Sentence examples for mouse fibroblasts results from inspiring English sources

Kapoor, M. et al. Loss of peroxisome proliferator-activated receptor gamma in mouse fibroblasts results in increased susceptibility to bleomycin-induced skin fibrosis.

Liu, S., Kapoor, M., Denton, C. P., Abraham, D. J. & Leask, A. Loss of β1 integrin in mouse fibroblasts results in resistance to skin scleroderma in a mouse model.

We also demonstated that removal of α-IPM from the culture of double transgenic primary mouse fibroblasts results in the repression of GFP expression with rapid kinetics compared to other inducible gene expression systems, such as tetracycline and FK506/rapamycin inducible systems with slow induction and reversibility kinetics [31].

Overexpression of TACC1 in mouse fibroblasts results in cellular transformation and anchorage independent growth (Still et al, 1999).

Overexpression of skeletal muscle determinant gene MyoD in the mouse fibroblasts results in the formation of myocytes [11,12].

Knockdown of either Stn1 or Ctc1 in human cancer cells and in mouse fibroblasts results in substantially elongated telomeric G-overhangs, consistent with its recently demonstrated role in facilitating telomeric C-strand synthesis and negatively regulating telomerase (Surovtseva et al., 2009; Dai et al., 2010; Chen et al., 2012; Wang et al., 2012; Wu et al., 2012).

Both c-kit receptor tyrosine kinase and insulin-like growth factor binding protein 3 have previously been described to be involved in hypoxia-induced angiogenesis [21], [22], and insulin growth factor 1 stimulation in mouse fibroblasts resulted in upregulation of DEAD [23].

Moreover, in a nude mouse xenograft model, coinjection of MDA-MB-231 breast cancer cells with Sdc-1 overexpressing and mock-transfected mouse fibroblasts resulted in significantly elevated microvessel density and a larger vessel area in tumours containing Sdc1 overexpressing stroma cells [ 33].

Overexpression of HDAC1 in mouse fibroblasts resulted in a partial G2/M block and aberrant nuclear morphology, whereas knock-down of HDAC1 in human tumor cells also led to impaired mitosis suggesting a requirement for balanced acetylation/deacetylation during mitosis (Bartl et al. 1997; Senese et al. 2007).

Although loss of PPARγ expression in cultured mouse embryonic fibroblasts results in enhanced, constitutive Smad3 phosphorylation and collagen production [ 8], loss of PPARγ expression in cultured adult mouse fibroblasts appears to be insufficient to result in either Smad 3 activation or collagen production [ 9].

Similarly, deletion of PHB2 in mouse embryonic fibroblasts results in severely impaired cellular proliferation [ 8].