Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0268596 (EMA)
 2,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The goal of this study was to determine the effects of tobacco compounds on gene expression in a human fetal lung cell line (WI38). In the present study, we investigated the effects of tobacco compounds (nicotine, benzo(a)pyrene (B(a)P), and 2-Naphthylamine) on gene expression profiles in human fetal fibroblasts using cDNA microarray and real-time PCR. WI38 cells were cultured in Eagle's minimum essential medium (MEM) supplemented with 10% fetal bovine serum, 2% 200 mM L-glutamine, and a 2% penicillin and streptomycin solution. Tissue culture flasks (T-25 cm(2)) containing confluent lung fibroblasts were incubated at 37 degrees C for 24 h with 5 mL of medium supplemented with 10 microM of a tobacco compound (nicotine, B(a)P, or 2-Naphthylamine). The gene expression profiles for the W138 cells varied depending on the tobacco compound. The cDNA microarray analysis revealed that apoptosis-related genes such as DNASE2, MADD, MST1, NME3, RARG, TNFRSF1A, BAD, and DFFB genes were down-regulated in tobacco compound-treated WI38 cells. We also observed significant increases in Arnt gene expression by real-time PCR in tobacco compound-treated WI38 cells. Tobacco compounds can affect apoptosis, immunity, and growth in WI38 cells. A microarray-based genomic survey is a high-throughput approach for the evaluation of gene expression in cell lines treated with tobacco compounds.
 ...
PMID:Effects of tobacco compounds on gene expression in fetal lung fibroblasts. 1824 14

In 1997, a German group demonstrated that the antigen of the biomarker EMA (endomysial antibodies) in coeliac disease is a calcium-dependent thiol enzyme, transglutaminase type 2 (TG2). This most important discovery opened up an exciting field of research aimed at a better understanding of the pathogenesis of coeliac disease, a T-cell-driven autoimmune disorder with a prevalence of about 1%. The accidental activation of TG2, possibly caused by a stress-induced local deficiency of zinc in the intestinal wall, might play a key role where the enzyme catalyzes an atypical deamidation of specific glutamine residues of food gliadins. The genetic contribution is HLA DQ2 or DQ8, which can form a complex with the TG2-modified gliadin residues, resulting in an immune response with the formation of antibodies against both gliadin and the enzyme. Indeed, the immunopathogenesis of coeliac disease can now be recognized partly at the molecular level. Progress has already improved the opportunities for laboratory diagnostics and, hopefully, new ways of treating and preventing coeliac disease will become available. These exciting developments might stimulate research within other fields of autoimmune disorders. With its focus on TG2, this review highlights some of the intriguing mechanisms of the pathogenesis of coeliac disease, such as the structure of the neo-antigen, the involvement of calcium and zinc, and the effects of coeliac antibodies on TG2 activity. Moreover, the many pitfalls due to dubious laboratory practice are addressed, as is the potential when a fundamental biological mechanism is understood at the molecular level.
 ...
PMID:Transglutaminase and the pathogenesis of coeliac disease. 1824 2