Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.99.3 (diaphorase)
 5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By differential hybridization, we have isolated 14 cDNA clones corresponding to genes that are more highly expressed in the flat revertant cell line R1 than in the parental human Ha-ras oncogene-transformed NIH/3T3 cell line (EJ-NIH/3T3). From cross-hybridization experiments, we determined that 5 sequence families accounted for the 14 clones. DNA sequencing revealed that four out of five selected cDNA clones represented mitochondrial genes (cytochrome b, cytochrome c oxidase subunit II, NADH dehydrogenase subunits 1 and 4, respectively), whereas one cDNA clone was homologous to the alpha 2 (type I collagen gene. Although a Southern blot analysis of the studied cell lines showed similar copy numbers of mitochondrial genomes, the transcript levels of the mitochondrial genes were high in R1, intermediate in NIH/3T3 and low in EJ-NIH/3T3 and partially revertant R2 cell lines. alpha 2 (type I) collagen mRNA levels were high in R1 and NIH/3T3, intermediate in R2 and low in EJ-NIH/3T3 cells. These results suggest that a complex alteration of the expression of mitochondrial and extracellular matrix components may be closely associated with the flat reversion of the transformed cells.
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PMID:Identification of genes that exhibit increased expression after flat reversion of NIH/3T3 cells transformed by human activated Ha-ras oncogene. 187 59

The flat revertant cell line R1, isolated from human activated Ha-ras oncogene transformed NIH/3T3 cells (EJ-NIH/3T3) by mutagen treatment, expresses a variant form of the actin-regulatory protein gelsolin, designated p92-5.7. To clone the gene encoding p92-5.7, gelsolin cDNAs were isolated from a cDNA library of R1 cells. In vitro transcription-translation and nucleotide sequence analyses of the cloned cDNAs identified a point mutation in codon 321 at the cause for the expression of p92-5.7. Considering gelsolin's function as an actin binding protein, the expression of alpha-actin, which is downregulated in many transformed fibroblasts, was analyzed. In EJ-NIH/3T3 cells no alpha-actin transcript was detected, whereas in R1 cells alpha-actin mRNA expression was restored to a level similar to NIH/3T3 cells. Immunofluorescence staining of the cells with an alpha-actin specific monoclonal antibody did not detect any alpha-actin containing microfilaments in EJ-NIH/3T3 cells, but revealed an ordered microfilament pattern in R1 and NIH/3T3 cells. In order to identify other genetic alterations that may also contribute to the revertant phenotype, genes with an elevated expression in R1 cells compared with the parental EJ-NIH/3T3 cells were isolated by using a differential hybridization approach. The identified sequences represented mitochondrial (cytochrome b, cytochrome c oxidase subunit II, NADH dehydrogenase subunits 1 and 4) and alpha 2 (type I) collagen genes. In summary, these results suggest that a complex alteration of the expression of cytoskeletal, mitochondrial and extracellular matrix components is closely associated with the flat reversion of R1 cells.
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PMID:[A study on alterations of gene expression in a flat revertant R1 from ras-oncogene transformed NIH/3T3 cells]. 769 63