Gfp-lc3 Mice
Gfp-lc3 Mice - Related Videos
08:44
Activating Autophagy by Aerobic Exercise in Mice
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Cited by 37 •
2017
Autophagy activation is beneficial in the prevention of a number of diseases. One of the physiological approaches to induce autophagy in vivo is physical exercise. Here we show how to activate autophagy by aerobic exercise and measure autophagy levels in mice.
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.
07:13
Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
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Cited by 4 •
2017
Mice with acquired hypoparathyroidism would be useful for studying novel drug therapies for hypoparathyroidism. Two procedures to create such mice are demonstrated. The GFP-PTX mouse is generated by surgical parathyroidectomy guided by green fluorescing parathyroid glands. A second, non-surgical approach is based on parathyroid-specific expression of the diphtheria toxin receptor.
06:19
In Vivo Imaging of Cx3cr1gfp/gfp Reporter Mice with Spectral-domain Optical Coherence Tomography and Scanning Laser Ophthalmoscopy
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Cited by 5 •
2017
This protocol describes how high-resolution imaging techniques such as spectral domain optical coherence tomography and scanning laser ophthalmoscopy can be utilized in small rodents, using an ophthalmic imaging platform system, to obtain information on retinal thickness and microglial cell distribution, respectively.
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.
FAQs
The key molecular event is LC3 lipidation: cytosolic LC3-I is converted into LC3-II, which becomes recruited to autophagosomal membranes. In GFP-LC3 mice, this relocation changes the fluorescence pattern from diffuse cellular signal toward puncta. That visual shift provides a way to examine where autophagosome formation occurs in tissues during immune or infectious responses.
Fluorescent puncta serve as visual markers of LC3 associated with autophagosomal membranes, so their distribution can reveal changes in autophagy across cells or organs. Comparing puncta patterns between experimental conditions helps identify responses to pathogens, inflammation, or cellular stress. The readout is therefore especially useful for mapping spatial differences in autophagic activity.
Because the transition links a molecular change in LC3 to a visible tissue signal, it connects autophagy regulation with host responses that can be examined during infection. This makes the reporter useful for asking whether immune cells or infected tissues alter autophagic activity under pathogen-associated stress, rather than treating autophagy as an unlocalized cellular event.
Researchers examine fluorescence in living tissues and can pair imaging with tissue analysis to assess LC3-associated patterns. They then compare autophagic activity across organs, cell populations, or experimental conditions involving pathogens, inflammation, or cellular stress. This workflow links visual localization of puncta with tissue-level interpretation of immune and infection-related responses.
Imaging different organs can show whether autophagic activity is distributed uniformly or changes according to tissue context. When combined with tissue analysis, the reporter can identify organ-specific changes associated with infection or inflammation. Such comparisons help researchers determine where host responses are most closely associated with altered autophagy and guide follow-up studies of those tissues.
They allow investigators to connect pathogen exposure or inflammatory conditions with autophagy patterns in immune cells and infected tissues. The resulting observations can inform studies of host defense and pathogen survival by showing where autophagic activity changes. They also provide a model for evaluating therapeutic strategies that target autophagy-related pathways.