Abstract: V29A subtype, with one consistent amino acid change at residue 29 (V A) and several nucleotide changes, showed higher frequency in
Abstract: The relatively higher prevalence of type f/V29A/SPM strains in NPC may also suggest the association between these variations in multiple viral genes and NPC.
Abstract: Two major subtypes of BARF1 gene, designated as B95-8 and V29A, were identified.
Abstract: Type f isolates was specially correlated with the V29A/SPM genotype in NPC isolates and type f/V29A/SPM was preferentially found in NPC.
Genomic sequencing and comparative analysis of Epstein-Barr virus genome isolated from primary nasopharyngeal carcinoma biopsy.
Abstract: Variations in LMP1 and EBNA3B epitopes and mutations in Cp (11404 C>T) and Qp (50134 G>C) found in GD1, GD2 and HKNPC1 could potentially affect CD8(+) T cell recognition and latent gene expression pattern in NPC, respectively.
Result: Although no mutations were identified in known and predicted TATA boxes, sequence changes of 11,324 G>T and 11,404 C>T in Cp, and 49,937 G>A and 50,134 G>C in Qp were observed.
Result: Based on strain-determining amino acids of EBNA1 (A487V, D499E and
Epstein-Barr virus nuclear protein 3C binds to the N-terminal (NTD) and beta trefoil domains (BTD) of RBP/CSL; only the NTD interaction is essential for lymphoblastoid cell growth.
Result: EBNA3C binding to the beta trefoil domain containing constructs (B and B+C) was eliminated by W227S mutation, confirming the role of this motif as a Notch RAM-like interaction sequence in yeast.
Result: Expressed as a GST fusion protein in bacteria, EBNA3C aa164-366 bound RBP/CSL, while EBNA3C aa164-366 W227S was deficient in RBP/CSL binding, despite equal expression levels (Fig 3C).
Result: GST-EBNA3C aa164-366 efficie
Cellular transcription factor Oct-1 interacts with the Epstein-Barr virus BRLF1 protein to promote disruption of viral latency.
Abstract: In addition, we demonstrate that an Oct-1 mutant defective in DNA binding (the S335D mutant) still retains the ability to enhance BRLF1 transcriptional effects.
Abstract: We find that Oct-1 interacts directly with BRLF1 in vitro and that a mutant BRLF1 protein (the M140A mutant) attenuated for the ability to interact with Oct-1 in vitro is also resistant to Oct-1-mediated transcriptional enhancement in 293 BRLF1-stop cells.
Transmembrane peptides used to investigate the homo-oligomeric interface and binding hotspot of latent membrane protein 1.
Method: pRSV-LMP-1-D150A was generated using site-directed mutagenesis (Agilent Technologies 210519, CA, USA) to substitute D150 to alanine with the forward primer 5'-CCTAGCCTTCTTCCTAGCCCTCATCCTGCTC-3' and its reverse complement.
Method: pTox7 TM5 D150A was created using standard site directed mutagenesis with a commercially available Stratagene Quikchange II kit (Agilent, CA, USA).
Discussion: Our results are consistent with a model in which the oligomeric state of LMP-1 is trimeric, and that of LMP-1 D150A is dimeric.
Discussion: Replacement of D150 with alanine in TM5 abolishes trimerization and the resulting peptide (TM5 D150A) is primarily dimeric.
Discussion: Substitution of D150 with alanine in full-leng
Efficient induction of nuclear aggresomes by specific single missense mutations in the DNA-binding domain of a viral AP-1 homolog.
PMID: 21233201
2011
The Journal of biological chemistry
Abstract: Co-transfection of WT ZEBRA with aggresome-inducing mutants Z(R183E) and Z(R179E) inhibited late lytic viral protein expression and lytic viral DNA amplification.
Abstract: Four non-DNA-binding mutants, Z(R179E), Z(R183E), Z(R190E), and Z(K178D) localized to the periphery of large intranuclear spheres, to discrete nuclear aggregates, and to the cytoplasm.
Abstract: Other non-DNA-binding mutants, Z(N182K),
Abstract: S393A mutant EBNA1 was deficient in supporting EBNA1- and oriP-dependent transcription and episome persistence, and roscovitine had little further effect on the diminished S393A mutant EBNA1-mediated transcription or episome persistence.
Abstract: Moreover, roscovitine decreased nuclear EBNA1 and often increased cytoplasmic EBNA1, whereas S393A mutant EBNA1 was localized equally in the nucleus and cytoplasm and was unaffected by roscovitine treatment.
The Epstein-Barr virus-encoded BILF1 protein modulates immune recognition of endogenously processed antigen by targeting major histocompatibility complex class I molecules trafficking on both the exocytic and endocytic pathways.
Abstract: We now demonstrate that disruption of the EKT signaling motif of BILF1 by a K122A mutation impairs the ability of BILF1 to enhance endocytosis of surface MHC-I molecules, while subsequent lysosomal degradation was impaired by deletion of the 21-residue C-terminal tail of BILF1.
The Epstein-Barr virus BZLF1 protein inhibits tumor necrosis factor receptor 1 expression through effects on cellular C/EBP proteins.
Abstract: Furthermore, we find that the Z(A204D) mutant is attenuated in the ability to inhibit the TNFR1p but mediates lytic viral reactivation and replication in vitro in 293 cells as well as wild-type Z.
Abstract: The Z(A204D) mutant has reduced interaction with the TNFR1p in vivo but is similar to wild-type Z in its ability to complex with the IL-8 promoter.
Polymorphisms of Epstein-Barr virus BHRF1 gene, a homologue of bcl-2.
EBV mutation literature information.
PMID: 
2012
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