Sentence examples for mice express mutant from inspiring English sources

P301S tau transgenic mice express mutant human tau protein and develop progressive tau pathology.

These mice express mutant cGKI-alpha protein that is incapable of binding to myosin light chain phosphatase, one key protein of vascular smooth muscle cell (VSMC) contractile apparatus.

Furthermore, the LRRK2/TauP301L mice express mutant tau, which has reduced tubulin binding [ 25, 27], potentially decreasing our ability to uncover tubulin-dependent LRRK2 phosphorylation of tau.

Our L126Z mice express mutant protein at a level that induces paralysis by 7 months of age with the co-expression of WT SOD1 (via mating to the Gurney WT) reducing the age to paralysis by 1 2 months.

Developed by Oddo et al., 3 × Tg-AD mice express mutant versions of the human presenilin 1 (PS1 M146V ) and tau (P 301L ) genes on a Tg2576 (amyloid precursor protein (APP Swe mutant) background, resulting in the formation of both A β plaques and neurofibrillary tangles with a similar spatial and temporal distribution to that observed in human AD patients.

Transgenic mice expressing mutant prion proteins spontaneously develop neurologic dysfunction and spongiform neuropathology.

"Knock-in" mice expressing mutant GABAA subunits engineered to be insensitive to benzodiazepines or general anaesthetics have proved invaluable in evaluating the role of GABAA receptor subtypes in complex behaviours such as sedation, cognition and anxiety [Rudolph, U., Mohler, H., 2006. GABA-based therapproachesproaches: GABAA receptor subtype functions. Curr. Opin. Pharmacol. 6, 18 23].

Aberrant axonal transport contributes toward pathogenesis in sporadic ALS and in mice expressing mutant SOD1 [26] [28].

Conversely, mice expressing mutant tau associated with familial fronto-temporal dementia (FTD) recapitulate robust tauopathy [14] [17].

Transgenic mice expressing mutant forms of SOD1 (mice1 mice) recapitulate the phenotype of ALS and provide the only currently available faithful model of ALS [1], [2].

To test this, we crossed αB-crystallin/HspB2 deficient (CRYAB-/-HSPB2-/) mice with AD model transgenic mice expressing mutant human amyloid precursor protein.