Sentence examples for mouse intestinal cells from inspiring English sources

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.

The genes embedded in these regions showed a dynamic and autonomous regulation during mouse intestinal cell differentiation, indicating that, in the framework considered here, the coordinated regulation in LRES is restricted to cancer.

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).

Recently, it was reported that inhibition of Rho/ROCK pathway by Y-27632 also enhances in vitro survival of mouse ES cell derived neural precursors [9], mouse intestinal stem cells [10] and human keratinocytes [11].

They also suggest that although neonatal mouse intestine is structurally fully developed, with the proper crypt-villus organization similar to that in the adult mouse, the embryonic/neonatal mouse intestinal stem cells are molecularly distinct from those in the adult mouse intestine.

Such behavior theoretically could underlie the observation of tumor-initiating cells in certain types of cancer (Reya et al, 2001) and has recently been reported for mouse intestinal stem cells (Vermeulen et al, 2013; Snippert et al, 2014).

In vivo studies further revealed that JNK2 deficiency led to upregulation of β-catenin and increase of GSK3-β phosphorylation in JNK2-/ mouse intestinal epithelial cells.