Sentence examples for mouse heart tissues from inspiring English sources

The anti-sera were affinity purified and tested on cell transfections or mouse heart tissues by western blotting.

ATP5b and Ndufs1 were significantly increased in the acute phase of CVB-infected myocarditis mouse heart tissues.

However, they were significantly decreased during the chronic phase of CVB-infected myocarditis mouse heart tissues [ 11].

Strikingly, of the 39 up-regulated proteins identified in this experiment (Table 1, Figure 2, Additional file 3), UPR target genes, such as GRP78, GRP94, Hspb1, Calr, and Pdia3, were also increased in the acute phase of CVB3-infected myocarditis mouse heart tissues [ 20].

The structure of mouse heart tissue was normal, and there was no hyperemia and hydroncus in the mesenchyme, as well as no infiltration of inflammatory corpuscles such as lymphocytes, plasma cells, neutrophilic granulocytes and eosinophil granulocytes.

Even more intriguing, the team discovered that the mutant protein failed to stop cells from spewing calcium into the valve cells of mouse heart tissue.

For Atf6, overexpression was studied in mouse heart tissue [46] (GEO accession: GSE8311).

Sub-cellular fractions (cytoplasmic and nuclear) from mouse heart tissue was prepared using methods primarily described by Charlet et al, 2002 [49] with some modifications.

The fifteen mouse heart tissue cRNA samples were labeled with Cy5 and the Universal Mouse reference cRNA was labeled with Cy3, yielding a total of 5 biological replicates per condition.

RNA extraction and northern blots were performed using mouse heart tissue, as previously described.[1] RNA (10 µg per sample lane) was resolved by electrophoresis in a formaldehyde-agarose gel and then transferred to a nitrocellulose membrane.

Moreover, although TMEM135 expression was not highly expressed in normal mouse heart tissue, TMEM135 was upregulated 3.25 (±0.03 -fold upon fasting (p<0.05) and 8.2 (±0.03 -fold upon cold exposure (p<0.02) (fasting and 5D).