Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of prenatal ethanol exposure on the intestinal maturation of rat fetuses was investigated to understand the nutritional alterations found in the offspring of alcoholic mothers. Female Wistar rats were maintained on solid diet and 25% ethanol solution as drinking fluid during pregnancy, and non-alcoholic isocaloric pregnant mothers were used as controls. At birth, intestines from unsuckled pups were removed for study. The weight and length of the intestine decreased significantly when ethanol was present in utero. Ultrastructural evaluation of the epithelium revealed loss of contact between neighboring enterocytes and abnormal dilation of the cisternae of the Golgi apparatus in ethanol-exposed pups. Further, increased lysosome-like vesiculation and enhanced lysosomal beta-galactosidase activity was observed in these neonates. The total number of absorptive enterocytes in the epithelium was reduced by 30% in ethanol-exposed neonates as compared to controls, due to altered cell growth and death during fetal life. Ethanol in utero stimulated epithelial cell migration which compensated cell loss, as demonstrated by 5'-Bromodeoxyuridine labeling. These findings could have important implications for the assimilation of nutrients and failure to thrive in infants with fetal alcohol syndrome.
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PMID:Ethanol in utero induces epithelial cell damage and altered kinetics in the developing rat intestine. 903 46

CD95(FAS/Apo-1) belongs to the family of TNF receptor related molecules and is expressed on many benign and malignant types of cells. CD95 triggering is involved in the apoptotic death of lymphoid cells and may also be important in myelopoiesis. Myeloid leukemia cells are in most cases resistant to CD95 triggering despite expressing the antigen. We reasoned that myeloid leukemic cells can become sensitized to the Fas pathway of cell death if CD95 expression is restored by gene transfer. As a model, we utilized the cell line K562 which does not express CD95 on their cell surface. The gene for CD95 was introduced into K562 cells (by electroporation). As a control, the gene coding for beta-galactosidase was used. The CD95 transfected K562 cells stably expressed CD95, and had a growth pattern comparable to untransfected cells, but still remained resistant to Fas-triggering (tested using recombinant Fas-ligand). Our experiment shows that antigen expression is not a critical determinant of Fas-mediated apoptosis, but further down-stream mechanisms determine the fate of the cells. The transfected cells also had a comparable susceptibility to NK-mediated lysis which shows that the expression of CD95 does not interfere with NK-mediated lysis of target cells.
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PMID:Expression of CD95(FAS) by gene transfer does not sensitize K562 to Fas-killing. 916 3