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)

Human papillomavirus type 6 (HPV-6) is predominantly associated with benign genital warts whereas HPV-16 and HPV-18 are detected predominantly in carcinomas of the lower genital tract; HPV-6 is found rarely in such carcinomas. Experiments were designed to discriminate between two hypotheses concerning the role of HPV-6 in the genesis of a genital tract carcinoma: (i) the HPV-6 in the carcinoma (HPV6-T70) differs genetically from HPV-6 in a benign lesion (HPV6-W50), giving HPV6-T70 properties similar to those of HPV-16/18: (ii) HPV6-T70 and HPV6-W50 have similar biological activity, suggesting that the role of HPV-6 in oncogenesis is different from that of HPV-16/18. Restriction enzyme digestion and DNA sequence determination established that HPV6-T70 differs from HPV6-W50 in the upstream regulatory region (URR) but not in the proteins encoded by open reading frames (ORFs) E5, E6 or E7, ORFs implicated in oncogenesis. To determine whether the difference in the URR sequence could alter the level of expression of viral genes, the URRs were cloned into the enhancerless plasmid pSVEcat. Analysis of chloramphenicol acetyltransferase activity after transfection into HeLa and Vero cells showed that the URRs had comparable enhancer activity. Cotransfection of baby rat kidney (BRK) cells with HPV6-T70 and an activated ras gene indicated that, in contrast to HPV-16 and HPV-18, this HPV-6 genome could not cooperate with ras to transform BRK cells. The data suggest that HPV6-T70 and HPV6-W50 have similar enhancer activity and transforming potential.
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PMID:Relative enhancer activity and transforming potential of authentic human papillomavirus type 6 genomes from benign and malignant lesions. 184 89

Human c-myb is normally involved in the regulation of proliferation and differentiation of hematopoietic cells. Until now, only a few reports have described elevated c-myb gene expression in epithelial tissue, suggesting that under certain circumstances, c-Myb protein might play a role during the process of malignant transformation of epithelial cells. To investigate a possible role of c-myb during papillomavirus-associated carcinogenesis, we investigated the c-myb mRNA expression in human papillomavirus (HPV)-associated tumors and tumor cell lines. Seven of nine cervical carcinomas and two of three carcinoma cell lines exhibited elevated c-myb transcriptional activity. In contrast to malignant cervical neoplasias, only 3 of 15 condylomata acuminata expressed a sparse signal for c-myb mRNA. Since the c-Myb protein has been described as a potent transcriptional regulator, we investigated the transactivating properties of c-Myb on the HPV-16 promoter/enhancer. Cotransfection of a chloramphenicol acetyltransferase-reporter plasmid containing the HPV-16 enhancer/promoter element with a full-length c-Myb-expressing plasmid resulted in a significant induction (4.3-fold) of the HPV-16 promoter, whereas expression of a carboxy-terminally deleted c-Myb protein led to no effects. Gel shift experiments showed a specific binding of recombinant c-Myb protein on the HPV-16 P97 enhancer. These data indicate that elevated c-myb expression occurs with HPV-associated cell transformation. Since c-Myb has been shown to stimulate the HPV-derived oncoprotein expression via transcriptional activation, it may play a role in the process of HPV-associated cervical carcinogenesis.
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PMID:Human c-myb is expressed in cervical carcinomas and transactivates the HPV-16 promoter. 767 Dec 56

Human papillomavirus type 6 (HPV-6) DNA is the predominant HPV type found in condyloma acuminata: it is rarely found in carcinomas. We have previously reported cloning and characterizing an HPV-6 from a vulvar condyloma (HPV6-W50) and an HPV-6 from a vulvar carcinoma (HPV6-T70). The E5, E6 and E7 proteins encoded by the two genomes were identical, however, the two genomes differed in the long control region (LCR). Cloning of the entire LCR into the enhancerless plasmid pSVEcat showed that the two LCRs had comparable enhancer activity. Since the major differences between the two LCRs resided in the 5' end of the LCR, upstream of the L1 polyadenylation signal, we subcloned the two LCRs to analyse more closely their effect on cat gene expression. The data indicated that LCR subclones of the two genomes had comparable chloramphenicol acetyltransferase (CAT) activity. A negative regulatory region was detectable when the test plasmids were transfected into HeLa and C33A cells and in primary keratinocytes. A decrease in CAT activity was also detected when the SV40 early promoter was replaced with the putative HPV-6 E6 promoter. The negative regulatory region functioned in a position- and orientation-independent manner, thus fulfilling the definition of a silencer.
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PMID:Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions. 904 28