Sentence examples for muscle cell expression from inspiring English sources

We generated transgenic C. elegans expressing Luc GFP regulated by a promoter for neuronal or body wall muscle cell expression (Figure 1A) and found a tissue-specific stability of the reporter protein upon chronic heat stress.

The objective of the present study is to reveal mechanisms through which skeletal muscle cell expression of ICAM-1 augments regenerative and hypertrophic processes of myogenesis.

Furthermore, when the number of muscle cells expressing reporter protein at 3, 6 and 9 dpf was quantified from all imaged larvae, rest MO-injected larvae showed clear increases in muscle cell expression compared to controls.

If we were to combine samples using the sub-facet groupings then we would produce a disproportionately large number of vascular-associated smooth muscle cell expression profiles, which would potentially have a deleterious effect on the later analyses.

When the same larvae were imaged three days later (7 dpf), muscle cell expression had faded, fragmenting with time and eventually disappearing, while neuronal expression in the spinal cord and gut was maintained.

While some ERβ expression was observed in the adventitia and smooth muscle cells, expression was largely endothelial.

In endothelial cells, PI3K, Akt kinase, ERK1/2, striatin, and phosphorylation of eNOS have been described to be required for ERα MISS, whereas in vascular smooth muscle cells, expression and activity of several phosphatases such as MKP-1, SHP-1, PTEN, and PP2A mediate this pathway (Ueda & Karas, 2013).

In addition, muscle cell reporter expression was maintained in rest MO-injected larvae at 6 and 9 dpf, well after the sparse muscle expression evident in 3-dpf control larvae had dissipated.

RNAi knockdown of smooth muscle cell VEGF expression phenocopied the effect of VEGF signaling inhibitors.

It is assumed that variation in lesion development at different sites is sensitive to several parameters, such as genetic background, immune status, gender, hemodynamic factors and differences in endothelial or smooth muscle cell gene expression [31], [33].

The most significant GO pathways up-regulated by disease at PND 0 are related to muscle cell gene expression, which is difficult to reconcile with the known literature on pulmonary macrophages.