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For cells with an X∶A ratio≥0.5 we used a cell division rate of once every two days, based on our cell division analysis (described above).
We demonstrated that LPS is a potent inducer of SAA3 expression in cultured colonic epithelial cells and suggest a model (Figure 7) whereby the gut microbiota significantly induces both SAA3 and TNF-α expression in colonic epithelial cells and macrophages; however, based on our cell culture models, the fold-induction of TNF-α in macrophages may be higher than is observed for SAA3.
It was of great interest to note that for both SNPs, the AD risk allele was associated with decreased Teashirt3 expression, which, based on our cell biological and postmortem studies, we would predict would lead to increased expression of caspase-4.
Based on our cell culture data we further hypothesized that zebrafish trilobite/ vangl2 mutant embryos have increased matrix metalloproteinase activity.
The ratio of decreasing to increasing trends (intially taken as 35%30%0 % based on our cell culture data) was set to 60%5%5 % as well as 5%60%0 %.
Based on our cell culture studies and biochemical studies on postmortem brains of patients carrying familial Alzheimer's disease PS1 mutations, we favour the notion that the disturbed ER calcium homeostasis is mediated by the elevation of PS1 holoprotein levels [ 85] possibly as a consequence of altered presenilin autocleavage.
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Based on our cell-culture studies, we propose a model to explain the tubulin modifications and neurite outgrowth in the presence of rHIgM12 (Fig. 6).
Herein, we present new findings based on our optimized cell.
Based on our single cell labelings we doubt such a distinction.
Based on our data, cell death does not seem to be associated with physiologic adult neurogenesis (n = 20 left OLs), but further analysis with higher temporal resolution will be required to corroborate these results.
Based on our live cell analyses and in vitro data obtained by others we suggest that oligomerization and segregation of Cx43 in the ER, normally induced by 14-3-3 14-3-3 14-3-3bindingicanly impaired be β-COPI binding.
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