Sentence examples for mutation under control from inspiring English sources

APP23 mice express the K670M/N671L-mutated human APP (Swedish double mutation) under control of the neuron-specific Thy1 promoter element at about 7-fold over endogenous (murine) APP.

pR5 mice express the longest human tau isoform carrying the pathogenic P301L mutation, under control of the murine Thy1.2 promoter that drives neuronal expression of the transgene.

Transgenic mice (Tg2576) overexpressing human amyloid precursor protein (hAPP) carrying the Swedish (K670N/M671L) familial AD mutation under control of the prion promoter [ 36] were used.

This mouse model harbors the human amyloid precursor protein (APP) gent containing Swedish mutant and human presenilin 1 (PS1) gene encoding the deleted exon 9 mutation under control of mouse PrP promoter which directs the transgene expression predominantly in brain neurons [ 18], and develops amyloid plaques at 6 months of age [ 17].

To examine how wild-type and mutant ARs (expressed at physiologically relevant levels) respond to various experimental manipulations, HeLa cell lines were generated that stably express either wild type (GFP-AR), mutant GFP-ART877A (LNCaP mutation; [13]), or GFP-ARF764L (AIS mutation; [21]) under control of the CMV promoter.

To readdress this question by rigorous quantitative methods, we analyzed transgenic mice expressing human β-CTF with the I45F mutation (SPA4CT) under control of the prion protein promoter by stereological techniques.

Line H6 also expresses hAPP with the Indiana mutation under the control of a PDGF promoter [ 344].

This can be achieved by introducing the JAK2V617F mutation under the control of the endogenous Jak2 promoter via homologous recombination in embryonic stem (ES) cells.

> -wrap-foot> In the present study, we generated and characterized a mouse line that expresses the human dominant-negative Cx30T5M mutation under the control of the endogenous Cx30 promoter after homologous recombination in mouse embryonic stem cells (Fig.  1).

A third rat line carrying both mutant APP (K670N/M671L) and a human PS1 transgene with the FAD M146V mutation under the control of the rat synapsin 1 promoter develops plaques at 7 months of age (Flood et al. 2009).

The only mouse model that develops significant cerebrovascular amyloid with virtually no parenchymal amyloid is the APPDutch mouse, which overexpresses hAPP751 bearing the E693Q (E22Q in Aβ) mutation under the control of the Thy1 promoter (Herzig et al. 2004).