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)

The 5'-flanking region of the human FcRn alpha-chain gene was analyzed for its ability to directly express the chloramphenicol acetyltransferase (CAT) reporter gene in NIH3T3 and Lu106 cells. Transient transfection of the CAT constructs revealed that there was promoter activity in the region -660 to +300 of the 5'-flanking sequence. Electrophoretic mobility-shift assays showed that there are functional binding sites for Sp1 or Sp1-like factors, AP1 or a related factor, and additional unidentified proteins in the promoter region.
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PMID:Analysis of the promoter region of the human FcRn gene. 1100 87

The role of c-Fos in neurodegeneration or neuroprotection after cerebral ischemia is controversial. To investigate whether early c-Fos induction after ischemia is associated with neuroprotection, rats were subjected to 10 minutes of transient forebrain ischemia and c-Fos expression was examined. Resistant dentate granule cells and neurons in CA2-4 displayed more robust immunoreactivity than vulnerable neurons in the CA1 region of hippocampus during early hours of reperfusion. By 6 hours after reperfusion, c-Fos immunoreactivity was greatly diminished in all areas of the hippocampus. Administration of N-acetyl-O-methyldopamine (NAMDA), a compound previously shown to protect CA1 neurons against ischemia, increased c-Fos immunoreactivity in the CA1 vulnerable region at 6 hours after ischemia and protected SK-N-BE(2)C neurons from oxygen glucose deprivation. Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. In vivo and in vitro results showed that a neuroprotectant, NAMDA, in concert with another stimulus (for example, ischemia or PMA) up-regulates c-Fos expression and suggested that the early rise of NAMDA-induced c-Fos expression in vulnerable CA1 neurons may account for neuroprotection by means of up-regulating late gene expression for survival.
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PMID:Early c-Fos induction after cerebral ischemia: a possible neuroprotective role. 1133 65

We previously reported that the rat aldolase C 115 bp promoter is sufficient to ensure the brain specific expression of the chloramphenicol acetyltransferase reporter gene in transgenic mice. We identify in a further reduced 84 bp promoter several putative binding sites for the transcriptional factors Sp1, USF, AP1, and AP2. Deletion or mutation of these partially overlapping binding sites results in inactivation of the cognate transgenes. Moreover, we show that the 115 bp sequence is able to direct bidirectional transcription in vivo but, surprisingly, transcriptional activity in the opposite direction is no more brain specific.
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PMID:Bidirectional activity and orientation-dependent specificity of the rat aldolase C promoter in transgenic mice. 1141 29

The lactoferrin gene in the mouse uterus is a target gene for natural estrogens and xenoestrogens. One of the xenoestrogens is methyoxychlor, an insecticide that displays both estrogenic and antiandrogenic activities. Recently, methyoxychlor was found to stimulate lactoferrin gene expression in the uterus of an estrogen receptor null mouse. The present study is designed to uncover the methoxychlor response region in the mouse lactoferrin gene promoter. A series of different lengths of the mouse lactoferrin gene 5' flanking region were linked to a chloramphenicol acetyltransferase (CAT) reporter construct and transfected into human endometrial carcinoma HEC-1B cells, an estrogen receptor null cell line, in order to examine the methoxychlor response. The transfected cells were treated with methoxychlor or the metabolite of methoxychlor, HPTE, and the CAT reporter activities were measured. Constructs that contain a mouse lactoferrin 5' region longer than 100 bp were activated more than twofold by both methoxychlor and HPTE. The activation of the CAT reporter by the chemicals was dose dependent and reached saturation. Additional deletion mutants within the 100-bp region were tested, and a GC-rich sequence (GC-II) that we have previously characterized as an epidermal growth factor (EGF) response element was identified to be the region for the methoxychlor response. GC-II binds Sp1, Sp3, and IKLF transcription factors, collaborates with the AP1/CREB binding element, and confers the EGF response. Whether the effect of methoxychlor requires the AP1/CREB binding element has yet to be established; however, the present finding provides an alternative signaling pathway for the xenoestrogens.
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PMID:Methoxychlor stimulates the mouse lactoferrin gene promoter through a GC-rich element. 1190 39

To study the transcriptional mechanisms by which expression of the dopamine receptor regulating factor (DRRF) gene is regulated, a murine genomic clone was isolated using a DRRF cDNA as probe. A 24 kb genomic fragment which comprises 13 kb upstream of the transcription initiation site was sequenced. The promoter region lacks a TATA box and CAAT box, is rich in G+C content, and has multiple putative binding sites for the transcription factor Sp1. The DRRF gene also has consensus sequences for AP1 and AP2 binding sites. The transcriptional activity of five deletion mutants of a 1.5 kb fragment was analyzed by modulating transcription of the heterologous chloramphenicol acetyltransferase (CAT) gene in the promoterless plasmid pCAT-Basic. All mutants showed significant transcriptional activity in the murine neuroblastoma cell line NB41A3, except the construct stretching from -901 to +17. These transient expression assays suggested the presence of positive regulators between -1153 and -901 and between -118 and -93 while a negative regulator was found in the region between -901 and -118. Comparison among cell types revealed strong transcriptional activity of the DRRF promoter in neuronal NB41A3 cells and moderate activity in hepatic HepG2 and renal OK cells, but none in skeletal muscle C2C12 or glial C6 cells. These findings confirm the tissue-specific activity of the DRRF promoter and suggest that this gene shares structural and functional similarities with the dopamine receptor genes that it regulates.
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PMID:Genomic organization and promoter characterization of the murine dopamine receptor regulating factor (DRRF) gene. 1256 28

Anchoring fibrils at the cutaneous basement membrane zone of the stratified squamous epithelia are essential to maintaining skin integrity, as absence of these structures leads to the chronic blistering disease, dystrophic epidermolysis bullosa. Type VII collagen, the major component of anchoring fibrils, is synthesized primarily by basal keratinocytes and to a lesser degree by dermal fibroblasts. To elucidate the transcriptional control elements of the type VII collagen gene (Col7a1), 3 kb of 5' flanking sequence of the mouse gene was cloned, sequenced, and fused to the chloramphenicol acetyltransferase reporter gene. Promoter deletion analyses revealed that 560 bp of Col7a1 5' flanking sequence was sufficient and necessary for basal level of transcription in cultured murine keratinocytes. Mutagenesis of DNA sequences with similarity to consensus binding sites for transcription factors, including Sp1/Sp3, AP2, AP1, and Smads, within the p-560Col7a1 promoter/chloramphenicol acetyltransferase construct, coupled with DNA binding assays, revealed the importance of these sites for basal Col7a1 expression. The effect of transforming growth factor beta, an activator of Col7a1 expression in keratinocytes and dermal fibroblasts, was examined using the same Col7a1 promoter/chloramphenicol acetyltransferase constructs. These analyses demonstrated that transforming growth factor beta1 stimulation of Col7a1 transcription is dependent on a putative interaction between Smads and AP1. Interestingly, the Smad-like binding site was essential for both basal and transforming growth factor beta1 stimulated Col7a1 transcription. Collectively, these findings attest to the complex regulation of Col7a1 transcription in epidermal keratinocytes.
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PMID:Transcriptional control of the mouse Col7a1 gene in keratinocytes: basal and transforming growth factor-beta regulated expression. 1467 98


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