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

We have recently isolated cDNA clones representing four alternative splice forms of a T cell-specific transcription factor, TCF-1. Here we report the characterization of the human gene encoding this factor. The TCF-1 gene is contained in 10 exons including an untranslated first exon. The DNA-binding high mobility group (HMG) box of TCF-1 is encoded by the closely spaced exons VI and VII. Differential splicing involves an alternative exon (IX) and three splice acceptor sites in exon X. Based on comparison of sequence and on the placement of an alternative exon, TCF-1 appears closely related to the recently characterized HMG box transcription factor TCF-1 alpha/LEF. In particular, the HMG boxes encoded by the two TCF genes are virtually identical. The TCF-1 gene resides on chromosome 5 band q31.1. The TCF-1 promoter coincides with a CpG island. As determined by chloramphenicol acetyltransferase analysis, the promoter is preferentially active in T cells. The promoter does not contain TCF-1/TCF-1 alpha binding sites and is therefore not autoregulated. This observation implies the existence of yet uncharacterized T cell transcription factors that are active during early T cell differentiation.
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PMID:The human T cell transcription factor-1 gene. Structure, localization, and promoter characterization. 156 1

Neuron-specific enolase (NSE) occurs in mature neurons and paraneurons. We have isolated the genomic clone coding for rat NSE and clarified its gene structure. In order to analyze the regulatory sequence in the 5'-upstream region and introns, we carried out transient expression experiments of NSE genomic DNA fragments fused to chloramphenicol acetyltransferase (CAT) gene which were transfected into several cultured cells. The used cells were primary cultured rat neurons, PC12, neuroblastoma 35, neuroblastoma 103, C6, primary cultured rat glial cells and HeLa cells. The promoter sequence (190 bp) upstream to the transcription initiation site was important in the expression of CAT gene in these cells. From the experiments with external and internal deletion mutants of the fusion gene, the cis-acting regulatory region responsible for the enhanced expression of the CAT activity in the primary cultured neuron and PC12 cells was found to be localized at upstream 500 bp sequence of the intron 1 and 1.5 kbp upstream sequence of the transcription initiation site. In the upstream important sequences, there were the nearest sequences for AP-1 binding motif, AP-2 binding element, SP-1 binding sequence, cAMP response element, half site of glucocorticoid receptor (GRE) binding sequence, half site of thyroid hormor receptor (TR) or retinoic acid receptor (RAR) binding sequence and MTF-1 binding sequence. Furthermore, Octamer-6 binding motifs also were found. In the intron 1, 5' end upstream 50 bp and downstream 100 bp were the most important sequences. We found the nearest sequences for cAMP response element, E2F binding sequence, early growth response (EGR)-1 binding motif, half site of TCF-1 binding sequence and a neuron-specific element-like sequence in the intron 1.
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PMID:Upstream and intron regulatory regions for expression of the rat neuron-specific enolase gene. 770 74

We previously reported that expression of the T-cell receptor (TCR) alpha and lck genes is extinguished in hybrids between mouse T-lymphoma EL4 cells and mouse fibroblast B82 cells. In the present study, we found that the activities of the TCRalpha minimum enhancer and the lck promoter monitored by the luciferase or chloramphenicol acetyltransferase (CAT) assays were markedly inhibited in the hybrids. Expression of the TCF-1, LEF-1, GATA-3, Ikaros, c-myb and Fli-1 genes, which encode the haematopoietic cell-restricted transcription factors that appear to be responsible for the activities of the enhancer and the promoter, was fully extinguished or markedly suppressed in the hybrids. On the other hand, expression of the transcription factor genes observed in both parental cells, such as the AML1 and c-ets-1 genes, and that of the genes encoding ubiquitously expressed transcription factors, such as the E2A, CREB and c-ets-2 genes, was not significantly suppressed in the hybrids. These results suggest that the genes encoding haematopoietic cell-restricted transcription factors are targets for negative regulation in fibroblastic background and that the repression of these genes may consequently lead to suppression of the promoter and/or enhancer activities of several T-cell-specific structural genes in T-lymphoma x fibroblast cell hybrids.
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PMID:Extinction of expression of the genes encoding haematopoietic cell-restricted transcription factors in T-lymphoma x fibroblast cell hybrids. 1168 56