Co-expression of multiple transgenes in mouse CNS: a comparison of strategies.

By J. Jankowsky, H. Slunt, T. Ratovitski, Nancy A. Jenkins, N. Copeland, D. Borchelt. Biomolecular Engineering, 2001

820 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/19961d9d89935a4fbcc17f70a467234b4dfdf4fb

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Citations in the corpus

Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase. (2004, background): “The two transgenes co-integrated and co-segregate as a single locus (55).”
Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxy quinoline analogs is associated with decreased interstitial Abeta. (2008, neutral): “We then compare the effects of PBT2 with those of CQ on behavior and neuropathology in two well-established amyloid protein precursor (APP) Tg mouse models of AD, the APPswe/PS1 dE9 (APP/PS1) ( Jankowsky et al., 2001 ) and Tg2576 (Hsiao et al., 1996) models.”
The Diabetes Drug Liraglutide Prevents Degenerative Processes in a Mouse Model of Alzheimer's Disease (2011, background): “DOI:10.1523/JNEUROSCI.0529-11.2011 Copyright © 2011 the authors 0270-6474/11/316587-08$15.00/0 crosses the BBB, and show the effect of 8 weeks of liraglutide intraperitoneal administration in an APPswe/PS1 E9 mouse model of AD (Jankowsky et al., 2001).”
Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006, methodology): “Previous work has demonstrated that coinjection results in efficient transgene cointegration, often together at the same genomic locus, thus enabling stable germ-line transmission and transgene coinheritance (Jankowsky et al., 2001; Oddo et al., 2003).”
Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice (2008, methodology): “…hypothesis, we developed a method to isolate fresh adult mouse microglia from the bigenic APPswe/PSEN1dE9 (PS1-APP) mice (Borchelt et al., 1997; Jankowsky et al., 2001), a robust mouse model of AD, and from their nontransgenic littermates at various ages and stages of AD-like pathology, and…”
Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques (2009, methodology): “plaques,ADtransgenicmice (13)expressingmutanthumanpresenilin1 (DeltaE9)”
Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014, background): “The numbers within each cell correspond to the following references: 1: (Jankowsky et al., 2001), 2: (Park et al., 2006), 3: (Cramer et al., 2012), 4: (Reiserer et al., 2007), 5:(Cao et al., 2007) 6:(Lalonde et al., 2004), 7: (Volianskis et al., 2010), 8: (Sood et al., 2007), 9: (Zhang et al.,…”
Aβ plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks (2008, neutral): “5 month old APP/PS1 mice – an age prior to the development of plaques but consistent with robust transgene expression (Garcia-Alloza et al., 2006; Jankowsky et al., 2001).”