds, 0.4 cm lateral to the midline). (B) Representative images of scar progression in vehicle-, FR-1-, TA-, and blank (surgery only)-treated groups at indicated time points (white boxes: scar areas; n = 10 scars from 5 mice per group). Quantification of (C) scar dynamic changes (line plots) and (D) scar area at day 12 (bar graph). (E) H&E-stained scar sections (scale bars, 1000 μm in low-power field, 200 μm in high-power field), (F) scar width quantification ( n = 5 mice). (G) Representative images of epidermal architecture in treated vs. normal skin (H&E; scale bars, 100 μm). Quantification of (H) epidermal thickness and (I) nuclear density ( n = 5 mice). (J) Hair follicle density ( n = 4 randomly selected representative high-power fields [HPFs] from 3 to 4 mice). (K) α-SMA/β-catenin co-staining (scale bars, 100 μm). Split channels (β-catenin, red; α-SMA, green) highlight follicular structures, and (L) correlation coefficients ( n = 4 HPFs from 2 to 3 mice). (M) Representative polarized light images of Sirius Red staining; separated type I (red) and type III (green) collagen signals are shown, along with corresponding vector field maps visualizing fiber orientation (scale bars, 50 μm). Quantification includes (N) type I/III collagen ratio ( n = 3 mice), (O) coherency index ( n = 6 HPFs), and (P) fiber angle distribution. (Q) Masson’s trichrome staining (scale bars, 500 μm) and (R) CVF analysis ( n = 5 mice). Note: “Blank” represents the baseline for untreated pathological scarring, “Vehicle” indicates the ointment base control, serving as the strict negative control to isolate pharmacological effects from baseline healing variation. Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant by one-way ANOVA.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: FR-1 attenuates established scars and preserves hair follicles in a murine linear excisional wound model (A) Schematic and timeline of the murine linear excisional wound model (1.5 × 0.2 cm wounds, 0.4 cm lateral to the midline). (B) Representative images of scar progression in vehicle-, FR-1-, TA-, and blank (surgery only)-treated groups at indicated time points (white boxes: scar areas; n = 10 scars from 5 mice per group). Quantification of (C) scar dynamic changes (line plots) and (D) scar area at day 12 (bar graph). (E) H&E-stained scar sections (scale bars, 1000 μm in low-power field, 200 μm in high-power field), (F) scar width quantification ( n = 5 mice). (G) Representative images of epidermal architecture in treated vs. normal skin (H&E; scale bars, 100 μm). Quantification of (H) epidermal thickness and (I) nuclear density ( n = 5 mice). (J) Hair follicle density ( n = 4 randomly selected representative high-power fields [HPFs] from 3 to 4 mice). (K) α-SMA/β-catenin co-staining (scale bars, 100 μm). Split channels (β-catenin, red; α-SMA, green) highlight follicular structures, and (L) correlation coefficients ( n = 4 HPFs from 2 to 3 mice). (M) Representative polarized light images of Sirius Red staining; separated type I (red) and type III (green) collagen signals are shown, along with corresponding vector field maps visualizing fiber orientation (scale bars, 50 μm). Quantification includes (N) type I/III collagen ratio ( n = 3 mice), (O) coherency index ( n = 6 HPFs), and (P) fiber angle distribution. (Q) Masson’s trichrome staining (scale bars, 500 μm) and (R) CVF analysis ( n = 5 mice). Note: “Blank” represents the baseline for untreated pathological scarring, “Vehicle” indicates the ointment base control, serving as the strict negative control to isolate pharmacological effects from baseline healing variation. Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Staining, Plasmid Preparation, Ointment, Control, Negative Control

FR-1 attenuates fibrotic scarring and preserves hair follicles in a murine splinted excisional wound model (A and B) Schematic and timeline (A) of the murine splinted excisional wound model (silicone ring: 8/15 mm inner/outer diameter) (B). (C) Representative images of wound healing and scar formation progression (D0–D60) with vehicle or FR-1 treatment. (D) Quantification of wound/scar areas over time ( n = 6–10 scars from 3 to 5 mice per group). Representative (E) H&E (black lines mark scar width) and (F) Masson’s trichrome staining (scale bars, 500 μm; high-magnification H&E: 200 μm). (G) Quantification of hair follicle density ( n = 4 HPFs from 2 to 3 mice) and (H) CVF ( n = 3 mice). (I) β-catenin/α-SMA colocalization in scar tissue (day 60). Left: Representative IF images with split channels (β-catenin, red; α-SMA, green) (scale bars, 200 μm). Right: Scatterplots (diagonal distribution) and fluorescence intensity curves showing colocalization. (J) Pearson’s Rr and Overlap R coefficients ( n = 4 HPFs from 2 mice; Rr = 0.5–1.0, overlap R = 0.6–1.0 indicate colocalization). Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001 vs. vehicle by Student’s t test (D, G, and H) or by one-way ANOVA (J).

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: FR-1 attenuates fibrotic scarring and preserves hair follicles in a murine splinted excisional wound model (A and B) Schematic and timeline (A) of the murine splinted excisional wound model (silicone ring: 8/15 mm inner/outer diameter) (B). (C) Representative images of wound healing and scar formation progression (D0–D60) with vehicle or FR-1 treatment. (D) Quantification of wound/scar areas over time ( n = 6–10 scars from 3 to 5 mice per group). Representative (E) H&E (black lines mark scar width) and (F) Masson’s trichrome staining (scale bars, 500 μm; high-magnification H&E: 200 μm). (G) Quantification of hair follicle density ( n = 4 HPFs from 2 to 3 mice) and (H) CVF ( n = 3 mice). (I) β-catenin/α-SMA colocalization in scar tissue (day 60). Left: Representative IF images with split channels (β-catenin, red; α-SMA, green) (scale bars, 200 μm). Right: Scatterplots (diagonal distribution) and fluorescence intensity curves showing colocalization. (J) Pearson’s Rr and Overlap R coefficients ( n = 4 HPFs from 2 mice; Rr = 0.5–1.0, overlap R = 0.6–1.0 indicate colocalization). Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001 vs. vehicle by Student’s t test (D, G, and H) or by one-way ANOVA (J).

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Staining, Fluorescence

FR-1 suppresses keloid progression in patient-derived ex vivo and xenograft models (A) Keloid tissue explants were pre-cultured and subsequently treated with vehicle (DMSO), 1 μM FR-1, or 1 μM TA (designated as treatment day 0). (B) Representative micrographs illustrating cell outgrowth from the explants, captured at identical fields of view on treatment days 0, 2, 4, and 7 (Scale bars, 100 μm). (C) The number of migrated cells was quantified at treatment days 0, 2, 4, and 7 ( n = 3). (D) Schematic timeline of the experimental design. (E) Representative images of the surgical implantation and wound closure. (F) Macroscopic appearance of explanted grafts at day 63. (G) Scatterplot analysis of explanted graft volume from vehicle- and FR-1 (0.1 μM)-treated groups, measured by digital calipers and calculated as V = 0.5 × length × width 2 ( n = 3 mice). (H) Body weight changes of mice during the treatment period. Red arrows indicate injection time points ( n = 3 mice). (I) Representative H&E staining of explanted grafts at day 63. Stars indicate hyalinized collagen bundles; arrows indicate microvessels; arrowheads indicate representative inflammatory cells. Scale bars, 500 μm (left) and 200 μm (middle and right). (J) Representative immunohistochemical staining (scale bars, 100 μm) and (K) quantification of α-SMA at the graft-host interface ( n = 3 mice). Note: All xenografts were derived from the keloid tissue of a single patient donor. Data represent mean ± SEM; n represents the number of independent biological replicates, except for (C), where n represents technical replicates. ∗∗ p < 0.01; ns, not significant vs. vehicle by Student’s t test.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: FR-1 suppresses keloid progression in patient-derived ex vivo and xenograft models (A) Keloid tissue explants were pre-cultured and subsequently treated with vehicle (DMSO), 1 μM FR-1, or 1 μM TA (designated as treatment day 0). (B) Representative micrographs illustrating cell outgrowth from the explants, captured at identical fields of view on treatment days 0, 2, 4, and 7 (Scale bars, 100 μm). (C) The number of migrated cells was quantified at treatment days 0, 2, 4, and 7 ( n = 3). (D) Schematic timeline of the experimental design. (E) Representative images of the surgical implantation and wound closure. (F) Macroscopic appearance of explanted grafts at day 63. (G) Scatterplot analysis of explanted graft volume from vehicle- and FR-1 (0.1 μM)-treated groups, measured by digital calipers and calculated as V = 0.5 × length × width 2 ( n = 3 mice). (H) Body weight changes of mice during the treatment period. Red arrows indicate injection time points ( n = 3 mice). (I) Representative H&E staining of explanted grafts at day 63. Stars indicate hyalinized collagen bundles; arrows indicate microvessels; arrowheads indicate representative inflammatory cells. Scale bars, 500 μm (left) and 200 μm (middle and right). (J) Representative immunohistochemical staining (scale bars, 100 μm) and (K) quantification of α-SMA at the graft-host interface ( n = 3 mice). Note: All xenografts were derived from the keloid tissue of a single patient donor. Data represent mean ± SEM; n represents the number of independent biological replicates, except for (C), where n represents technical replicates. ∗∗ p < 0.01; ns, not significant vs. vehicle by Student’s t test.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Derivative Assay, Ex Vivo, Cell Culture, Injection, Staining, Immunohistochemical staining

The mode of action for FR-1’s fibrosis-reversal effects is mitochondrial uncoupling (A) RT-qPCR analysis of COL1A1, COL3A1 , and ACTA2 in human keloid fibroblasts after treatment with different PKC family inhibitors ( n = 3). (B) Mitochondrial membrane potential detection (TMRE) in keloid fibroblasts treated with increasing concentrations of FR-1 (scale bars, 200 μm, n = 4). (C) Mitochondrial uncoupling morphology detection and puncta quantification in human keloid fibroblasts treated with increasing concentrations of FR-1 (scale bars, 10 μm, n = 2). (D) ATP/ADP mass spectrometry detection following treatment of keloid fibroblasts with increasing concentrations of FR-1 ( n = 3). (E) Seahorse XF analysis of real-time oxygen consumption rate (OCR) profiles in fibroblasts treated with FR-1 or DMSO ( n = 4). (F) RT-qPCR analysis of fibrosis biomarkers in human keloid fibroblasts after treatment with different mitochondrial uncoupling compounds, FCCP and BAM15 ( n = 3). (G) Mitochondrial membrane potential detection in keloid fibroblasts treated with different mitochondrial uncoupling compounds (scale bars, 200 μm, n = 4). (H) RT-qPCR analysis of fibrosis biomarkers in human keloid fibroblasts after overexpression of mitochondrial uncoupling proteins ( n = 3). Data are mean ± SD; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO or vector by one-way ANOVA.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: The mode of action for FR-1’s fibrosis-reversal effects is mitochondrial uncoupling (A) RT-qPCR analysis of COL1A1, COL3A1 , and ACTA2 in human keloid fibroblasts after treatment with different PKC family inhibitors ( n = 3). (B) Mitochondrial membrane potential detection (TMRE) in keloid fibroblasts treated with increasing concentrations of FR-1 (scale bars, 200 μm, n = 4). (C) Mitochondrial uncoupling morphology detection and puncta quantification in human keloid fibroblasts treated with increasing concentrations of FR-1 (scale bars, 10 μm, n = 2). (D) ATP/ADP mass spectrometry detection following treatment of keloid fibroblasts with increasing concentrations of FR-1 ( n = 3). (E) Seahorse XF analysis of real-time oxygen consumption rate (OCR) profiles in fibroblasts treated with FR-1 or DMSO ( n = 4). (F) RT-qPCR analysis of fibrosis biomarkers in human keloid fibroblasts after treatment with different mitochondrial uncoupling compounds, FCCP and BAM15 ( n = 3). (G) Mitochondrial membrane potential detection in keloid fibroblasts treated with different mitochondrial uncoupling compounds (scale bars, 200 μm, n = 4). (H) RT-qPCR analysis of fibrosis biomarkers in human keloid fibroblasts after overexpression of mitochondrial uncoupling proteins ( n = 3). Data are mean ± SD; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; ns, not statistically significant vs. DMSO or vector by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

Techniques: Quantitative RT-PCR, Membrane, Mass Spectrometry, Over Expression, Plasmid Preparation

Mitochondrial uncoupling by FCCP also attenuates skin fibrosis (A) Schematic and timeline for assessing mitochondrial uncoupling in the murine linear excisional wound model. (B) Representative scar images (white boxes: scar margins) from vehicle-, FR-1-, and FCCP-treated mice at indicated time points. (C) Scar area quantification on day 16 ( n = 10 scars from 5 mice per group). Representative (D) H&E staining (black lines: scar width, scale bars, 500 μm) and (E) Masson’s trichrome staining (scale bars, 500 μm) of scar tissues. Quantitative data of (F) scar width ( n = 4 mice) and (G) CVF analysis ( n = 5 mice). (H) Schematic and timeline of the murine splinted excisional wound model. (I) Representative images of wound healing and scar formation progression (D0–D60) with vehicle, FR-1, or FCCP treatment. (J) Quantification of wound/scar areas over time (n = 6–10 scars from 3 to 5 mice per group). Representative (K) H&E staining (scale bars, 500 μm; black lines mark scar width) and (L) Masson’s trichrome staining (scale bars, 200 μm). (M) Quantification of CVF ( n = 3–4 mice). (N) Schematic diagram illustrating the mechanism by which FR-1 reverses fibrosis through promoting mitochondrial uncoupling. Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ns, not statistically significant vs. vehicle by one-way ANOVA.

Journal: Cell Reports Medicine

Article Title: Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling

doi: 10.1016/j.xcrm.2026.102821

Figure Lengend Snippet: Mitochondrial uncoupling by FCCP also attenuates skin fibrosis (A) Schematic and timeline for assessing mitochondrial uncoupling in the murine linear excisional wound model. (B) Representative scar images (white boxes: scar margins) from vehicle-, FR-1-, and FCCP-treated mice at indicated time points. (C) Scar area quantification on day 16 ( n = 10 scars from 5 mice per group). Representative (D) H&E staining (black lines: scar width, scale bars, 500 μm) and (E) Masson’s trichrome staining (scale bars, 500 μm) of scar tissues. Quantitative data of (F) scar width ( n = 4 mice) and (G) CVF analysis ( n = 5 mice). (H) Schematic and timeline of the murine splinted excisional wound model. (I) Representative images of wound healing and scar formation progression (D0–D60) with vehicle, FR-1, or FCCP treatment. (J) Quantification of wound/scar areas over time (n = 6–10 scars from 3 to 5 mice per group). Representative (K) H&E staining (scale bars, 500 μm; black lines mark scar width) and (L) Masson’s trichrome staining (scale bars, 200 μm). (M) Quantification of CVF ( n = 3–4 mice). (N) Schematic diagram illustrating the mechanism by which FR-1 reverses fibrosis through promoting mitochondrial uncoupling. Data are mean ± SEM; n represents the number of independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ns, not statistically significant vs. vehicle by one-way ANOVA.

Article Snippet: Single-crystal X-ray diffraction data collection of compound FR-1 , The Cambridge Crystallographic Data Center (CCDC) , CCDC: 2498324.

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