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HIV type 1 Tat inhibits tumor necrosis factor alpha-induced repression of tumor necrosis factor receptor p55 and amplifies tumor necrosis factor alpha activity in stably tat-transfected HeLa Cells.
AIDS Res Hum Retroviruses. 2001 Aug 10; 17(12):1125-32.AR

Abstract

The human immunodeficiency virus type 1 (HIV-1) Tat protein is a key regulatory protein in the HIV-1 replication cycle. Tat interacts with cellular transcriptional factors and cytokines, such as tumor necrosis factor (TNF-alpha), and alters the expression of a variety of genes in HIV-1-infected and noninfected cells. To further elucidate the mechanisms by which HIV-1 Tat amplifies the activity of TNF-alpha, we transfected the HIV-1 tat gene into an epithelial (HeLa) cell line. We observed that Tat-expressing cells had increased NF-kappa B-dependent trans-activational activity due to enhanced NF-kappa B--DNA binding in response to TNF-alpha treatment. Tumor necrosis factor receptor (TNFR) p55 was the prominent receptor, as neutralizing antibodies to TNFR p55, but not to TNFR p75, blocked TNF-alpha-mediated NF-kappa B activation. Furthermore, tat-transfected cells were more sensitive to TNF-alpha-induced cytotoxicity and only the neutralizing antibodies to TNFR p55 completely protected the cells. To determine whether TNFR p55 was involved in amplification of cellular response to TNF-alpha by HIV-1 Tat, we investigated the effect of TNF-alpha on TNFR p55 expression in the tat-transfected cells. TNF-alpha treatment resulted in a reduction in both TNFR p55 mRNA and protein levels in the control cells but not in the tat-transfected cells as determined with Northern blot and Western blot analyses, respectively. Our results indicate that HIV-1 Tat may inhibit TNF-alpha-induced repression of TNFR p55 and thereby amplify TNF-alpha activity in these stably transfected cells.

Authors+Show Affiliations

Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health and Science, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11522182

Citation

Chiao, C, et al. "HIV Type 1 Tat Inhibits Tumor Necrosis Factor Alpha-induced Repression of Tumor Necrosis Factor Receptor P55 and Amplifies Tumor Necrosis Factor Alpha Activity in Stably Tat-transfected HeLa Cells." AIDS Research and Human Retroviruses, vol. 17, no. 12, 2001, pp. 1125-32.
Chiao C, Bader T, Stenger JE, et al. HIV type 1 Tat inhibits tumor necrosis factor alpha-induced repression of tumor necrosis factor receptor p55 and amplifies tumor necrosis factor alpha activity in stably tat-transfected HeLa Cells. AIDS Res Hum Retroviruses. 2001;17(12):1125-32.
Chiao, C., Bader, T., Stenger, J. E., Baldwin, W., Brady, J., & Barrett, J. C. (2001). HIV type 1 Tat inhibits tumor necrosis factor alpha-induced repression of tumor necrosis factor receptor p55 and amplifies tumor necrosis factor alpha activity in stably tat-transfected HeLa Cells. AIDS Research and Human Retroviruses, 17(12), 1125-32.
Chiao C, et al. HIV Type 1 Tat Inhibits Tumor Necrosis Factor Alpha-induced Repression of Tumor Necrosis Factor Receptor P55 and Amplifies Tumor Necrosis Factor Alpha Activity in Stably Tat-transfected HeLa Cells. AIDS Res Hum Retroviruses. 2001 Aug 10;17(12):1125-32. PubMed PMID: 11522182.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - HIV type 1 Tat inhibits tumor necrosis factor alpha-induced repression of tumor necrosis factor receptor p55 and amplifies tumor necrosis factor alpha activity in stably tat-transfected HeLa Cells. AU - Chiao,C, AU - Bader,T, AU - Stenger,J E, AU - Baldwin,W, AU - Brady,J, AU - Barrett,J C, PY - 2001/8/28/pubmed PY - 2001/11/3/medline PY - 2001/8/28/entrez SP - 1125 EP - 32 JF - AIDS research and human retroviruses JO - AIDS Res. Hum. Retroviruses VL - 17 IS - 12 N2 - The human immunodeficiency virus type 1 (HIV-1) Tat protein is a key regulatory protein in the HIV-1 replication cycle. Tat interacts with cellular transcriptional factors and cytokines, such as tumor necrosis factor (TNF-alpha), and alters the expression of a variety of genes in HIV-1-infected and noninfected cells. To further elucidate the mechanisms by which HIV-1 Tat amplifies the activity of TNF-alpha, we transfected the HIV-1 tat gene into an epithelial (HeLa) cell line. We observed that Tat-expressing cells had increased NF-kappa B-dependent trans-activational activity due to enhanced NF-kappa B--DNA binding in response to TNF-alpha treatment. Tumor necrosis factor receptor (TNFR) p55 was the prominent receptor, as neutralizing antibodies to TNFR p55, but not to TNFR p75, blocked TNF-alpha-mediated NF-kappa B activation. Furthermore, tat-transfected cells were more sensitive to TNF-alpha-induced cytotoxicity and only the neutralizing antibodies to TNFR p55 completely protected the cells. To determine whether TNFR p55 was involved in amplification of cellular response to TNF-alpha by HIV-1 Tat, we investigated the effect of TNF-alpha on TNFR p55 expression in the tat-transfected cells. TNF-alpha treatment resulted in a reduction in both TNFR p55 mRNA and protein levels in the control cells but not in the tat-transfected cells as determined with Northern blot and Western blot analyses, respectively. Our results indicate that HIV-1 Tat may inhibit TNF-alpha-induced repression of TNFR p55 and thereby amplify TNF-alpha activity in these stably transfected cells. SN - 0889-2229 UR - https://www.unboundmedicine.com/medline/citation/11522182/HIV_type_1_Tat_inhibits_tumor_necrosis_factor_alpha_induced_repression_of_tumor_necrosis_factor_receptor_p55_and_amplifies_tumor_necrosis_factor_alpha_activity_in_stably_tat_transfected_HeLa_Cells_ L2 - https://www.liebertpub.com/doi/full/10.1089/088922201316912736?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -