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Type 1 interferon has been found to be present in epithelial layers and epidermis in humans and identified as an endogenous inhibitor of angiogenesis in skin[52].
Indeed, sPLA2-IID and sPLA2-V were found to be present in epithelial cells of normal mucosa, and their expression was markedly reduced in tumours.
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Somatic nonsense or insertion/deletion (indel) mutations that result in loss of the RING finger domain of BIRC3 were found to be present in a wide range of epithelial tumors and were also shown to be oncogenic.
nAChR subunits were found to be present in a wide variety of non-neuronal cells, including those of epithelial and endothelial origin [9].
All epithelial cell types were found to be present within these clonal normal populations including luminal, myoepithelial, ductal and lobule-committed epithelial progenitors and fully competent mammary epithelial stem cells.
Finally, some of these proteins were found to be adherent to intestinal epithelial cells in vitro.
In contrast to a previous report showing that leptin was absent in normal mucosa, we found that leptin was present in epithelial cells and the lamina propria layer in both control and IBD patients.
In some tissue samples, epithelial basal cells were also found to be positive for probe hybridization.
ERα staining was present in epithelial cells throughout the tumour.
DCAMKL1 cells were present in epithelial cell linings, since the cells had desmosomes in the junction with adjacent epithelial cells.
IK channels may also be present in the epithelial cells of guinea-pig jejunum because they have been identified in rat colonic epithelial cells [43].
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