Lc3 Recruitment
Lc3 Recruitment - Related Videos
11:39
Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry
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Cited by 94 •
2017
Here, multispectral imaging flow cytometry with an analytical feature that compares bright detail images of 3 autophagy markers and quantifies their co-localization, along with LC3 spot counting, was used to measure autophagy in an objective, quantitative, and statistically robust manner.
06:58
Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles
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Cited by 7 •
2024
Here, we present the methodology for concisely assessing autophagosome marker LC3-II levels in extracellular vesicles (EVs) by immunoblotting. Analysis for LC3-II levels in EVs, autolysosome formation, and omegasome formation suggests the new role of STX6 in the release of LC3-II-positive EVs when autophagosome-lysosome fusion is inhibited.
05:52
An In Vitro Flow Investigation of the Effect of Stromal Cells on Leukocyte Recruitment
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2025
The video demonstrates a method for investigating the impact of stromal cells on leukocyte recruitment. In a parallel plate flow chamber model, pro-inflammatory cytokines induce the expression of adhesion receptors by endothelial cells, facilitating neutrophil recruitment and migration. The cross-talk between stromal cells and endothelial cells diminishes neutrophil recruitment to the endothelial cells.
04:28
Lung Tumor Cell Recruitment Assay
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2019
This manuscript describes a method to quantify tumor cell accumulation in the lungs in an animal model of tumor metastasis.
11:30
Analyzing the Effects of Stromal Cells on the Recruitment of Leukocytes from Flow
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Cited by 28 •
2015
The ability of inflamed endothelium to recruit leukocytes from flow is regulated by mesenchymal stromal cells. We describe two in vitro models incorporating primary human cells that can be used to assess neutrophil recruitment from flow and examine the role that mesenchymal stromal cells play in regulating this process.
FAQs
The autophagy machinery modifies LC3 by attaching phosphatidylethanolamine, a membrane-associated lipid. This lipidation enables LC3 to associate with phagophore membranes during autophagosome formation and with pathogen-containing vacuoles during LC3-associated phagocytosis. The resulting membrane association supports the organization and maturation of structures that direct cellular material or microbes toward lysosomal degradation.
LC3 recruitment provides more than a marker of membrane association. By attaching to phagophore or pathogen-containing vacuole membranes, LC3 helps organize membrane maturation and links these structures with downstream lysosomal degradation. In infection studies, this makes recruitment relevant to both the development of autophagic compartments and the processing of microbe-containing cellular structures.
The associated membrane compartment distinguishes these two contexts. During autophagy, LC3 is recruited to the phagophore as an autophagosome forms around cellular material or damaged components. During LC3-associated phagocytosis, it is recruited to a pathogen-containing vacuole. Both pathways use LC3 lipidation and membrane association, but they address different cellular structures and targets.
Measurements of LC3 recruitment can help distinguish autophagic responses, examine host-pathogen interactions, and evaluate intracellular clearance pathways. The location of recruited LC3 is especially informative because association with a phagophore suggests autophagosome formation, whereas association with a pathogen-containing vacuole relates to LC3-associated phagocytosis and antimicrobial defense.
The relevant membranes depend on the process under investigation. Autophagy studies examine phagophore or autophagosome-associated membranes, while infection studies may focus on pathogen-containing vacuoles. Researchers can relate LC3 association at these sites to membrane maturation and subsequent delivery of damaged components or microbes toward lysosomal degradation.
In infection research, LC3 recruitment provides a way to investigate whether microbes encounter cellular clearance pathways and how host-pathogen interactions affect those responses. Studies can use the recruitment pattern to evaluate antimicrobial defense and to examine how bacteria, viruses, or parasites manipulate intracellular clearance pathways involving autophagy-related membranes and lysosomal degradation.