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Nevertheless, our data indicate that HDAC1 and HDAC2 may regulate intestinal epithelial cell fate, in part through Notch pathway regulation, as well as the relative production and maturation of differentiated cells from progenitors.
NFAT5 may regulate intestinal cell differentiation via the inhibition of the Wnt/ β-catenin pathway.
As PTL-1 regulates kinesin-based transport (Tien et al., 2011), neuronal PTL-1 may regulate intestinal SKN-1 via signalling molecules carried by SVs.
Inhibition of NO synthesis has been shown to increase intestinal permeability via mast cells, which suggests that NO may regulate intestinal barrier function [ 43, 44].
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In vivo, some additional contributions from the intestinal environment may differentially regulate intestinal homeostasis.
It has a protective role in intestinal injury models, and may regulate proliferation of intestinal epithelial cells by modulating responsiveness to growth factors [ 25, 26].
Zimberlin, C. D. et al. HDAC1 and HDAC2 collectively regulate intestinal stem cell homeostasis.
Gil-Cruz, C. et al. Fibroblastic reticular cells regulate intestinal inflammation via IL-15-mediated control of group 1 ILCs.
Tian, H. et al. Opposing activities of notch and wnt signaling regulate intestinal stem cells and gut homeostasis.
Tian, H. et al. Opposing activities of Notch and Wnt signaling regulate intestinal stem cells and gut homeostasis.
In addition, AAs modulate growth and metabolism, and regulate intestinal microbiota (Wu et al. 2013, 2014).
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