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 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

Epidemiologic studies show an association between infection with human immunodeficiency virus type 1 (HIV-1) and human papillomavirus (HPV) associated anogenital disease. To investigate possible molecular mechanisms of HIV-1 modulation of HPV expression, we studied the effect of an HIV-1 regulatory protein, tat1, on gene expression directed by the upstream regulatory region (URR) of HPV type 16 (HPV 16). HPV 16 URR-directed chloramphenicol acetyltransferase (CAT) expression driven by the native HPV 16 promoter (P97) was increased in the presence of tat1 alone. Tat1 also reversed E2-mediated repression of P97-directed CAT expression. E2 mediated CAT expression with URR constructs containing the SV40 promoter was enhanced when tat1 and E2 were cotransfected. Using a cervical carcinoma cell line (SiHa), E2 enhancement of URR-directed gene expression was elevated in the presence of extracellular tat1 or during cocultivation with HIV-1-infected cells. These results show HIV can modulate HPV gene expression in cell culture and that the increased rate of HPV-associated cervical disease in asymptomatic HIV-seropositive women may result from HPV-HIV molecular interactions.
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PMID:The HIV-1 tat protein enhances E2-dependent human papillomavirus 16 transcription. 838 65