Sentence examples for mutant rat model from inspiring English sources

In this study, we designed rat-specific siRNA sequences for Erc/mesothelin, which is a tumor-specific gene expressed in the Eker (Tsc2 mutant) rat model of hereditary renal cancer and confirmed the efficacy of gene silencing in vitro.

Autophagy can promote oligodendrocyte precursor survival and myelin development in a myelin mutant rat model (57), and it is possible that it may play a similar function after CNS trauma.

The data presented here tries to look at the gravity of metabolic insult during the early and prolonged phases of obesity/insulin resistance (IR) depicted in WNIN/Ob strain of rats an obese euglycemic mutant rat model developed indigenously at our institute which is highly vulnerable for a variety of degenerative diseases.

In line with this, neuroprotective strategies not directly targeting transcription (e.g. chaperones and calcineurin) block the loss of DARPP32 produced by mutant Htt in our rat model [12], [13], [61].

To examine the probiotic properties of the non-genotoxic Nissle 1917 mutant, we first used a rat model in which colonic inflammation was chemically induced by the administration of Dextran Sodium Sulfate (DSS) in drinking water.

In addition in the Eker rat model, a mutant Tsc2 gene that fails to inhibit mTOR is still able to suppress tumourigenesis (Shiono et al, 2008), and administration of rapamycin reduces the development of macroscopic tumours while having no effect on the number of microscopic precursor lesions (Kenerson et al, 2005).

Only the mouse model that expresses mutant rat Notch3 protein from a genomic DNA construct shows early onset vascular Notch3 accumulation with subsequent development of brain parenchymal lesions [ 9].

The present study was designed to extend our previous results obtained in rd1 mouse (a relevant model of human recessive RP) to transgenic rhodopsin P23H mutant rat, a frequent mutation in dominant human disease and a good model for studying long-term effects and functional phenomena.

As an in vivo model for studying the effect of these mutants after their extracellular application, we used the rat model of cerebral ischemia.

The HCM mouse model used in this study expresses a mutant rat α-MyHC with expression driven by an α-MyHC promoter on a C57Bl/6 background (Vikstrom et al, 1996).

It is thus possible that age-dependent alterations to CREB signaling may interact synergistically with CREB deficits induced by mutant Htt, increasing DARPP-32 loss and striatal degeneration in our rat model.