about
Termination of NF-kappaB activity through a gammaherpesvirus protein that assembles an EC5S ubiquitin-ligaseDefining immune engagement thresholds for in vivo control of virus-driven lymphoproliferationCrystal Structure of the Gamma-2 Herpesvirus LANA DNA Binding Domain Identifies Charged Surface Residues Which Impact Viral LatencyRole of Src homology domain binding in signaling complexes assembled by the murid γ-herpesvirus M2 protein.Intrabodies targeting the Kaposi sarcoma-associated herpesvirus latency antigen inhibit viral persistence in lymphoma cells.Murine gamma-herpesvirus 68 latency protein M2 binds to Vav signaling proteins and inhibits B-cell receptor-induced cell cycle arrest and apoptosis in WEHI-231 B cells.The Gammaherpesvirus m2 protein manipulates the Fyn/Vav pathway through a multidocking mechanism of assemblyA single CD8+ T cell epitope sets the long-term latent load of a murid herpesvirusActivation of Vav by the gammaherpesvirus M2 protein contributes to the establishment of viral latency in B lymphocytesEstablishment of murine gammaherpesvirus latency in B cells is not a stochastic event.Identification of H-type BSE in PortugalThe Kaposi Sarcoma Herpesvirus Latency-associated Nuclear Antigen DNA Binding Domain Dorsal Positive Electrostatic Patch Facilitates DNA Replication and Episome Persistence.Murine gammaherpesvirus 68 LANA acts on terminal repeat DNA to mediate episome persistence.A secreted chemokine binding protein encoded by murine gammaherpesvirus-68 is necessary for the establishment of a normal latent load.KSHV but not MHV-68 LANA induces a strong bend upon binding to terminal repeat viral DNA.Maternal retinoids control type 3 innate lymphoid cells and set the offspring immunity.Type I Interferons and NK Cells Restrict Gammaherpesvirus Lymph Node Infection.GLUT1-mediated glucose uptake plays a crucial role during Plasmodium hepatic infection.T cell apoptosis and induction of Foxp3+ regulatory T cells underlie the therapeutic efficacy of CD4 blockade in experimental autoimmune encephalomyelitis.Anthracyclines induce DNA damage response-mediated protection against severe sepsis.Murid Gammaherpesvirus Latency-Associated Protein M2 Promotes the Formation of Conjugates between Transformed B Lymphoma Cells and T Helper Cells.Effector γδ T Cell Differentiation Relies on Master but Not Auxiliary Th Cell Transcription Factors.Cross-species conservation of episome maintenance provides a basis for in vivo investigation of Kaposi's sarcoma herpesvirus LANA.Latency-Associated Nuclear Antigen E3 Ubiquitin Ligase Activity Impacts Gammaherpesvirus-Driven Germinal Center B Cell Proliferation.The M2 gene product of murine gammaherpesvirus 68 is required for efficient colonization of splenic follicles but is not necessary for expansion of latently infected germinal centre B cells.K3-mediated evasion of CD8(+) T cells aids amplification of a latent gamma-herpesvirus.Putative emergence of classical scrapie in a background of enzootic atypical scrapie.ORF73 of murine herpesvirus-68 is critical for the establishment and maintenance of latency.Gamma-herpesvirus colonization of the spleen requires lytic replication in B cells.Murine gammaherpesvirus 68 bcl-2 homologue contributes to latency establishment in vivo.Identification of putative atypical scrapie in sheep in Portugal.In vivo persistence of chimeric virus after substitution of the KSHV LANA DNA binding domain with that of MuHV-4Vaccine protection against murid herpesvirus-4 is maintained when the priming virus lacks known latency genes
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P50
description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
J Pedro Simas
@ast
J Pedro Simas
@en
J Pedro Simas
@es
J Pedro Simas
@nl
J Pedro Simas
@sl
type
label
J Pedro Simas
@ast
J Pedro Simas
@en
J Pedro Simas
@es
J Pedro Simas
@nl
J Pedro Simas
@sl
prefLabel
J Pedro Simas
@ast
J Pedro Simas
@en
J Pedro Simas
@es
J Pedro Simas
@nl
J Pedro Simas
@sl
P106
P108
P1153
7003457329
P21
P31
P496
0000-0001-6982-9253