α-Linolenic acid, an endogenous ligand of FFA1, induces GLP-1 secretion in GLUTag cells and in primary fetal mouse intestinal cells.
Co-culture of m-ICcl2 mouse intestinal cells with H. muridarum resulted in increased transcription and synthesis of two CXC chemokines, Cxcl1 and Cxcl2.
Although both gain- and loss-of-function approaches used in this report highlighted a positive role for PTK6 in anchorage-independent survival, other studies utilizing mouse intestinal cells and rat fibroblasts suggest that PTK6 may be required for cell death triggered by specific stimuli such as DNA damage [41], [42].
These data indicate that the apparently high expression of Limk2 in mouse intestinal cells becomes repressed, probably via promoter methylation and consequent inhibition, during tumorigenesis.
Altogether, these data clearly indicate that ectopic expression of ApoA-IV in HeLa cells lead to its partial targeting to lipid droplets, as observed in Caco-2/TC7 enterocytes and mouse intestinal cells.
Consistent with the absence of Paneth cells, which are essential components of the mouse intestinal stem cell niche (Sato et al, 2011), isolated crypts from Src Fyn Yes KO intestines were unable to form organoids in culture (Sato et al, 2009; Fig 6L P).
In this regard, it is of interest to note that we detect mRNA expression of GPR119 in the GLUTag mouse intestinal L cell line as well as in the human line NCI-H716 cells (JA Hedrick, unpublished data).
Primary mouse intestinal epithelial cells and adenoma cells were isolated from C57BL/6- Apc Min mice (Apc Min mice) as reported (Zhang et al., 2010).
LIMK2 deletion increases mouse intestinal stem cell proliferation in vitro.
We next wished to determine whether there was a conserved role for Limk2 in regulating mouse intestinal stem cell homeostasis.
