We have investigated how mouse liver cells respond to increased cell size caused by Cdk1 inactivation and hepatectomy.
The yeast S. cerevisiae cells respond to increased intracellular osmolarity by activating of the high osmolarity glycerol (HOG MAPKK pathway.
C vs H and C' vs H' comparative analysis of the gene expression profiles of each cell line revealed that the mammary epithelial cells responded to increased temperature distinctly from the breast cancer lines, with altered regulation of gene networks controlling DNA damage response, cell cycle progression, apoptosis, and heat shock characterizing the mammary epithelial cell response.
The bacterial cells responded to increasing concentrations of NaCl by increasing both the degree of saturation of the membrane phospholipid fatty acids (Fig. 1a) and their cell surface hydrophobicity (Fig. 1b).
U87 cells responded to increasing amounts of fMLF in a dose-dependent manner with intracellular calcium mobilisation.
β-Cells respond to increased plasma glucose levels with an increase in insulin secretion, and Δ I/Δ G is modulated by severity of IR (128).
Unexpectedly, cells respond to increases in ROS by maintaining elevated levels of ROS scavenger proteins by posttranscriptional mechanisms.
In our previous model-based data reconciliation analysis of the response to NADPH demand modulation, we showed that yeast cells responded to increases in NADPH demand by increasing flux through the PP and acetate pathways, which covered 80%and20%0% of the NADPH demand, respectively [ 5].
Particularly attractive biomarkers might be circulating endothelial cells (CECs), as these may reflect damage to the tumour vasculature or circulating haematopoietic progenitor cells (HPCs), as they have been proposed to reflect a pro-angiogenic cell population, which may respond to increased hypoxia by effective anti-angiogenic therapy (Jain and Duda, 2003; Shaked et al, 2006; Zurita et al, 2009).
The increased expression of genes associated with definitive hematopoiesis was confirmed by that the progenitor cells responding to SCF/IL6/epo had increased 5-8-fold within the intact EB when Lhx2 was expressed during this time period compared to control EBs (Fig. 6B).
However, it has not been determined how cells depleted of GSH (∆gsh1) respond to increased GSH uptake.
