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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 <t>and</t> <t>Dectin-1</t> 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.
Dectin 1 Rabbit Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rat anti dectin 1 clec7a  (InvivoGen)
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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 <t>and</t> <t>Dectin-1</t> 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.
Rat Anti Dectin 1 Clec7a, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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 <t>and</t> <t>Dectin-1</t> 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.
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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 <t>and</t> <t>Dectin-1</t> 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.
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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 <t>and</t> <t>Dectin-1</t> 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.
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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 <t>and</t> <t>Dectin-1</t> 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.
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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 <t>and</t> <t>Dectin-1</t> 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.
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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 <t>and</t> <t>Dectin-1</t> 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.
Anti Dectin 1, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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