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)

Interferon-gamma (IFN-gamma) regulates a variety of immunoregulatory functions through the induction of a specific set of IFN-gamma response genes. This includes the invariant chain associated with the major histocompatibility complex class II molecules. To investigate the mechanism involved in the invariant chain (In) response to IFN-gamma we constructed chloramphenicol acetyltransferase (CAT) hybrid genes in which the CAT gene is under the control of the In promoter. The glioblastoma cell line, U-373 MG, transfected with a CAT construct having the In promoter sequence -790 to +1 bp showed over 3-fold increased CAT activity when treated with IFN-gamma indicating that this region confers IFN-gamma responsiveness to the CAT gene. The IFN-gamma response element in the promoter was further sublocalized to the region -120 to -61 base pairs (bp). This region contains homology to the interferon-stimulated response elements identified in other IFN responsive genes. By gel shift analyses, an IFN-gamma-induced sequence-specific DNA-binding factor was identified. This induced complex binds to an oligonucleotide corresponding to -107 to -79 bp of the In promoter. Mutations of this binding site at -94 and -92 bp drastically decreased binding of the constitutive and IFN-gamma-induced complexes. This IFN-gamma induced factor also binds to an oligonucleotide corresponding to -91 to -62 bp of the interferon-beta (IFN-beta) gene promoter, a region necessary for the induction of the IFN-beta gene by virus and double-stranded RNA. This binding specificity is characteristic of a family of DNA binding factors that bind both the interferon-stimulated response elements and the IFN-beta gene promoter.
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PMID:Interferon-gamma-inducible regulation of the human invariant chain gene. 189 64

We report a functional analysis of the human thymidine kinase (tk) gene promoter. We have linked the tk promoter to the chloramphenicol acetyltransferase (CAT) gene to allow direct measurement of promoter strength by assaying chloramphenicol acetyltransferase enzyme activity after transfection into mouse L cells. Putative transcription elements have been identified by deletion and mutation analysis of this promoter. The promoter relies primarily on two "CCAAT" elements and a series of "GC" elements found farther upstream. Two-thirds of promoter activity is maintained by a construct containing 139 base pairs of sequence upstream of the initiation of transcription that contains only one GC and one of the CCAAT elements. In addition, an evolutionary comparison identifies two highly conserved promoter elements: the -40 CCAAT element and a "TATA" element located at -21. We have further characterized both CCAAT elements using a mutational as well as protein binding analysis. From this study we have determined that both the -70 and -40 CCAAT elements bind strongly to the same factor, with a slightly higher affinity for the -40 CCAAT. Competition studies suggest that the CCAAT factor that binds to this promoter is homologous to protein nuclear factor Y, which binds to the major histocompatibility complex class II E alpha gene promoter. In addition, either CCAAT element is capable of supplying almost as much promoter strength as is supplied in the presence of both.
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PMID:The human thymidine kinase gene promoter. Deletion analysis and specific protein binding. 291 10

The function of the 5'-flanking region of the mouse major histocompatibility complex gene Ed alpha has been studied by deletion analysis with the chloramphenicol acetyltransferase gene as a transient expression marker in various cell lines. This analysis reveals the presence of several control regions on the 5' side of the gene. Sequences between base pair (bp) -873 and bp -353 have a negative function in human and mouse fibroblasts but not in the mouse macrophage line WEHI-3. Additional positive and negative elements have been mapped between bp -353 and bp -38. A gamma-interferon response region has been also identified within that sequence. the 5' and 3' boundaries of the gamma-interferon response region have been located between bp -164 and bp -43. Inducible human cell lines showed the same gamma-interferon response region endpoints with the mouse cell line WEHI-3. A DNA fragment spanning the equivalent region of the mouse Ed beta gene confers gamma-interferon inducibility to the simian virus 40 and alpha-globin promoters in an orientation-independent manner. We further provide evidence that the conserved sequence motifs on the 5' side of all major histocompatibility complex class II genes are indispensable for gamma-interferon induction.
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PMID:Multiple regulatory regions on the 5' side of the mouse E alpha gene. 312 25

Cellular adherence is important for monocyte migration and function and is known to induce monocyte activation, leading to the production of mRNA for several proto-oncogenes and cytokines. In addition, since cellular adherence has important intracellular signalling function, it has the potential to enhance human immunodeficiency virus (HIV) replication in monocytic cells. We have investigated the effects of adhesion of the monocytic cell line THP-1 transfected with HIV1 or HIV2 long terminal repeat chloramphenicol acetyltransferase (LTR CAT) constructs. These studies have shown that adherence to tissue culture plastic or confluent endothelial cells is essential for enhanced HIV LTR CAT expression in lipopolysaccharide-stimulated cells. In addition, we have investigated the effects of engagement of specific adhesion molecules, using immobilized antibodies, on HIV replication in the promonocytic cell line OM101, which contains a single latent proviral copy of HIV. Such studies have demonstrated that engagement of CD18, the beta subunit of the lymphocyte function-related antigen-1 (LFA-1) and major histocompatibility complex class II (MHC II) enhanced HIV replication. LFA-1 is involved in both monocyte-endothelial cell interactions and monocyte-T-cell interactions, and MHC II is involved in monocyte interaction with antigen-specific T cells. These data suggest that such interactions of membrane adhesion molecules with their appropriate ligand enhance HIV replication in vivo. Thus, this study has demonstrated that cellular adherence is a key regulatory factor of HIV replication in monocytic cells.
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PMID:Cellular adherence enhances HIV replication in monocytic cells. 780 Sep 38

In the present report, the effects of IFN-gamma and transforming growth factor beta1 (TGF-beta1) on major histocompatibility complex class II (MHC-II) gene expression in isolated mouse brain microglial cells, in the MH-S macrophage cell line and in the primary mouse macrophage cultures were examined. IFN-gamma is a potent inducer of MHC-II gene and this induction was further elevated in microglia by TGF-beta1, while TGF-beta1 inhibited IFN-gamma, induction in macrophages. The enhancing effect of TGF-beta1 was also detected in microglia at the protein level. Transient transfection of microglia with 5' deletional mutants of the MHC-II IAalpha promoter linked to the chloramphenicol acetyltransferase reporter gene demonstrated that TGF-beta1 acts at the transcriptional level to enhance the MHC-II expression induced by IFN-gamma.
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PMID:Effect of transforming growth factor-beta1 on microglial MHC-class II expression. 1069 7