1,721,012 research outputs found
p65/RelA binds and activates the beclin-1 promoter
No full textWe unveiled novel p65/RelA consensus sites in the promoter
of the beclin 1 gene and demonstrate that p65/RelA positively
modulates canonical autophagy in various human cell lines
both under basal conditions and upon induction by ceramide.
Interestingly, we find that T cell receptor-dependent activation
of Jurkat cells triggers an increase in the binding of p65/RelA
to the beclin 1 promoter accompanied by enhanced autophagy,
suggesting that p65/RelA could regulate T-cell activation and
homeostasis through autophagy
Inhibitors of the ubiquitin-proteasome system are not all alike: Identification of a new necrotic pathway
No full textHuman Immunodeficiency Virus type 1 Tat protein activates transcription factor NF-kappaB through the cellular interferon-inducible, double-stranded RNA-dependent protein kinase, PKR
No full textJ. VIROL
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
In vivo footprinting analysis of constitutive and inducible protein-DNA interactions at the long terminal repeat of human immunodeficiency virus type 1.
No full textThe regulation of the rate of transcription of human immunodeficiency virus type 1 is mainly exerted through the long terminal repeat (LTR) at the 5' end of the provirus. A large number of cis-acting regulatory elements have been identified in the LTR by in vitro binding studies; the biological role of these sites within living infected cells, however, is still not clear. We have studied the interactions of nuclear proteins with the LTR in the U1 monocytic cell line by in vivo dimethylsulfate footprinting, using the ligation-mediated polymerase chain reaction technique. In this cell line, transcription of the virus, which is very low under basal conditions, is highly inducible by treatment with phorbol esters; therefore, this system is likely to represent a suitable cellular model to study viral latency. Independently of the level of viral transcription, major in vivo footprints appear at the two Sp1 sites adjacent to the enhancer, the downstream-positioned enhancer repeat, the NFAT binding site, and one of the purine-rich sites of the negative regulatory element. Upon transcriptional activation by phorbol myristate acetate, the only perturbation in the footprinting pattern is a dramatic increase in dimethylsulfate sensitivity of guanine at position -92 in the downstream enhancer repeat. This modification is correlated with the transient induction of two enhancer-binding activities, as determined by gel retardation assays. While the transcriptional rate is still increasing and the in vivo footprinting pattern is unchanged at up to 24 h postactivation, these enhancer-binding factors are considerably reduced at this time. Therefore, further levels of regulation have to be considered to explain the maintenance of the induced state
p65/RelA modulates Beclin transcription and Autophagy
No full textRecently, autophagy has emerged as a critical process in the control of T-cell homeostasis. Given the pivotal
role of NF-B in the signaling events of T cells, we have analyzed and unveiled a conserved NF-B binding site
in the promoter of the murine and human BECN1 autophagic gene (Atg6). Accordingly, we demonstrate that
the NF-B family member p65/RelA upregulates BECN1 mRNA and protein levels in different cellular systems.
Moreover, p65-mediated upregulation of BECN1 is coupled to increased autophagy. The newly identified B
site in the BECN1 promoter specifically interacts with p65 both in vitro and in living Jurkat cells upon phorbol
myristate acetate (PMA)-ionomycin stimulation, where p65 induction is coupled to BECN1 upregulation and
autophagy induction. Finally, anti-CD3- and PMA-ionomycin-mediated activation of T-cell receptor signaling
in peripheral T cells from lymph nodes of healthy mice results in an upregulation of BECN1 expression that
can be blocked by the NF-B inhibitor BAY 11-7082. Altogether, these data suggest that autophagy could
represent a novel route modulated by p65 to regulate cell survival and control T-cell homeostasis
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