1. Regulation of intestinal epithelial gene expression in hypoxia
Cormac T. Taylor 
Kidney International 
Volume 66, Issue 2, Pages (August 2004)
DOI: /j _12.x
Copyright © 2004 International Society of Nephrology Terms and Conditions

2. Figure 1
Autocrine regulation of intestinal epithelial permeability in hypoxia. Mucosal hypoxia occurs coincidentally with inflammation in chronic mucosal inflammatory disease. Hypoxia-elicited epithelial tumor necrosis factor-alpha (TNF-α) synergizes with immune cell-derived interferon-gamma (IFN-γ) to cause increased epithelial permeability, an event which leads to the non-specific movement of luminal antigenic material to the lamina propria, which houses the mucosal immune system, thus potentiating the inflammatory state.
Kidney International  , DOI: ( /j _12.x)
Copyright © 2004 International Society of Nephrology Terms and Conditions

3. Figure 2
Phosphorylation-dependent targeting of cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) to ubiquitination/degradation in hypoxia. In normoxia, CREB is maintained in its unphosphorylated (stable) state through the activity of PP1γ. Under these conditions, CREB acts as a repressor of tumor necrosis factor-alpha (TNF-α) transcription. In hypoxia, decreased PP1γ activity leads to CREB phosphorylation, ubiquitination and degradation. Coincidentally IκB is degraded, nuclear factor-κB (NF-κB) becomes activated and transcription of the TNF-α gene ensues.
Kidney International  , DOI: ( /j _12.x)
Copyright © 2004 International Society of Nephrology Terms and Conditions