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ATCC human bone osteosarcoma cells
Human Bone Osteosarcoma Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 2486 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human bone osteosarcoma cells/product/ATCC
Average 98 stars, based on 2486 article reviews

human bone osteosarcoma cells - by Bioz Stars, 2026-05

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(A) Schematic representation of the time-of-drug-addition assay. U2OS cells were treated with (B) 2 µM JG98 or (C) 1 µM JG345 at the indicated time points (conditions 1-8) or with the DMSO control. Virus inoculum (CHIKV-LR at MOI 1) was present for 1.5 h, after which the inoculum was removed, and fresh medium was added with or without the Hsp70 inhibitors or DMSO control. At 9 hpi, the infectious virus particle production was assessed using the plaque assay. Data are presented as mean±SEM from at least three independent experiments. One-way ANOVA was used to evaluate statistical differences from the non-treated control and was presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: (A) Schematic representation of the time-of-drug-addition assay. U2OS cells were treated with (B) 2 µM JG98 or (C) 1 µM JG345 at the indicated time points (conditions 1-8) or with the DMSO control. Virus inoculum (CHIKV-LR at MOI 1) was present for 1.5 h, after which the inoculum was removed, and fresh medium was added with or without the Hsp70 inhibitors or DMSO control. At 9 hpi, the infectious virus particle production was assessed using the plaque assay. Data are presented as mean±SEM from at least three independent experiments. One-way ANOVA was used to evaluate statistical differences from the non-treated control and was presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Article Snippet: The human bone osteosarcoma epithelial cell line U2OS (ATCC HTB-96) and human foreskin fibroblast cell line HFF-1 (ATCC SCRC-1041) were maintained in Dulbecco’s minimal essential medium (DMEM), high glucose, GlutaMAX tm, and sodium pyruvate (Gibco), supplemented with penicillin-streptomycin (P/S; 100U/mL, Gibco) and 10% or 15% fetal bovine serum (FBS, Lonza), respectively.

Techniques: Control, Virus, Plaque Assay

(A) U2OS cells were treated with increasing concentrations of the Hsp70 inhibitors or the equivalent volume of the DMSO control. The metabolic activity of the cells was assessed after 16 hours (h) of treatment using the MTS assay and was normalized to the DMSO control. A decrease of 15% in metabolically active cells was considered non-toxic (dotted line represents 85%). (B-F) U2OS cells were infected with CHIKV-LR OPY1 at multiplicity of infection (MOI) 1 in the presence of increasing concentrations of the (B) DMSO control (0.002% matches 0.1 µM JG-compound, 0.01% DMSO matches 0.5 µM JG-compound, etc.) or the Hsp70 inhibitors concentrations of (C) JG18, (D) JG40, (E) JG98, (F) JG345. Supernatants were collected at 9 hpi, and the number of infectious CHIKV particles was quantified using plaque assay on Vero-WHO cells. (B-F) Percentage inhibition was determined relative to the DMSO control, and IC50 (which corresponds to a 50% reduction in viral titer) per Hsp70 inhibitor was determined via non-linear regression. Data are presented as mean±SEM from three independent experiments. (B) Statistical differences were determined using One-way ANOVA and were presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: (A) U2OS cells were treated with increasing concentrations of the Hsp70 inhibitors or the equivalent volume of the DMSO control. The metabolic activity of the cells was assessed after 16 hours (h) of treatment using the MTS assay and was normalized to the DMSO control. A decrease of 15% in metabolically active cells was considered non-toxic (dotted line represents 85%). (B-F) U2OS cells were infected with CHIKV-LR OPY1 at multiplicity of infection (MOI) 1 in the presence of increasing concentrations of the (B) DMSO control (0.002% matches 0.1 µM JG-compound, 0.01% DMSO matches 0.5 µM JG-compound, etc.) or the Hsp70 inhibitors concentrations of (C) JG18, (D) JG40, (E) JG98, (F) JG345. Supernatants were collected at 9 hpi, and the number of infectious CHIKV particles was quantified using plaque assay on Vero-WHO cells. (B-F) Percentage inhibition was determined relative to the DMSO control, and IC50 (which corresponds to a 50% reduction in viral titer) per Hsp70 inhibitor was determined via non-linear regression. Data are presented as mean±SEM from three independent experiments. (B) Statistical differences were determined using One-way ANOVA and were presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Techniques: Control, Activity Assay, MTS Assay, Metabolic Labelling, Infection, Plaque Assay, Inhibition

U2OS cells were infected with the (A) African S27 CHIKV strain or the (B) Caribbean 99659 strain at MOI 1 and simultaneously treated with 10 µM, 10 µM, 2 µM, or 1 µM of JG18, JG40, JG98, or JG345, respectively, or the DMSO control. Production of infectious virus particles was assessed at 9 hpi. (C) U2OS cells were infected with DENV A2 (16681) at MOI 0.5 and treated with 10 µM JG18 or JG40, or the vehicle control. 24 hpi, supernatants were collected and DENV progeny production was analyzed via plaque assay on BHK-21 cells. Data are presented as mean±SEM from three independent experiments, and statistical differences were determined via one-way ANOVA and presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: U2OS cells were infected with the (A) African S27 CHIKV strain or the (B) Caribbean 99659 strain at MOI 1 and simultaneously treated with 10 µM, 10 µM, 2 µM, or 1 µM of JG18, JG40, JG98, or JG345, respectively, or the DMSO control. Production of infectious virus particles was assessed at 9 hpi. (C) U2OS cells were infected with DENV A2 (16681) at MOI 0.5 and treated with 10 µM JG18 or JG40, or the vehicle control. 24 hpi, supernatants were collected and DENV progeny production was analyzed via plaque assay on BHK-21 cells. Data are presented as mean±SEM from three independent experiments, and statistical differences were determined via one-way ANOVA and presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Techniques: Infection, Control, Virus, Plaque Assay

U2OS cells were treated with 2 µM JG98, 1 µM JG345, or the DMSO control during CHIKV infection at MOI 10. Virus production was measured at 9 hpi using a plaque assay. Data are presented as mean±SEM from at least three independent experiments. One-way ANOVA was used to evaluate statistical differences from the DMSO control and was presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: U2OS cells were treated with 2 µM JG98, 1 µM JG345, or the DMSO control during CHIKV infection at MOI 10. Virus production was measured at 9 hpi using a plaque assay. Data are presented as mean±SEM from at least three independent experiments. One-way ANOVA was used to evaluate statistical differences from the DMSO control and was presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Techniques: Control, Infection, Virus, Plaque Assay

(A) The total intracellular vRNA and (B) genomic vRNA copy number were assessed at 4, 6, and 8 hpi in U2OS cells infected with CHIKV at MOI 10 and treated with vehicle control DMSO or 2μM JG98. Intracellular vRNA copies were quantified by RT-qPCR using specific primers against (A) E1 and (B) nsP1. (C) The number of subgenomic RNA copies was determined by subtracting the genomic vRNA copies from the total vRNA copies. Data is presented as mean ± SEM from at least three independent experiments. Student T-test was used to evaluate statistical differences from the DMSO control per timepoint and were presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: (A) The total intracellular vRNA and (B) genomic vRNA copy number were assessed at 4, 6, and 8 hpi in U2OS cells infected with CHIKV at MOI 10 and treated with vehicle control DMSO or 2μM JG98. Intracellular vRNA copies were quantified by RT-qPCR using specific primers against (A) E1 and (B) nsP1. (C) The number of subgenomic RNA copies was determined by subtracting the genomic vRNA copies from the total vRNA copies. Data is presented as mean ± SEM from at least three independent experiments. Student T-test was used to evaluate statistical differences from the DMSO control per timepoint and were presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Techniques: Infection, Control, Quantitative RT-PCR

Gating strategy to determine the percentage of cells positive for CHIKV E2 and capsid expression in U2OS cells treated with JG98, JG345, or the DMSO control. (A) Gating for cells and exclusion of doublets. (B and C) Gating to determine the percentage of cells positive for (B) capsid and (C) E2 based on mock-infected cells.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: Gating strategy to determine the percentage of cells positive for CHIKV E2 and capsid expression in U2OS cells treated with JG98, JG345, or the DMSO control. (A) Gating for cells and exclusion of doublets. (B and C) Gating to determine the percentage of cells positive for (B) capsid and (C) E2 based on mock-infected cells.

Techniques: Expressing, Control, Infection

(A-D) U2OS cells were infected with CHIKV at MOI 10 and treated with JG98 (2μM), JG345 (1μM), or the DMSO control. At 9hpi, E2 and capsid expression were assessed using flow cytometry to determine the (A and C) percentage of positive cells and (B and D) mean fluorescent intensity (MFI; geometric mean). (E and F) Representative western blot of capsid, E2, or vinculin expression from protein lysates of U2OS cells infected with CHIKV at MOI 10 and treated for 9 h with Hsp70 inhibitor JG-98 (2μM), JG-345 (1μM), or the DMSO control. (G and H) Quantification of Western blots from three independent experiments. Protein levels are normalized to vinculin and are expressed as relative protein level to vehicle control DMSO. Data are presented as mean±SEM from at least three independent experiments. One-way ANOVA was used to evaluate statistical differences from the DMSO control and was presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: (A-D) U2OS cells were infected with CHIKV at MOI 10 and treated with JG98 (2μM), JG345 (1μM), or the DMSO control. At 9hpi, E2 and capsid expression were assessed using flow cytometry to determine the (A and C) percentage of positive cells and (B and D) mean fluorescent intensity (MFI; geometric mean). (E and F) Representative western blot of capsid, E2, or vinculin expression from protein lysates of U2OS cells infected with CHIKV at MOI 10 and treated for 9 h with Hsp70 inhibitor JG-98 (2μM), JG-345 (1μM), or the DMSO control. (G and H) Quantification of Western blots from three independent experiments. Protein levels are normalized to vinculin and are expressed as relative protein level to vehicle control DMSO. Data are presented as mean±SEM from at least three independent experiments. One-way ANOVA was used to evaluate statistical differences from the DMSO control and was presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Techniques: Infection, Control, Expressing, Flow Cytometry, Western Blot

U2OS cells were infected with the (A-C, G-I) CHIKV-LR or the (D-F) CHIKV S27 strain for 9 h in the presence of (A-F) 2 µM JG98, 1 µM JG345, (G-I) 20 µM VER-155008, or the DMSO control. Supernatants were collected and the number of (A, D, and G) infectious particles and (B, E, and H) secreted genome equivalent copies (GECs) were measured using plaque assay and RT-qPCR, respectively. (C, F, and I) Specific infectivity is depicted as the ratio between produced infectious particles and GECs. Data are presented as mean± SEM from three independent experiments. One-way ANOVA was used to evaluate statistical differences from the DMSO control and was given when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: U2OS cells were infected with the (A-C, G-I) CHIKV-LR or the (D-F) CHIKV S27 strain for 9 h in the presence of (A-F) 2 µM JG98, 1 µM JG345, (G-I) 20 µM VER-155008, or the DMSO control. Supernatants were collected and the number of (A, D, and G) infectious particles and (B, E, and H) secreted genome equivalent copies (GECs) were measured using plaque assay and RT-qPCR, respectively. (C, F, and I) Specific infectivity is depicted as the ratio between produced infectious particles and GECs. Data are presented as mean± SEM from three independent experiments. One-way ANOVA was used to evaluate statistical differences from the DMSO control and was given when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Techniques: Infection, Control, Plaque Assay, Quantitative RT-PCR, Produced

Metabolic activity of the U2OS cells was assessed after 16 hours of treatment with increasing concentrations of the VER155008 or the equivalent volume of the DMSO control. The percentage of metabolically active cells relative to the DMSO control. A decrease of 15% in metabolically active cells was considered non-toxic (dotted line represents 85%). Data are presented as mean±SEM from three independent experiments.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: Metabolic activity of the U2OS cells was assessed after 16 hours of treatment with increasing concentrations of the VER155008 or the equivalent volume of the DMSO control. The percentage of metabolically active cells relative to the DMSO control. A decrease of 15% in metabolically active cells was considered non-toxic (dotted line represents 85%). Data are presented as mean±SEM from three independent experiments.

Techniques: Activity Assay, Control, Metabolic Labelling

Metabolic activity of (A) U2OS and (B) HFF-1 cells was assessed after 16 h of treatment with increasing concentrations of JG231 or the equivalent volume of the DMSO control. The percentage of metabolically active cells is presented relative to the DMSO control. A decrease of 15% in metabolically active cells was considered non-toxic (dotted line represents 85%). (C) U2OS cells and (D) HFF-1 cells were infected with CHIKV-LR for 9 h in the presence of 2 µM JG231 or the DMSO control. Supernatants were collected, and the number of infectious particles in the supernatant was determined using the plaque assay. (E and F) Mouse skin explants were infected with 10 6 PFU/mL of the CHIKV 899 strain during treatment with 2 µM JG231 or an equal volume of DMSO. (E) Infectious virus production (tissue culture infectious dose 50% (TCID 50 )) and (F) total virus production (GEC) at 2 dpi is displayed per mg tissue. The dotted line indicates the limit of quantification (LOQ). To evaluate statistical differences from the DMSO control, we used a Student T-test, and differences are presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Journal: bioRxiv

Article Title: The Heat shock protein 70 machinery is crucial in the production of infectious chikungunya virus progeny

doi: 10.64898/2026.01.26.701664

Figure Lengend Snippet: Metabolic activity of (A) U2OS and (B) HFF-1 cells was assessed after 16 h of treatment with increasing concentrations of JG231 or the equivalent volume of the DMSO control. The percentage of metabolically active cells is presented relative to the DMSO control. A decrease of 15% in metabolically active cells was considered non-toxic (dotted line represents 85%). (C) U2OS cells and (D) HFF-1 cells were infected with CHIKV-LR for 9 h in the presence of 2 µM JG231 or the DMSO control. Supernatants were collected, and the number of infectious particles in the supernatant was determined using the plaque assay. (E and F) Mouse skin explants were infected with 10 6 PFU/mL of the CHIKV 899 strain during treatment with 2 µM JG231 or an equal volume of DMSO. (E) Infectious virus production (tissue culture infectious dose 50% (TCID 50 )) and (F) total virus production (GEC) at 2 dpi is displayed per mg tissue. The dotted line indicates the limit of quantification (LOQ). To evaluate statistical differences from the DMSO control, we used a Student T-test, and differences are presented when p≤0.05 with *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.001.

Techniques: Activity Assay, Control, Metabolic Labelling, Infection, Plaque Assay, Virus

( A ) A schematic illustrates the process of LatA treatment assay in U2OS cell lines on nanostructures. ( B ) Average confocal images of LifeAct-mApple-expressed U2OS live cells cultured on nanobars ranging from 300 to 1000 nm in width demonstrate F-actin recovery following a 1 h treatment with 100 nM LatA and a 20 min washout. Scale bar, 2 μm. ( C ) Normalized actin signal density was calculated based on the actin intensity in the flat area, at nanobars ranging from 300–1000 nm in width. Sample sizes for treatments under DMSO, LatA and washout were N = 6, 6, and 8 averaged nanobar ends, respectively. Each data point represents the mean ± SEM. ( D ) The normalized actin repolymerization ratio (Washout/LatA) in ( C ) at nanobars ranging from 300–1000 nm in width. N = 8 averaged nanobars, each point represents mean ± SEM. ( E ) Original and averaged confocal images of U2OS fixed cells cultured on 300-nm-wide nanobars with the expression of mScarlet3-N-WASP and the staining with Phalloidin-ATTO-488. Cells were fixed after a 1 h treatment with DMSO, 20 or 50 μM ML141. Scale bar, 10 μm (left) and 1 μm (right). Contrast(averaged): 12–30. ( F ) Actin signal end-to-center ratio at nanobars 300 nm in width. Sample sizes for treatments under DMSO, 20 or 50 µM ML141 were N = 634, 324, 689 nanobar ends, respectively. Each data point represents the mean ± SD. (**** P < 0.0001). ( G ) mScarlet-N-WASP signal end-to-center ratio at nanobars 300 nm in width. Sample sizes for treatments under DMSO, 20 or 50 µM ML141 were N = 634, 324, 689 nanobar ends, respectively. Each data point represents the mean ± SD. ( H ) Average confocal images of U2OS cells cultured on nanobar arrays with bar widths ranging from 1000 to 300 nm, immuno-stained with anti-FBP17. Cells were treated with DMSO, 20 μM ML141, or 50 μM ML141. Scale bars: 2 μm. ( I ) Quantification of FBP17 intensity at nanobar ends across bar widths for each treatment condition in ( H ). Data represent mean ± SEM from N = 45–57 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). ( J ) Average confocal images of U2OS cells cultured on nanobar arrays with bar widths ranging from 1000 to 300 nm, stained with phalloidin-565. Cells were treated with DMSO, 20 μM ML141, or 50 μM ML141. Scale bars: 2 μm. ( K ) Quantification of Phalloidin-565(F-actin) intensity at nanobar ends across bar widths for each treatment condition in ( J ). Data represent mean ± SEM from N = 34–54 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. See also Fig. . .

Journal: The EMBO Journal

Article Title: Membrane curvature initiates Cdc42-FBP17-N-WASP clustering and actin nucleation

doi: 10.1038/s44318-025-00677-w

Figure Lengend Snippet: ( A ) A schematic illustrates the process of LatA treatment assay in U2OS cell lines on nanostructures. ( B ) Average confocal images of LifeAct-mApple-expressed U2OS live cells cultured on nanobars ranging from 300 to 1000 nm in width demonstrate F-actin recovery following a 1 h treatment with 100 nM LatA and a 20 min washout. Scale bar, 2 μm. ( C ) Normalized actin signal density was calculated based on the actin intensity in the flat area, at nanobars ranging from 300–1000 nm in width. Sample sizes for treatments under DMSO, LatA and washout were N = 6, 6, and 8 averaged nanobar ends, respectively. Each data point represents the mean ± SEM. ( D ) The normalized actin repolymerization ratio (Washout/LatA) in ( C ) at nanobars ranging from 300–1000 nm in width. N = 8 averaged nanobars, each point represents mean ± SEM. ( E ) Original and averaged confocal images of U2OS fixed cells cultured on 300-nm-wide nanobars with the expression of mScarlet3-N-WASP and the staining with Phalloidin-ATTO-488. Cells were fixed after a 1 h treatment with DMSO, 20 or 50 μM ML141. Scale bar, 10 μm (left) and 1 μm (right). Contrast(averaged): 12–30. ( F ) Actin signal end-to-center ratio at nanobars 300 nm in width. Sample sizes for treatments under DMSO, 20 or 50 µM ML141 were N = 634, 324, 689 nanobar ends, respectively. Each data point represents the mean ± SD. (**** P < 0.0001). ( G ) mScarlet-N-WASP signal end-to-center ratio at nanobars 300 nm in width. Sample sizes for treatments under DMSO, 20 or 50 µM ML141 were N = 634, 324, 689 nanobar ends, respectively. Each data point represents the mean ± SD. ( H ) Average confocal images of U2OS cells cultured on nanobar arrays with bar widths ranging from 1000 to 300 nm, immuno-stained with anti-FBP17. Cells were treated with DMSO, 20 μM ML141, or 50 μM ML141. Scale bars: 2 μm. ( I ) Quantification of FBP17 intensity at nanobar ends across bar widths for each treatment condition in ( H ). Data represent mean ± SEM from N = 45–57 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). ( J ) Average confocal images of U2OS cells cultured on nanobar arrays with bar widths ranging from 1000 to 300 nm, stained with phalloidin-565. Cells were treated with DMSO, 20 μM ML141, or 50 μM ML141. Scale bars: 2 μm. ( K ) Quantification of Phalloidin-565(F-actin) intensity at nanobar ends across bar widths for each treatment condition in ( J ). Data represent mean ± SEM from N = 34–54 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test. See also Fig. . .

Article Snippet: Homo sapiens bone osteosarcoma U2OS cells (ATCC) were maintained in DMEM with GlutaMAX (Gibco) supplemented medium with 10% fetal bovine serum (FBS) and 1% Penicillin/Streptomycin (PS).

Techniques: Cell Culture, Expressing, Staining

( A ) Representative confocal images of Lifeact-mApple-labeled actin filaments in cells treated with DMSO (control), LatA, or after LatA washout, cultured on flat surfaces (top row) or nanobar arrays (bottom row). White boxes in nanobar images indicate regions of interest (ROIs) corresponding to bar widths ranging from 300 to 1000 nm. Scale bars: 10 µm. Zoomed-in views of nanobar ROIs, highlighting actin alignment and curvature adaptation across different bar widths (300–1000 nm). ( B ) Original and averaged confocal images of U2OS fixed cells cultured on 300-nm-wide nanobars with the expression of mScarlet3-N-WASP and the staining with Phalloidin-ATTO-488. Cells were fixed after a 1 h treatment with 40 μM CK666. Scale bar, 10 μm (left) and 1 μm (right). Contrast(averaged): 12–30. ( C ) Normalized Actin signal end-to-center ratio at nanobars 300 nm in width. Sample sizes for treatments under DMSO, 20 or 50 µM ML141, 40 µM CK666 were N = 634, 324, 689, and 425 nanobar ends, respectively. Each data point represents the mean ± SEM. ( D ) Normalized mScarlet-N-WASP signal end-to-center ratio at nanobars 300 nm in width. Sample sizes for treatments under DMSO, 20 or 50 µM ML141, 40 µM CK666 were N = 634, 324, 689, and 425 nanobar ends, respectively. Each data point represents the mean ± SEM. Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test (ns p > 0.05, **** p < 0.0001).

Journal: The EMBO Journal

Article Title: Membrane curvature initiates Cdc42-FBP17-N-WASP clustering and actin nucleation

doi: 10.1038/s44318-025-00677-w

Figure Lengend Snippet: ( A ) Representative confocal images of Lifeact-mApple-labeled actin filaments in cells treated with DMSO (control), LatA, or after LatA washout, cultured on flat surfaces (top row) or nanobar arrays (bottom row). White boxes in nanobar images indicate regions of interest (ROIs) corresponding to bar widths ranging from 300 to 1000 nm. Scale bars: 10 µm. Zoomed-in views of nanobar ROIs, highlighting actin alignment and curvature adaptation across different bar widths (300–1000 nm). ( B ) Original and averaged confocal images of U2OS fixed cells cultured on 300-nm-wide nanobars with the expression of mScarlet3-N-WASP and the staining with Phalloidin-ATTO-488. Cells were fixed after a 1 h treatment with 40 μM CK666. Scale bar, 10 μm (left) and 1 μm (right). Contrast(averaged): 12–30. ( C ) Normalized Actin signal end-to-center ratio at nanobars 300 nm in width. Sample sizes for treatments under DMSO, 20 or 50 µM ML141, 40 µM CK666 were N = 634, 324, 689, and 425 nanobar ends, respectively. Each data point represents the mean ± SEM. ( D ) Normalized mScarlet-N-WASP signal end-to-center ratio at nanobars 300 nm in width. Sample sizes for treatments under DMSO, 20 or 50 µM ML141, 40 µM CK666 were N = 634, 324, 689, and 425 nanobar ends, respectively. Each data point represents the mean ± SEM. Statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparisons test (ns p > 0.05, **** p < 0.0001).

Techniques: Labeling, Control, Cell Culture, Expressing, Staining

( A ) Model of N-WASP activation by FBP17 (upper) and Cdc42 binding (lower). ( B ) Domain organization of FBP17, the HR1-deleted mutant (FdHR1), and the tip-to-tip oligomerization-deficient mutant (K166A). ( C ) Schematic and representative single-molecule imaging of FBP17 and K166A clustering (10% AF647 labeled). Scale bars, 1 μm. ( D ) Quantification of total intensity for FBP17 and K166A clusters. ( E ) Frequency distribution of total intensity for FBP17 and K166A clusters. ( F ) Average confocal images of U2OS cells seeded on nanobar arrays, expressing FBP17, FdHR1, or K166A. Scale bars, 2 μm. ( G ) Average confocal images of N-WASP recruitment in U2OS cells expressing FBP17, FdHR1, or K166A. Scale bars, 2 μm. ( H ) Average confocal images of phalloidin staining (F-actin) in U2OS cells expressing N-WASP with FBP17, FdHR1, or K166A. Scale bars, 2 μm. ( I ) Quantification of nanobar end-to-center ratio for FBP17, FdHR1, and K166A in ( F ). Data represent mean ± SEM from N = 22–64 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). ( J ) Quantification of nanobar end-to-center ratio for N-WASP in ( G ). Data represent mean ± SEM from N = 23–64 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). ( K ) Quantification of nanobar end-to-center ratio for phalloidin in ( H ). Data represent mean ± SEM from N = 20–70 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). Statistical analysis was performed using unpaired t -test or two-way ANOVA followed by Tukey’s multiple comparisons test. Outliers were identified and excluded using the ROUT method ( Q = 1%). .

Journal: The EMBO Journal

Article Title: Membrane curvature initiates Cdc42-FBP17-N-WASP clustering and actin nucleation

doi: 10.1038/s44318-025-00677-w

Figure Lengend Snippet: ( A ) Model of N-WASP activation by FBP17 (upper) and Cdc42 binding (lower). ( B ) Domain organization of FBP17, the HR1-deleted mutant (FdHR1), and the tip-to-tip oligomerization-deficient mutant (K166A). ( C ) Schematic and representative single-molecule imaging of FBP17 and K166A clustering (10% AF647 labeled). Scale bars, 1 μm. ( D ) Quantification of total intensity for FBP17 and K166A clusters. ( E ) Frequency distribution of total intensity for FBP17 and K166A clusters. ( F ) Average confocal images of U2OS cells seeded on nanobar arrays, expressing FBP17, FdHR1, or K166A. Scale bars, 2 μm. ( G ) Average confocal images of N-WASP recruitment in U2OS cells expressing FBP17, FdHR1, or K166A. Scale bars, 2 μm. ( H ) Average confocal images of phalloidin staining (F-actin) in U2OS cells expressing N-WASP with FBP17, FdHR1, or K166A. Scale bars, 2 μm. ( I ) Quantification of nanobar end-to-center ratio for FBP17, FdHR1, and K166A in ( F ). Data represent mean ± SEM from N = 22–64 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). ( J ) Quantification of nanobar end-to-center ratio for N-WASP in ( G ). Data represent mean ± SEM from N = 23–64 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). ( K ) Quantification of nanobar end-to-center ratio for phalloidin in ( H ). Data represent mean ± SEM from N = 20–70 averaged nanobar ends per bar width per condition (exact n values are provided in the Source Data). Statistical analysis was performed using unpaired t -test or two-way ANOVA followed by Tukey’s multiple comparisons test. Outliers were identified and excluded using the ROUT method ( Q = 1%). .

Techniques: Activation Assay, Binding Assay, Mutagenesis, Imaging, Labeling, Expressing, Staining

$a Sketch of an immunolabeled microtubule with primary and secondary antibodies. The secondary antibody is conjugated with a docking DNA strand complementary to the Cy3B-labeled imager strand. b Super-resolution and diffraction-limited images of the microtubule network of fixed U2OS cells obtained with the smartphone-based microscope. The super-resolved image represents the localization density, while the diffraction-limited image is the actual fluorescence intensity. Scale bar: 2 µm. c , d Comparison of super-resolved images of the microtubule network obtained with the smartphone-based setup ( c ) – a magnified image of the region marked in ( b ) - and with the high-end microscope ( d ). Scale bar: 2 µm. e Line profiles across super-resolved microtubules as indicated in ( c ) and ( d ). Black solid lines: smartphone-based microscope. Pink dashed lines: high-end microscope. In total, four different videos were obtained in which the immunolabeled microtubules could be resolved with the smartphone-based microscope. Source data are provided as a Source Data file.$

Journal: Nature Communications

Article Title: Direct single-molecule detection and super-resolution imaging with a low-cost portable smartphone-based microscope

doi: 10.1038/s41467-025-63993-z

Figure Lengend Snippet: a Sketch of an immunolabeled microtubule with primary and secondary antibodies. The secondary antibody is conjugated with a docking DNA strand complementary to the Cy3B-labeled imager strand. b Super-resolution and diffraction-limited images of the microtubule network of fixed U2OS cells obtained with the smartphone-based microscope. The super-resolved image represents the localization density, while the diffraction-limited image is the actual fluorescence intensity. Scale bar: 2 µm. c , d Comparison of super-resolved images of the microtubule network obtained with the smartphone-based setup ( c ) – a magnified image of the region marked in ( b ) - and with the high-end microscope ( d ). Scale bar: 2 µm. e Line profiles across super-resolved microtubules as indicated in ( c ) and ( d ). Black solid lines: smartphone-based microscope. Pink dashed lines: high-end microscope. In total, four different videos were obtained in which the immunolabeled microtubules could be resolved with the smartphone-based microscope. Source data are provided as a Source Data file.

Article Snippet: A human bone osteosarcoma epithelial (U2OS) cell culture with immunolabeled microtubules was purchased from Massive Photonics.

Techniques: Immunolabeling, Labeling, Microscopy, Fluorescence, Comparison

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