Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have stably expressed a trans-activation suppressing deletion mutant of the human c-jun gene (TAM-67) in the malignant mouse epidermal cell lines 10Gy5 and PDV. Expression of the p26 mJUN protein blocked both constitutive and inducible transcriptional trans-activation of several AP-1 responsive reporter chloramphenicol acetyltransferase constructs. p26 mJUN was able to block both 12-O-tetradecanoylphorbol-13-acetate (TPA) and okadaic acid induced expression of the mouse stromelysin gene in 10Gy5 cells and TPA induced expression of the urokinase-type plasminogen activator gene in PDV cells as determined by Northern analyses. Both genes contain TPA response elements in their promoter regions and are known to be AP-1 responsive. The presence of p26 mJUN in nuclear extracts, as determined by Western blotting, did not detectably alter the DNA binding activity of endogenous AP-1 as determined by gel shift analysis with an oligonucleotide containing a single high affinity AP-1 binding site. UV cross-linking studies coupled with Western analyses identified DNA bound cJUN but not mJUN in nuclear extracts of stably transfected cell lines, suggesting that the mutant JUN protein may exert some of its antioncogenic effects in malignant mouse epidermal cells by a mechanism(s) not involving DNA binding. Malignant mouse epidermal cells which stably expressed the mutant JUN protein were not only inhibited in their AP-1 trans-activation response, but also in their ability to form s.c. tumors in nude mice. These results indicate that inhibition of AP-1 mediated transcriptional trans-activation alone can be sufficient to suppress the tumorigenic phenotype in a subset of malignant mouse epidermal cells.
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PMID:Stable expression of a c-JUN deletion mutant in two malignant mouse epidermal cell lines blocks tumor formation in nude mice. 812 97

An enzyme, 8-oxo-7,8-dihydrodeoxyguanosine triphosphatase (8-oxo-dGTPase), is present in various organisms and plays an important role in the control of spontaneous mutagenesis. The enzyme hydrolyzes 8-oxo-dGTP, an oxidized form of dGTP, to 8-oxo-dGMP, thereby preventing the occurrence of A:T to C:G transversion, caused by misincorporation. We isolated the mouse genomic sequence encoding the enzyme and elucidated its structure. The gene, named MTH1 for mutT homologue 1, is composed of at least five exons and spans approximately 9 kilobase pairs. A genomic region containing the pseudogene was also isolated. The promoter region for the gene is GC-rich, contains many AP-1 and AP-2 recognition sequences, and lacks a typical TATA box. Primer extension and S1 mapping analyses revealed the existence of multiple transcription initiation sites, among which a major site was defined as +1. The putative promoter region was placed upstream of the chloramphenicol acetyltransferase reporter gene, and control of expression of the gene was examined by introducing the construct into mouse NIH 3T3 cells. Deletion analysis indicated that a sequence from -321 to +9 carries the basic promoter activity while an adjacent region, spanning from +352 to +525 stimulates the frequency of transcription.
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PMID:Organization and expression of the mouse MTH1 gene for preventing transversion mutation. 901 34