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As discussed in detail these findings both corroborate and contrast with studies of other mice with altered Mecp2 levels.
We used MMTV-PyMT mice to study the effects of S14 loss because they rapidly develop mammary tumors at a young age, providing an opportunity to observe any delay in tumor latency in mice with altered mammary de novo fatty acid synthesis.
Epidemiological studies in humans carrying an inactive ALDH2, genetic models in mice with altered ALDH2 levels, and small molecule activators of ALDH2 all highlight the role of ALDH2 in cardioprotection and suggest a promising new direction in cardiovascular research and the development of new treatments for cardiovascular diseases.
Discordant behavioral effects of psychotomimetic drugs in mice with altered NMDA receptor function.
The mutant mice with altered nurturing leave their young scattered around the nest to die of exposure.
New results from genetically engineered mice with altered catecholamine signaling, as well as possibilities for future experiments, are discussed.
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UBB+1 tg mice are not the only mouse model with altered respiration.
During the past decade, a large number of genetically engineered mouse models with altered cardiac function have been generated.
Previous mouse models with altered neural progenitor maintenance and survival develop smaller brain (Chae and Walsh, 2007).
To date, a total of six mouse models with altered p53 activity have been generated, and in all of them age-associated events and lifespan are altered.
Examples include three mouse lines with altered bacterial susceptibility and multiple lines with minimal/absent hepatic lipidosis despite high-fat diet challenge.
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