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Increased <t>LC3-II</t> expression and monolayer membrane-coated autophagosome formation in Beas2B cells following conidia infection. (A) Expression of LC3-I and LC3-II in Beas2B following infected by B5233 wild-type live conidia at 0, 2, 4, 6, 8, and 10 h. (B) Relative expression levels of LC3-I and LC3-II at the various time points. (C) Fluorescence microscopy images of GFP-LC3 (green), mCherry-labeled conidia (red), and DAPI staining (blue) in Beas2B cells following infected by conidia at 0, 4, 6, and 8 h. (D) Quantification of cells with LC3 + vesicles and average number of LC3 + vesicles per cell at 4, 6, and 8 h. (E) Electron microscopy images of cellular structural changes over time at 2, 4, 8, and 12 h. The magnification progressively increases from left to right, with each subsequent column of images depicting the area enclosed within the red box of the preceding image. The red arrow in each image points to the monolayer membrane encapsulating the A. fumigatus spores. * p < 0.05; ** p < 0.01; *** p < 0.001.
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Increased <t>LC3-II</t> expression and monolayer membrane-coated autophagosome formation in Beas2B cells following conidia infection. (A) Expression of LC3-I and LC3-II in Beas2B following infected by B5233 wild-type live conidia at 0, 2, 4, 6, 8, and 10 h. (B) Relative expression levels of LC3-I and LC3-II at the various time points. (C) Fluorescence microscopy images of GFP-LC3 (green), mCherry-labeled conidia (red), and DAPI staining (blue) in Beas2B cells following infected by conidia at 0, 4, 6, and 8 h. (D) Quantification of cells with LC3 + vesicles and average number of LC3 + vesicles per cell at 4, 6, and 8 h. (E) Electron microscopy images of cellular structural changes over time at 2, 4, 8, and 12 h. The magnification progressively increases from left to right, with each subsequent column of images depicting the area enclosed within the red box of the preceding image. The red arrow in each image points to the monolayer membrane encapsulating the A. fumigatus spores. * p < 0.05; ** p < 0.01; *** p < 0.001.
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The effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) The effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) The effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) The effect of miR-27a-5p on human renal cancer cell cycle. (D) The effect of miR-27a-5p on the expression of <t>LC3</t> protein in human renal cancer cells *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.
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The effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) The effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) The effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) The effect of miR-27a-5p on human renal cancer cell cycle. (D) The effect of miR-27a-5p on the expression of <t>LC3</t> protein in human renal cancer cells *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.
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The effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) The effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) The effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) The effect of miR-27a-5p on human renal cancer cell cycle. (D) The effect of miR-27a-5p on the expression of <t>LC3</t> protein in human renal cancer cells *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.
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The effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) The effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) The effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) The effect of miR-27a-5p on human renal cancer cell cycle. (D) The effect of miR-27a-5p on the expression of <t>LC3</t> protein in human renal cancer cells *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.
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The effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) The effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) The effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) The effect of miR-27a-5p on human renal cancer cell cycle. (D) The effect of miR-27a-5p on the expression of <t>LC3</t> protein in human renal cancer cells *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.
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HDAC8 PROTAC (1) decreased the expression of Bcl-2, an anti-apoptotic protein, in U-87 MG cells. Representative Western blots and bar graphs of HDAC8, Bcl-2, Bax and <t>LC3</t> compared to GAPDH after 72-h treatment with the HDAC8 PROTAC (1) , HDAC8i (2) , and pomalidomide (3) at 10 μM. Data are represented as the mean ± S.D. of five independent experiments. (*** p < 0.001).
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Image Search Results


Increased LC3-II expression and monolayer membrane-coated autophagosome formation in Beas2B cells following conidia infection. (A) Expression of LC3-I and LC3-II in Beas2B following infected by B5233 wild-type live conidia at 0, 2, 4, 6, 8, and 10 h. (B) Relative expression levels of LC3-I and LC3-II at the various time points. (C) Fluorescence microscopy images of GFP-LC3 (green), mCherry-labeled conidia (red), and DAPI staining (blue) in Beas2B cells following infected by conidia at 0, 4, 6, and 8 h. (D) Quantification of cells with LC3 + vesicles and average number of LC3 + vesicles per cell at 4, 6, and 8 h. (E) Electron microscopy images of cellular structural changes over time at 2, 4, 8, and 12 h. The magnification progressively increases from left to right, with each subsequent column of images depicting the area enclosed within the red box of the preceding image. The red arrow in each image points to the monolayer membrane encapsulating the A. fumigatus spores. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Frontiers in Microbiology

Article Title: ULK1 mediated autophagy in airway cells during Aspergillus infection

doi: 10.3389/fmicb.2026.1756294

Figure Lengend Snippet: Increased LC3-II expression and monolayer membrane-coated autophagosome formation in Beas2B cells following conidia infection. (A) Expression of LC3-I and LC3-II in Beas2B following infected by B5233 wild-type live conidia at 0, 2, 4, 6, 8, and 10 h. (B) Relative expression levels of LC3-I and LC3-II at the various time points. (C) Fluorescence microscopy images of GFP-LC3 (green), mCherry-labeled conidia (red), and DAPI staining (blue) in Beas2B cells following infected by conidia at 0, 4, 6, and 8 h. (D) Quantification of cells with LC3 + vesicles and average number of LC3 + vesicles per cell at 4, 6, and 8 h. (E) Electron microscopy images of cellular structural changes over time at 2, 4, 8, and 12 h. The magnification progressively increases from left to right, with each subsequent column of images depicting the area enclosed within the red box of the preceding image. The red arrow in each image points to the monolayer membrane encapsulating the A. fumigatus spores. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: LC3 Rabbit Polyclonal antibody(#14600-1-AP, 1:1000), Rubicon Rabbit Polyclonal Antibody (#21444-1-AP, 1:1000), GAPDH Polyclonal antibody(#10494-1-AP, 1:2000) were purchased from proteintech, Phospho-UKL1(Ser555) Rabbit monoclonal antibody (#5869, 1:500), Phospho-UKL1(Ser757) Rabbit monoclonal antibody (#6888, 1:500), ULK1 rabbit monoclonal antibody (#8054, 1:1000), SQSTM1/p62 antibody (#5114, 1:1000), Atg5 Rabbit monoclonal antibody (#12994, 1:1000), Dectin-1 Rabbit monoclonal antibody (#60128, 1:1000), AMPKalpha Antibody (#2532, 1:1000), Phospho-AMPKalpha (Thr172) Rabbit monoclonal antibody(#50081, 1:1000), β -tubulin Rabbit monoclonal antibody(#2128, 1:2000) were purchased from Cell Signaling Technology (USA).

Techniques: Expressing, Membrane, Infection, Fluorescence, Microscopy, Labeling, Staining, Electron Microscopy

ULK1 and CR3 receptor modulated conidia-induced autophagy in Beas2B cells. (A) Expression levels of ULK1, p-ULK1 (Ser555), and p-ULK1 (Ser757) in Beas2B after internalization by B5233 wild-type live conidia at 0, 1, 2, 4, 6, and 8 h. (B) Expression levels of LC3-I and LC3-II in ULK1-silenced Beas2B cells after internalization by conidia. (C) Expression levels of LC3-I, LC3-II, ULK1, p-ULK1 (Ser555), and p-ULK1 (Ser757) in Beas2B cells treated with 2 μM and 5 μM SBI-0206965 inhibitor targeting ULK1/2 with conidia infection. (D) Expression levels of LC3-I and LC3-II in Beas2B cells with CR3 knockdown or overexpression after internalization by conidia. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Frontiers in Microbiology

Article Title: ULK1 mediated autophagy in airway cells during Aspergillus infection

doi: 10.3389/fmicb.2026.1756294

Figure Lengend Snippet: ULK1 and CR3 receptor modulated conidia-induced autophagy in Beas2B cells. (A) Expression levels of ULK1, p-ULK1 (Ser555), and p-ULK1 (Ser757) in Beas2B after internalization by B5233 wild-type live conidia at 0, 1, 2, 4, 6, and 8 h. (B) Expression levels of LC3-I and LC3-II in ULK1-silenced Beas2B cells after internalization by conidia. (C) Expression levels of LC3-I, LC3-II, ULK1, p-ULK1 (Ser555), and p-ULK1 (Ser757) in Beas2B cells treated with 2 μM and 5 μM SBI-0206965 inhibitor targeting ULK1/2 with conidia infection. (D) Expression levels of LC3-I and LC3-II in Beas2B cells with CR3 knockdown or overexpression after internalization by conidia. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: LC3 Rabbit Polyclonal antibody(#14600-1-AP, 1:1000), Rubicon Rabbit Polyclonal Antibody (#21444-1-AP, 1:1000), GAPDH Polyclonal antibody(#10494-1-AP, 1:2000) were purchased from proteintech, Phospho-UKL1(Ser555) Rabbit monoclonal antibody (#5869, 1:500), Phospho-UKL1(Ser757) Rabbit monoclonal antibody (#6888, 1:500), ULK1 rabbit monoclonal antibody (#8054, 1:1000), SQSTM1/p62 antibody (#5114, 1:1000), Atg5 Rabbit monoclonal antibody (#12994, 1:1000), Dectin-1 Rabbit monoclonal antibody (#60128, 1:1000), AMPKalpha Antibody (#2532, 1:1000), Phospho-AMPKalpha (Thr172) Rabbit monoclonal antibody(#50081, 1:1000), β -tubulin Rabbit monoclonal antibody(#2128, 1:2000) were purchased from Cell Signaling Technology (USA).

Techniques: Expressing, Infection, Knockdown, Over Expression

Model of a novel ULK1-mediated LAP-like pathway in airway cells during A. fumigatus conidial internalization. During the interaction between A. fumigatus conidia and airway cells, several changes occur: intracellular LC3-II levels, phosphorylation of AMPK and ULK1, and reactive oxygen species (ROS) content all increase. Additionally, the release of cytokines—including IL-6, IL-8, and MCP-1—also rises. Inhibiting ULK1 activity or silencing its expression can suppress the increase in LC3-II levels and cytokine release triggered by A. fumigatus . Notably, common fungal polysaccharides and Dectin-1 did not impact this process, but the loss of complement receptor 3 elevated both basal and conidia-induced autophagy, correlating with increased AMPK expression. Dashed lines indicate signal pathway interactions hypothesized to occur in airway cells.

Journal: Frontiers in Microbiology

Article Title: ULK1 mediated autophagy in airway cells during Aspergillus infection

doi: 10.3389/fmicb.2026.1756294

Figure Lengend Snippet: Model of a novel ULK1-mediated LAP-like pathway in airway cells during A. fumigatus conidial internalization. During the interaction between A. fumigatus conidia and airway cells, several changes occur: intracellular LC3-II levels, phosphorylation of AMPK and ULK1, and reactive oxygen species (ROS) content all increase. Additionally, the release of cytokines—including IL-6, IL-8, and MCP-1—also rises. Inhibiting ULK1 activity or silencing its expression can suppress the increase in LC3-II levels and cytokine release triggered by A. fumigatus . Notably, common fungal polysaccharides and Dectin-1 did not impact this process, but the loss of complement receptor 3 elevated both basal and conidia-induced autophagy, correlating with increased AMPK expression. Dashed lines indicate signal pathway interactions hypothesized to occur in airway cells.

Article Snippet: LC3 Rabbit Polyclonal antibody(#14600-1-AP, 1:1000), Rubicon Rabbit Polyclonal Antibody (#21444-1-AP, 1:1000), GAPDH Polyclonal antibody(#10494-1-AP, 1:2000) were purchased from proteintech, Phospho-UKL1(Ser555) Rabbit monoclonal antibody (#5869, 1:500), Phospho-UKL1(Ser757) Rabbit monoclonal antibody (#6888, 1:500), ULK1 rabbit monoclonal antibody (#8054, 1:1000), SQSTM1/p62 antibody (#5114, 1:1000), Atg5 Rabbit monoclonal antibody (#12994, 1:1000), Dectin-1 Rabbit monoclonal antibody (#60128, 1:1000), AMPKalpha Antibody (#2532, 1:1000), Phospho-AMPKalpha (Thr172) Rabbit monoclonal antibody(#50081, 1:1000), β -tubulin Rabbit monoclonal antibody(#2128, 1:2000) were purchased from Cell Signaling Technology (USA).

Techniques: Phospho-proteomics, Activity Assay, Expressing

The effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) The effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) The effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) The effect of miR-27a-5p on human renal cancer cell cycle. (D) The effect of miR-27a-5p on the expression of LC3 protein in human renal cancer cells *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.

Journal: Frontiers in Oncology

Article Title: Study on the mechanism of 18β-glycyrrhetinic acid inhibiting the proliferation of renal cancer cells by inducing autophagy through the miR-27a-5p/LC3 axis

doi: 10.3389/fonc.2026.1762770

Figure Lengend Snippet: The effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) The effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) The effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) The effect of miR-27a-5p on human renal cancer cell cycle. (D) The effect of miR-27a-5p on the expression of LC3 protein in human renal cancer cells *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.

Article Snippet: LC3 rabbit polyclonal antibody , Wuhan Sanying Biotechnology Co.Ltd. , Cat No. 14600-1-AP.

Techniques: Expressing

18-GA regulates the effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) 18-GA regulates the effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) 18-GA regulates the effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) 18-GA regulates the effect of miR-27a-5p on the cell cycle of human renal cancer cells. (D) 18-GA regulates the effect of miR-27a-5p on the expression of LC3 protein in human renal cancer cells. *p < 0.05, **p < 0.01, ***p < 0.001, *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.

Journal: Frontiers in Oncology

Article Title: Study on the mechanism of 18β-glycyrrhetinic acid inhibiting the proliferation of renal cancer cells by inducing autophagy through the miR-27a-5p/LC3 axis

doi: 10.3389/fonc.2026.1762770

Figure Lengend Snippet: 18-GA regulates the effect of miR-27a-5p on the proliferation phenotype of human renal cancer cells. (A) 18-GA regulates the effect of miR-27a-5p on the clone formation ability of human renal cancer cells. (B) 18-GA regulates the effect of miR-27a-5p on the apoptosis of human renal cancer cells. (C) 18-GA regulates the effect of miR-27a-5p on the cell cycle of human renal cancer cells. (D) 18-GA regulates the effect of miR-27a-5p on the expression of LC3 protein in human renal cancer cells. *p < 0.05, **p < 0.01, ***p < 0.001, *p < 0.05, **p < 0.01, ***p < 0.001 indicate that the results are statistically significant.

Article Snippet: LC3 rabbit polyclonal antibody , Wuhan Sanying Biotechnology Co.Ltd. , Cat No. 14600-1-AP.

Techniques: Expressing

HDAC8 PROTAC (1) decreased the expression of Bcl-2, an anti-apoptotic protein, in U-87 MG cells. Representative Western blots and bar graphs of HDAC8, Bcl-2, Bax and LC3 compared to GAPDH after 72-h treatment with the HDAC8 PROTAC (1) , HDAC8i (2) , and pomalidomide (3) at 10 μM. Data are represented as the mean ± S.D. of five independent experiments. (*** p < 0.001).

Journal: Drug Design, Development and Therapy

Article Title: Targeted Degradation of Histone Deacetylase 8 Using Proteolysis Targeting Chimeras Technology: A Promising Approach for Glioblastoma Treatment

doi: 10.2147/DDDT.S555228

Figure Lengend Snippet: HDAC8 PROTAC (1) decreased the expression of Bcl-2, an anti-apoptotic protein, in U-87 MG cells. Representative Western blots and bar graphs of HDAC8, Bcl-2, Bax and LC3 compared to GAPDH after 72-h treatment with the HDAC8 PROTAC (1) , HDAC8i (2) , and pomalidomide (3) at 10 μM. Data are represented as the mean ± S.D. of five independent experiments. (*** p < 0.001).

Article Snippet: Rabbit polyclonal LC3 antibody , Cell Signaling Technology , CS#4108 , 1:1500.

Techniques: Expressing, Western Blot