Apc Min/+ Mice
Apc Min/+ Mice - Related Videos
05:21
Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy
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Cited by 1 •
2014
By using transgenic reporter mice and injectable fluorescent labels, long-term intravital spinning disk confocal microscopy enables direct visualization of myeloid cell behavior into intestinal adenoma in the ApcMin/+ colorectal cancer model.
05:16
Sleeve Gastrectomy in Mice using Surgical Clips
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Cited by 2 •
2020
The prevalence of diabetes and obesity is continuously increasing worldwide. The mechanisms between diabetes, obesity and their associated mortality and co-morbidities need to be further investigated. Here, we present a protocol for sleeve gastrectomy (SG) in animals as an uncomplicated preclinical model of bariatric surgery.
06:17
Measuring the Strength of Mice
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Cited by 287 •
2013
Deficits in muscular strength occur in many clinical conditions such as motor neuron disease. The inverted screen and weight lifting tests described here measure strength in mice almost exclusively, with minimal influence of factors such as coordination.
36:30
Small Bowel Transplantation In Mice
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Cited by 2 •
2007
The mouse small bowel transplantation model has been recognized as an important tool to study mechanismes of immune rejection and screen new immunosuppressive drugs. However, this model is limited to use because the techniques involved is an extremely technically challenge. Now we introduce the modified technique.
07:02
Trace Fear Conditioning in Mice
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Cited by 32 •
2014
In the following experiment we describe a protocol for trace fear conditioning in mice. This type of associative memory includes a trace period that separates the neutral stimulus and the unconditioned stimulus.
FAQs
The central molecular effect is impaired Apc-mediated control of β-catenin and Wnt signaling. When this regulation is disrupted, intestinal epithelial cells can proliferate abnormally, creating conditions that favor polyp formation. Additional genetic or environmental changes may intensify this process, allowing researchers to examine how signaling defects interact with broader influences on intestinal tissue behavior.
The inherited Apc alteration creates a defined susceptibility, but tumor development can also depend on subsequent genetic or environmental influences. Studying these added factors helps separate the initiating effect of altered tumor-suppressor signaling from events that promote progression. This makes the model useful for investigating how intestinal tumors emerge through interactions among epithelial abnormalities, external exposures, and tissue conditions.
Immune activity and inflammation provide biological context for tumor initiation and progression in the intestine. Changes in these processes can be examined alongside epithelial proliferation and polyp formation to determine how host defenses and inflammatory conditions influence tissue homeostasis. In immunology research, the model therefore connects abnormal tumor-related signaling with the local immune environment.
The gut microbiota can be evaluated as an environmental influence that may modify intestinal tumor development. Investigators can relate microbial conditions to immune responses, inflammation, tissue homeostasis, and tumor progression, while the defined genetic susceptibility provides a consistent background for comparison. This approach helps clarify how host genetics and microbial exposure jointly shape intestinal disease.
These mice provide a susceptibility framework for examining whether infectious or other microbial exposures alter intestinal tumor initiation or progression. Such studies can assess the relationship between exposure, immune responses, inflammation, and epithelial disease in the intestine. Their value lies in connecting microbial influences with genetically defined disruption of Apc-related regulation rather than examining infection in isolation.
Relevant outcomes include intestinal polyp formation, tumor initiation, tumor progression, immune responses, inflammatory conditions, microbiota-associated effects, and changes in tissue homeostasis. Examining these outcomes together can reveal whether a factor primarily affects early tumor development, later progression, or the surrounding intestinal environment. The model also supports assessment of cancer-prevention strategies in this defined susceptibility setting.