Francesca Avesani

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Raver2 is a putative modulator of the activity of the polypyrimidine-tract binding protein (PTB), one of the most intensively studied splicing repressors. Little is known about Raver2 expression, and all current data is from mice where it shows tissue specificity. In the present study, by comparing Raver2 transcript expression in human and mouse tissues, we(More)
HTLV-1 is more pathogenic than HTLV-2 despite having a similar genome and closely related transactivating oncoproteins. Both Tax-1 protein from HTLV-1 and Tax-2 from HTLV-2 activate the NF-κB pathway. The mechanisms involved in Tax-1 deregulation of this signalling pathway have been thoroughly investigated, but little is known about regulation by Tax-2. We(More)
Human T-lymphotropic viruses type 1 (HTLV-1) and type 2 (HTLV-2) present very similar genomic structures but HTLV-1 is more pathogenic than HTLV-2. Is this difference due to their transactivating Tax proteins, Tax-1 and Tax-2, which are responsible for viral and cellular gene activation? Do Tax-1 and Tax-2 differ in their cellular localization and in their(More)
The Tax protein expressed by human T-cell leukemia virus type 1 (HTLV-1) plays a pivotal role in the deregulation of cellular pathways involved in the immune response, inflammation, cell survival, and cancer. Many of these effects derive from Tax multiple interactions with host factors, including the subunits of the IKK-complex that are required for NF-κB(More)
Raver1 is a ribonucleoprotein, evolutionarily conserved in mammals, which acts as a polypyrimidine tract-binding protein (PTB/hnRNPI) co-repressor in regulating alternative splicing events. The mouse homologue has been identified as a dual compartment protein that interacts with PTB within perinucleolar structures, and localizes at microfilament plasma(More)
Post-translational modifications of HTLV-1 and HTLV-2 Tax-1 and Tax-2 proteins have been shown to play a critical role in their cellular localization, transactivation and protein interactions. Five of ten lysine residues were found to be major targets for Tax-1 modifications: Lys189(K4); Lys197(K5), Lys263(K6), Lys280(K7) and Lys284(K8), are essential for(More)
The Tax oncoprotein of HTLV-1 initiates T-cell transformation by dysregulating cell cycle progression and inhibiting DNA damage responses. The subsequent genomic instability might result in constitutive activation of the NF-B pathway observed in HTLV-1-transformed T lymphocytes. Our previous results indicated that differential modifications of Tax by(More)
The HTLV-1 infection is known to induce an alteration of type I interferon (IFN-I) signaling since it is capable of escaping IFN-mediated immune response in vitro and Tax-1 protein modulates the expression of factors involved in the interferon signaling. In the present study we have investigated the effect of Tax-1 and Tax-2 expression on the activation of(More)
HTLV-1 Tax de-regulates several cellular signaling pathways leading to cell transformation by altering gene expression, intracellular protein distribution and cell proliferation. Tax-1 induces persistent activation of several transcriptional factors and signal transduction pathways , including NF-B and CREB/ATF. It is known that Tax-1 constitutively(More)
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