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Therapeutic implications include the ability to establish new humanized disease models for understanding mechanisms, conduct high-throughput screening for novel biogenic compounds to reverse or prevent the disease phenotype, identify and engineer genetic rescue of causal mutations, and develop patient-specific cellular replacement strategies.
As these cells proliferate they accumulate further mutations and develop increased resistance to anticancer agents.
Tg2576 mice express human amyloid precursor protein with the Swedish mutations and develop numerous amyloid plaques in the cortex and hippocampus as they age (Hsiao et al., 1996).
The longer the patient is exposed to such treatment, the higher will be the chance to accumulate mutations and develop resistance [ 16].
Although antibiotic tolerance in persisters is thought to be phenotypic, it is possible that under some conditions, antibiotic tolerant persisters may acquire mutations and develop genetic resistance.
In 2005, endorsed by breeders and veterinarians, we established a heredo-surveillance platform to centralize relevant information and biological samples for emerging genetic anomalies, identify responsible genes and mutations, and develop diagnostic tests.
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By screening waxy Chinese sorghum accessions with the wx a and wx b markers, Lu et al. [ 11] identified two novel types of waxy mutations and developed cleaved amplified polymorphic sequence markers based on these new alleles to classify their germplasm.
We tested a mouse model of Alzheimer's disease-typical amyloid β pathology the tgCRND8 mouse, which overexpresses amyloid precursor protein with the Swedish and Indiana mutations and develops amyloid plaques like those in the brains of patients with Alzheimer's disease (Chishti et al., 2001)—on a modified version of the spontaneous object recognition paradigm (McTighe et al., 2010) (Fig. 1).
Tg2576 mice harbor the human APP transgene with the Swedish mutation and develop AD-like amyloidosis and memory deficits [15].
Human ESCs can be genetically modified to harbor a desired mutation and develop a phenotype of disease.
APP23 mice express APP with Swedish mutation and develop amyloid plaques late in their life, while cognitive deficits are observed in young age.
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