Sentence examples for model overexpressing human from inspiring English sources

Mougenot, A. L. et al. Transmission of prion strains in a transgenic mouse model overexpressing human A53T mutated alpha-synuclein.

In a transgenic mouse model overexpressing human EPO, the authors demonstrated that these mice fail to develop hypertension, stroke, myocardial infarction, or thromboembolism [67] but do have hematocrit levels of approximately 80% with generalized vasodilatation [68].

Recently the importance of cytokines was pointed out in a transgenic mouse model overexpressing human IL-1β in the pancreas.

In a transgenic mouse model overexpressing human EPO, the authors demonstrated that these mice fail to develop hypertension, stroke, myocardial infarction, or thromboembolism [ 67] but do have hematocrit levels of approximately 80% with generalized vasodilatation [ 68].

In similar experiments in another transgenic animal model, overexpressing human islet amyloid polypeptide did not reveal any ductal abnormalities (histology) or a change in ductal cell proliferation rates with sitagliptin, metformin, sitagliptin with metformin, or placebo treatment (15).

In this study, we have used a multidimensional approach including high-magnification and super-resolution microscopy, cerebro-spinal fluid (CSF) mass spectrometry analysis and ELISA to investigate the Aβ pathology and its associated cognitive impairments, in a novel transgenic rat model overexpressing human APP.

On the other hand, these Tg models overexpressing human APP only develop a partial AD-like phenotype and only recapitulate certain features of human AD.

Available models include transgenic models overexpressing human NOTCH3 from a cDNA construct [ 6– 8] or rat Notch3 from a genomic construct [ 9], and models in which a mutation was introduced into the endogenous Notch3 gene [ 10, 11].

Recently, transgenic mouse models, overexpressing human αSYN under specific oligodendroglial promotors have been developed to reproduce the specific GCI pathology of MSA (Kahle et al., 2002; Stefanova et al., 2005a; Yazawa et al., 2005; Shults et al., 2005).

To recapitulate the pathogenesis of human AD, APP23 mouse model overexpresses human APP with the Swedish mutation under the murine Thy1 promoter [ 57], while deltaE9 mice express APP with the Swedish mutation controlled by mouse prion protein promoter elements together with mutant human PS1 lacking exon 9, which is associated with familial AD [ 29, 52].

In addition, the results of the present study suggest that heterozygous Abca1 mice could be considered a valuable model when overexpressing human genes related to AD types of neurodegeneration, or with global disruption of genes involved in neurological disorders known for perturbed neuronal development or impaired synaptic plasticity.