Sentence examples for mouse myoblasts expressing from inspiring English sources

In order to quantitate the number of cells surviving in the device and optimize initial conditions leading to high-density survival, we implant devices containing C2C12 mouse myoblasts expressing a luciferase reporter in the mouse subcutaneous tissue.

Furthermore, this effect was also observed in primary cultures of mouse myoblasts expressing expPABPN1.

In conclusion, we find that LiCl rescues polyalanine expansion-associated cell death in our C2C12 OPMD cell model and in primary cultures of mouse myoblasts expressing expPABPN1.

To further confirm the observed protective effects of LiCl on C2C12 cells, we assessed both proliferation and differentiation in primary cultures of mouse myoblasts expressing GFP-expPABPN1 (13and and 17Ala) after LiCl treatment.

Mouse myoblasts express telomerase, but their proliferation is still limited, probably by the p16 pathway, since mouse myoblasts can be immortalized by the overexpression of cdk4 that traps p16, rendering it inactive (Douillard-Guilloux et al. 2009).

Both in vivo live-stage imaging microscopy and fluorescence-activated cell sorting (FACS) methods were used to measure the protective effect of LiCl in an OPMD cell model of murine myoblast (C2C12) cells expressing expPABPN1 as well as in primary culture of mouse myoblasts also expressing expPABPN1.

Populations were implanted into leg skeletal muscles of adult SCID mice to avoid immunologic response to myoblasts expressing xenogeneic LacZ protein (Misteli et al, 2010).

Engineered C2C12 mouse myoblast cells expressing Rab5-EGFP, Rab7-EGFP or Cav1-GFP were used to monitor the location of the plasmid DNA into the endocytic compartments by real time fluorescence confocal microscopy.

Six- to twelve-week-old immunodeficient SCID CB17 mice (Charles River Laboratories, Sulzfeld, Germany) were used to avoid any immunologic response to myoblasts expressing xenogenic LacZ protein.

In this study, we demonstrate decreased proliferation rates of myoblasts expressing FRG1, an attribute that could contribute to the long term reduction in muscle regenerative potential and muscular dystrophy observed in transgenic mice overexpressing FRG1.

The RNA foci were also found in myoblasts expressing 58 CAG repeats (CAG58).