about
Targeting of prosurvival pathways as therapeutic approaches against primary effusion lymphomas: past, present, and FuturePrimary effusion lymphoma cell death induced by bortezomib and AG 490 activates dendritic cells through CD91Latent membrane protein 1 of Epstein-Barr virus mimics a constitutively active receptor molecule.JNK and macroautophagy activation by bortezomib has a pro-survival effect in primary effusion lymphoma cells.The activation of KSHV lytic cycle blocks autophagy in PEL cells.HSP70 inhibition by 2-phenylethynesulfonamide induces lysosomal cathepsin D release and immunogenic cell death in primary effusion lymphoma.Kaposi sarcoma associated herpesvirus (KSHV) induces AKT hyperphosphorylation, bortezomib-resistance and GLUT-1 plasma membrane exposure in THP-1 monocytic cell line.Epstein-barr virus blocks the autophagic flux and appropriates the autophagic machinery to enhance viral replication.STAT3 activation by KSHV correlates with IL-10, IL-6 and IL-23 release and an autophagic block in dendritic cells.KSHV ORF67 encoded lytic protein localizes on the nuclear membrane and alters emerin distribution.The BFRF1 gene of Epstein-Barr virus encodes a novel protein.Identification and characterization of the product encoded by ORF69 of Kaposi's sarcoma-associated herpesvirusDeletion of Epstein-Barr virus BFLF2 leads to impaired viral DNA packaging and primary egress as well as to the production of defective viral particlesOxidant species are involved in T/B-mediated ERK1/2 phosphorylation that activates p53-p21 axis to promote KSHV lytic cycle in PEL cells.Regulation of the expression of the Epstein-Barr virus early gene BFRF1.Quercetin induces apoptosis and autophagy in primary effusion lymphoma cells by inhibiting PI3K/AKT/mTOR and STAT3 signaling pathways.Characterization and intracellular localization of the Epstein-Barr virus protein BFLF2: interactions with BFRF1 and with the nuclear lamina.BFRF1 of Epstein-Barr virus is essential for efficient primary viral envelopment and egress.KSHV reduces autophagy in THP-1 cells and in differentiating monocytes by decreasing CAST/calpastatin and ATG5 expression.Expression of tumor necrosis factor receptor-associated factor 1 in nasopharyngeal carcinoma: possible upregulation by Epstein-Barr virus latent membrane protein 1.Intracellular localization of the Epstein-Barr virus BFRF1 gene product in lymphoid cell lines and oral hairy leukoplakia lesions.Transcription of latent and replicative Epstein-Barr-virus genes in bone-marrow and peripheral-blood mononuclear cells of healthy donors.Activation of dendritic cells by tumor cell death.PKC theta and p38 MAPK activate the EBV lytic cycle through autophagy induction.Metformin triggers apoptosis in PEL cells and alters bortezomib-induced Unfolded Protein Response increasing its cytotoxicity and inhibiting KSHV lytic cycle activation.Bortezomib promotes KHSV and EBV lytic cycle by activating JNK and autophagy.HSP70 inhibition by 2-phenylethynesulfonamide induces lysosomal cathepsin D release and immunogenic cell death in primary effusion lymphoma.Lack of Serologic Association Between Human Herpesvirus-8 Infection and Multiple Myeloma and Monoclonal Gammopathies of Undetermined SignificanceEBV reduces autophagy, intracellular ROS and mitochondria to impair monocyte survival and differentiationEBV up-regulates PD-L1 on the surface of primary monocytes by increasing ROS and activating TLR signaling and STAT3Human herpesvirus 8 DNA sequences in CD8+ T cellsHHV-6 infection in Italy: characterization of an endemic isolate and seroepidemiologic analysis
P50
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P50
description
hulumtuese
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Roberta Gonnella
@ast
Roberta Gonnella
@en
Roberta Gonnella
@es
Roberta Gonnella
@nl
type
label
Roberta Gonnella
@ast
Roberta Gonnella
@en
Roberta Gonnella
@es
Roberta Gonnella
@nl
prefLabel
Roberta Gonnella
@ast
Roberta Gonnella
@en
Roberta Gonnella
@es
Roberta Gonnella
@nl
P106
P1153
6602365853
P21
P31
P496
0000-0003-4894-4986