Search results for " REPLICATION"
showing 10 items of 406 documents
FANCD2 promotes mitotic rescue from transcription-mediated replication stress in SETX-deficient cancer cells
2022
AbstractReplication stress (RS) is a leading cause of genome instability and cancer development. A substantial source of endogenous RS originates from the encounter between the transcription and replication machineries operating on the same DNA template. This occurs predominantly under specific contexts, such as oncogene activation, metabolic stress, or a deficiency in proteins that specifically act to prevent or resolve those transcription-replication conflicts (TRCs). One such protein is Senataxin (SETX), an RNA:DNA helicase involved in resolution of TRCs and R-loops. Here we identify a synthetic lethal interaction between SETX and proteins of the Fanconi anemia (FA) pathway. Depletion of…
Phosphatidylserine liposomes reduce inflammatory response, mycobacterial viability and HIV replication in coinfected human macrophages
2021
AbstractChronic immune activation is the key pathogenetic event of Mycobacterium tuberculosis-human immunodeficiency virus (HIV) coinfection. We assessed the therapeutic value of phosphatidylserine-liposome (PS-L) in an in vitro model of M. tuberculosis-HIV coinfection. PS-L reduced nuclear factor-κB activation and the downstream production of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in bacille Calmette-Guérin-infected macrophages and of TNF-α and IL-1β in M. tuberculosis-infected and M. tuberculosis-HIV–coinfected macrophages. Importantly, a significant reduction of intracellular M. tuberculosis viability and HIV replication were also observed. These results suppor…
The region 0.7615-0.796 m.u. of the HSV-1 genome determines suppression of humoral antibody formation against herpes simplex virus.
1991
The influence of genetic properties of parts of the HSV-1 genome on suppression of humoral antibody formation was investigated by using intratypic recombinants. The deleted strain HFEM (HSV-1) induces suppression. The MluI DNA fragment (coordinates 0.7615–0.796 m.u.) derived from the antibody inducing strain F1 (HSV-1) was transfected into the deleted strain HFEM to produce the recombinant virus R-MlCI and shown to restore antibody formation, as demonstrated by neutralization- and ELISA-tests. The intratypic recombinant viruses R-15, R-19 and R-26, produced by transfection of the Bam HI DNA-fragment B (0.738–0.809 m.u.) of strain Fl into the deleted strain HFEM, resulted in antibody formati…
Die Hemmung der Riesenzellbildung durch das sogenannte Compound 48/80 nach der Infektion mit dem Herpesvirus hominis
1969
Es wurde uber die Wirkung des Histamin-Liberators Compound 48/80 auf die Phasen der Synthese des Herpesvirus hominis und auf normale Zellstoffwechselprozessein vitro berichtet.
Molecular mechanisms of sorafenib action in liver cancer cells.
2012
Sorafenib, a multikinase inhibitor, recently received FDA approval for the treatment of advanced hepatocellular carcinoma (HCC). However, as the clinical application of sorafenib evolves, there is increasing interest in defining the mechanisms underlying its anti-tumor activity. Considering that this specific inhibitor could target unexpected molecules depending on the biologic context, a precise understanding of its mechanism of action could be critical to maximize its treatment efficacy, while minimizing adverse effects. Two human HCC cell lines (HepG2 and Huh7), carrying different biological and genetic characteristics, were used in this study to examine the intracellular events leading …
Replication invariance on NTU games
2001
Two concepts of replication (conflictual and non-conflictual) are extended from the class of pure bargaining games to the class of NTU games. The behavior of the Harsanyi, Shapley NTU, Egalitarian and Maschler-Owen solutions of the replica games is compared with that of the Nash and Egalitarian solutions in pure bargaining games.
Binding isotope effects as a tool for distinguishing hydrophobic and hydrophilic binding sites of HIV-1 RT.
2014
The current treatment for HIV-1 infected patients consists of a cocktail of inhibitors, in an attempt to improve the potency of the drugs by adding the possible effects of each supplied compound. In this contribution, nine different inhibitors of HIV-1 RT, one of the three key proteins responsible for the virus replication, have been selected to develop and test a computational protocol that allows getting a deep insight into the inhibitors’ binding mechanism. The interaction between the inhibitors and the protein have been quantified by computing binding free energies through FEP calculations, while a more detailed characterization of the kind of inhibitor–protein interactions is based on …
Synthesis and antiviral activity of scopadulane-rearranged diterpenes.
2009
A new bioactive diterpene skeleton resulting from a backbone rearrangement is described. Activity of the rearranged product and several derivatives against Herpes Virus Simplex type 2 is reported.
Evidence against a key role for transforming growth factor-beta1 in cytomegalovirus-induced bone marrow aplasia.
1998
During immunodeficiency after sublethal haematoablative treatment, cytomegalovirus (CMV) infection interferes with haematopoietic reconstitution and can cause lethal bone marrow (BM) aplasia. The in vivo model of murine CMV infection has identified the BM stroma as the principal target site of CMV in the haematopoietic cord. The infected cell type is the reticular stromal cell which forms the stromal network and produces essential haemopoietins, such as stem-cell factor (SCF). The expression of SCF was found to be reduced in the infected stroma, but the stromal network was not disrupted and the number of infected stromal cells was too low to explain the functional deficiency. These facts ca…
Echovirus 1 Endocytosis into Caveosomes Requires Lipid Rafts, Dynamin II, and Signaling EventsV⃞
2004
Binding of echovirus 1 (EV1, a nonenveloped RNA virus) to the α2β1 integrin on the cell surface is followed by endocytic internalization of the virus together with the receptor. Here, video-enhanced live microscopy revealed the rapid uptake of fluorescently labeled EV1 into mobile, intracellular structures, positive for green fluorescent protein-tagged caveolin-1. Partial colocalization of EV1 with SV40 (SV40) and cholera toxin, known to traffic via caveosomes, demonstrated that the vesicles were caveosomes. The initiation of EV1 infection was dependent on dynamin II, cholesterol, and protein phosphorylation events. Brefeldin A, a drug that prevents SV40 transport, blocked the EV1 infection…