Biochemical and Biophysical Research Communications
Regular ArticleExtracellular HIV-1 Tat Protein Induces a Rapid and Selective Activation of Protein Kinase C (PKC)-α, -ϵ, and -ζ Isoforms in PC12 Cells
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Host-based processes as therapeutic targets for Rift Valley fever virus
2018, Antiviral ResearchCitation Excerpt :Although mostly present in the cytoplasm, PKCε can alter its localization to the Golgi or mitochondria depending on the specific signal (Capuani et al., 2016). Extracellular HIV-1 Tat protein has been previous shown to activate PKCα, PKCε, and PKCζ when added to naïve serum-starved rat cells (Borgatti et al., 1998). Additionally, HIV-1 Nef decreased the expression and activation PKCε in astrocytes, which resulted in inhibition of the viral long terminal repeat activation and restriction of HIV-1 replication (Ambrosini et al., 1999).
Expression of HIV-Tat protein is associated with learning and memory deficits in the mouse
2012, Behavioural Brain ResearchCitation Excerpt :Of interest, Tat protein possesses multiple means to induce cellular dysfunction, potentially mediating the observed learning and memory impairments. Extracellular Tat protein also activates cell surface growth factor receptors [55], modulating signal transduction including the activation of PKC [56] and MAP kinases [55,57] associated with LTP and synaptic plasticity, the neuronal basis for hippocampal-dependent learning (see [58,59] for reviews). Tat exposure in vitro can result in CA1 hippocampal and entorhinal cell dysfunction, suppressing LTP [17,18].
HIV-1 Tat protein induces TNF-α and IL-10 production by human macrophages: Differential implication of PKC-βII and -δ isozymes and MAP kinases ERK1/2 and p38
2008, Cellular ImmunologyCitation Excerpt :Altogether, our results and those reported by others, indicate that the ability of Tat to activate PKC isoforms seems dependent on cell differentiation as well as on cell type. This statement is in agreement with results reported by Borgatti et al. (1998), who showed that stimulating the PC12 neuron line with Tat selectively activated PKC-α, -ε and -ζ among the isoforms present in this cell line (PKC-α, -βI, -βII, -δ, -ε, -η, -μ and -ζ) [55]. In this case, it is noteworthy that, despite the presence of PKC-βII and -δ in the PC12 cell line, they are not activated by Tat.
Limited role of COX-2 in HIV Tat-induced alterations of tight junction protein expression and disruption of the blood-brain barrier
2007, Brain ResearchCitation Excerpt :Exposure to Tat is known to activate a variety of redox-responsive signaling pathways and transcription factors, including those involved in COX-2 overexpression. For example, Tat can stimulate protein kinase C (Borgatti et al., 1998; Andras et al., 2005) and the Ras/MAPK pathway (Andras et al., 2005; Toschi et al., 2006) which were demonstrated to induce transcription of COX-2 (Chun and Surh, 2004). COX-2 gene promoter contains several enhancer elements which are sensitive to cellular redox balance.
HIV-dementia, Tat-induced oxidative stress, and antioxidant therapeutic considerations
2005, Brain Research Reviews