Biochemical and Biophysical Research Communications
Regular ArticleTumor Necrosis Factor α and Interleukin-1β Induce Specific Subunits of NF-κB to Bind the HIV-1 Enhancer: Characterization of Transcription Factors Controlling Human Immunodeficiency Virus Type 1 Gene Expression in Neural Cells
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Different molecular mechanisms of HTLV-1 and HIV LTR activation by TPA
2018, Biochemical and Biophysical Research CommunicationsCitation Excerpt :TPA is a strong activator of PKCs which are involved in the activation of different transcriptional factors such as NFқB [30]. Due to the fact that NFҝB has binding sites in different gene promoters including HIV promotor [30,31], we decided to examine possible involvement of NFҝB in TPA induced activation of HIV-1 and possibly HTLV-1 LTRs. Jurkat cells were transfected with either HTLV-1 luc or HIV-1 LTR luc and treated with TPA in the presence or absence of PS-34 (an inhibitor of NF-κ B activation).
Tat controls transcriptional persistence of unintegrated HIV genome in primary human macrophages
2018, VirologyCitation Excerpt :We observed a great enhancement of the LTR-driving luciferase expression following infection of 1G5 with D116N (Fig. 2A). However, the intrinsic leakiness of the LTR promoter in indicator cells such as 1G5 made the measurement of low-level HIV transcription problematic, as stimuli such as cytokines, mitogens (Aguilar-Cordova et al., 1994; Akan et al., 1997; Siekevitz et al., 1987; Sweet and Hume, 1995; Swingler et al., 1992, 1994), or the viral particle binding itself (Merzouki et al., 1995) may also trigger Tat-independent reporter expression. Thus, we pre-treated cells with a reverse transcriptase inhibitor, etravirine, which largely diminished the enhancement of the luciferase activity.
Thiamine deficiency results in release of soluble factors that disrupt mitochondrial membrane potential and downregulate the glutamate transporter splice-variant GLT-1b in cultured astrocytes
2014, Biochemical and Biophysical Research CommunicationsCitation Excerpt :TNF-α can be synthesized and released in the brain by astrocytes, microglia, and some neurons and the increased expression and release of TNF-α have been reported in various pathological conditions such as trauma, ischemia, and inflammatory diseases [17–19]. In addition, increased levels of TNF-α in the brain can lead to the activation of NF-κB [20]. Moreover, TNF-α dependent NF-κB activation is also implicated in the pathogenesis of glutamate neurotoxicity, with increased levels of TNF-α having been shown to inhibit glutamate transport activity in organotypic hippocampal slice cultures [7].
Orientation-Dependent Regulation of Integrated HIV-1 Expression by Host Gene Transcriptional Readthrough
2008, Cell Host and MicrobeCitation Excerpt :However, when the high- or low-expressing cells within the same cell population were sorted and subject to expansion, each population could reproduce the pattern of the entire population from which the cloned cell was sorted, suggesting that each clonal population exhibits significant variation in expression around a mean (Eszterhas et al., 2002). Since HIV-1 transcription can be activated by TNF-α through NF-κB signaling (Swingler et al., 1994), we tested whether TNF-α could reverse this transcriptional interference. After 3 hr of TNF-α treatment, the nuclear NF-κB levels were significantly increased in treated cells (Figure S5), and HIV-1 gene expression was increased in both Readthrough (+) and Readthrough (−) clones (compare Figures 3A and 3B).
IL-1β and TNFα regulate sodium absorption in rat distal colon
2004, Biochemical and Biophysical Research CommunicationsCitation Excerpt :A similar mechanism for transcriptional control has, e.g., been described for TNFα on the tight junction protein occludin[20]. A possible factor responsible for this effect could be the nuclear factor κB (NFκB) which is known to be the final stage in the signaling cascade of TNFα and also IL-1β [32]. This would also explain the similarity of the effects of both cytokines on β- and γ-ENaC subunit mRNA expression.