|
|
| Nomenclature |
|
Symbol:
|
Tg(Camk2a-IDE)1Selk
|
|
Name:
|
transgene insertion 1, Dennis J Selkoe
|
|
MGI ID: |
MGI:3043428 |
|
Synonyms: |
2xIDE |
|
Transgene:
|
Tg(Camk2a-IDE)1Selk
Location:
unknown
|
|
Transgene
origin |
|
Strain of Origin:
|
C57BL/6
|
|
Transgene
description |
|
Transgene
Type: | |
Transgenic (random, expressed) |
|
Mutation: | |
Insertion |
| |
|
Mutation details: Transgenic mice express human insulin-degrading enzyme (IDE) under the direction of the mouse calcium/calmodulin-dependent protein kinase II alpha (Camk2a) promoter. Transgene expression is approximately 2 fold relative to wildtype controls as detected by quantitative Western blot analysis and protease activity assay. The levels of soluble alpha beta-amyloid X-40 and soluble alpha beta-amyloid X-42 are reduced in 2 to 3 month old transgenic mice. (J:87150)
|
|
Phenotypes
|
View phenotypes for all genotypes (concatenated display).
|
| Find Mice (IMSR) |
Mouse strains and cell lines available from the
International Mouse Strain Resource
(IMSR)
|
|
Notes |
Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The levels of soluble alpha beta-amyloid X-40 and soluble alpha beta-amyloid X-42 are reduced in 2 to 3 month old transgenic mice. In conjunction with Tg(PDGFB-APPSwInd)20Lms, transgenic mice develop only about half the amyloid beta plaque burden displayed by transgenic mice carrying Tg(PDGFB-APPSwInd)20Lms alone.
|
| References |
|
Original: |
J:87150
Leissring MA et al.,
"Enhanced proteolysis of beta-amyloid in APP transgenic mice prevents plaque formation, secondary pathology, and premature death."
Neuron 2003 Dec 18;40(6):1087-93
|
|
All: |
1 reference(s)
|
|
Analysis Tools
