Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas
Transgene Detail
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Symbol: |
Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas |
Name: |
transgene insertion 6799, Robert Vassar |
MGI ID: |
MGI:3693208 |
Synonyms: |
5XFAD, 5XFAD APP/PS1, 5XFAD line Tg6799, Tg-5xFAD, Tg6799, Tg(APP*Swe*Fl*Lon,PSEN1*M146L*L286V)6799Vas |
Transgene: |
Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas Location: Chr3:62886057-62886058 bp Genetic Position: Chr3, Syntenic
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Alliance: |
Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas page
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Transgene Type: |
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Transgenic (Humanized sequence, Inserted expressed sequence) |
Mutation: |
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Insertion
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Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas expresses
2 genes
Transgene expresses:
Organism |
Expressed Gene |
Homolog in Mouse |
Note |
human |
APP (351) |
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"The gene encodes the Swedish, Florida and London mutations." |
human |
PSEN1 (5663) |
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The gene encodes the two FAD associated mutations. |
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Mutation details: Four familial Alzheimer disease- (FAD-) associated mutations were introduced into a single human amyloid precursor protein cDNA: the "Swedish" double mutation (K670N/M671L); the "Florida" mutation (I716V); and the "London" mutation (V717I). Two FAD-associated mutations, M146L and L286V, likewise were introduced into a human presenilin 1 cDNA. Each cDNA was then cloned independently into the mouse thymus cell antigen 1 gene, replacing a segment that contains thymus-specific elements so that expression of the transgenes is targeted only to the brain. Equal molar amounts of the two transgenes were coinjected into pronuclei of single-celled embryos.
(J:32213, J:112949)
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View phenotypes and curated references for all genotypes (concatenated display).
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Three transgenic lines coexpressing the APP and PSEN1 proteins at high, medium and low levels, respectively designated Tg6799, Tg7031, and Tg7092, were propagated for analysis, most of which employed Tg6799.
Phenotypic Similarity to Human Syndrome: Macular Degeneration, Age-Related J:214858.
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Original: |
J:112949 Oakley H, et al., Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. J Neurosci. 2006 Oct 4;26(40):10129-40 |
All: |
1003 reference(s) |
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