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1.
Fig. 3.

Fig. 3. From: An immunoreceptor tyrosine-based inhibition motif in varicella-zoster virus glycoprotein B regulates cell fusion and skin pathogenesis.

Phenylalanine substitution of Y881 within the gBcyt ITIM enhances gB/gH–gL–induced cell–cell fusion. Quantification of cell–cell fusion and cell-surface expression by flow cytometry of gB mutants compared with WT gB. Statistical differences were evaluated by two-way ANOVA. *P < 0.05, ***P < 0.001. SEM is indicated.

Stefan L. Oliver, et al. Proc Natl Acad Sci U S A. 2013 January 29;110(5):1911-1916.
2.
Fig. 4.

Fig. 4. From: An immunoreceptor tyrosine-based inhibition motif in varicella-zoster virus glycoprotein B regulates cell fusion and skin pathogenesis.

Extensive syncytia formation is triggered by Y881F substitution in the gBcyt ITIM. Confocal microscopy of melanoma cells infected with wild-type pOka and the gBcyt mutant, gB-Y881F, stained for gB (red), trans-Golgi network (green), and nuclei (blue) at 24 and 48 hpi. (Scale bar, 100 μm.)

Stefan L. Oliver, et al. Proc Natl Acad Sci U S A. 2013 January 29;110(5):1911-1916.
3.
Fig. 2.

Fig. 2. From: An immunoreceptor tyrosine-based inhibition motif in varicella-zoster virus glycoprotein B regulates cell fusion and skin pathogenesis.

Phenylalanine substitution of Y881 in the gBcyt ITIM does not prevent gB endocytosis. Confocal microscopy of melanoma cells at 24 h posttransfection with wild-type or gB mutant expression constructs and stained for gB (red) and early endosome antigen (EEA1; green). These high-magnification images are from boxed areas in Fig. S2A. White arrows highlight representative endocytic vesicles (EEA1) that contain gB. (Scale bar, 10 μm.) Diagram: epitope locations of the mAb SG2-2E6 (gB ectodomain in the endosome lumen, red), EEA1 rabbit polyclonal Ab (cytoplasmic surface, green), and gBcyt with Y881 and Y920 residues (red).

Stefan L. Oliver, et al. Proc Natl Acad Sci U S A. 2013 January 29;110(5):1911-1916.
4.
Fig. 5.

Fig. 5. From: An immunoreceptor tyrosine-based inhibition motif in varicella-zoster virus glycoprotein B regulates cell fusion and skin pathogenesis.

Increased syncytia formation induced by Y881F substitution in the gBcyt ITIM impairs VZV replication and plaque size in vitro. (A) Replication of pOka and the three gBcyt tyrosine mutants as determined by plaque assay. (B) Box and whisker (10–90% percentile) plots of plaques sizes measured (n = 30) in melanoma cells infected with pOka and the three gBcyt mutants. Black dots are outliers in the datasets. (A and B) Statistical differences between pOka and gB-Y881F (red asterisks) or gB-Y881/920F (blue asterisks) were determined by one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001. SEM is indicated. (C) Immunohistochemical staining of plaques in melanoma cells infected with pOka and gB-Y881F, gB-Y920F, and gB-Y881/920F. (Scale bars, 1 mm.)

Stefan L. Oliver, et al. Proc Natl Acad Sci U S A. 2013 January 29;110(5):1911-1916.
5.
Fig. 6.

Fig. 6. From: An immunoreceptor tyrosine-based inhibition motif in varicella-zoster virus glycoprotein B regulates cell fusion and skin pathogenesis.

Enhanced syncytia formation triggered by Y881F substitution in the gBcyt ITIM severely impairs VZV infection and spread in human skin xenografts in vivo. (A) Viral titers in skin xenografts at 10 and 21 dpi with pOka, gB-Y881F, gB-Y920F, or gB-Y881/920F. The frequency of virus-positive xenografts/number inoculated is indicated. (B) Viral genome copies/ng human DNA at 10 and 21 dpi. The frequency of VZV DNA-positive xenografts/number inoculated is indicated. (A and B) Statistical differences were evaluated by two-way ANOVA. *P < 0.05, ***P < 0.001. SEM is indicated. (C and D) Histopathology revealed by composite images of hematoxylin and eosin-stained 5-µm sections of infected skin xenografts at 21 dpi. Dotted lines outline the extent of virus penetration. Black boxes indicate where confocal microscopy images were captured on serial sections. Virus titers and genome copies/ng human DNA for each implant are indicated (red) in each panel. (E and F) Confocal microscopy of pOka- and Y881/920F-infected skin xenografts (21 dpi) stained for gE (cyan), capsid protein ORF23 (pink), TGN46 (brown), and nuclei (violet). Black boxes (Left) are shown in higher-magnification images (Right). (Scale bars, 100 μm.)

Stefan L. Oliver, et al. Proc Natl Acad Sci U S A. 2013 January 29;110(5):1911-1916.
6.
Fig. 1.

Fig. 1. From: An immunoreceptor tyrosine-based inhibition motif in varicella-zoster virus glycoprotein B regulates cell fusion and skin pathogenesis.

Cytoplasmic domain of VZV gB is a tyrosine kinase substrate. (A) Homology model of the gB ectodomain trimer and predicted transmembrane (TM) domain. The five domains of a single molecule in the gB trimer are as follows: domain I, blue; II, green; III, yellow; IV, orange; V, red; furin cleavage site (RSRR), red spacefill; residues W180 and Y185 in the predicted primary fusion loop, purple spacefill. (B) The gB cytoplasmic domain. The three predicted α-helices (pink cylinders), gB ITIM (879IKYMTL884), two YXXΦ motifs (residues 881–884 and 920–923), and dileucine endocytosis motif (residues 904–905) are shown. (C) Immunoprecipitation of gB from VZV-infected (V) or uninfected (UI) melanoma cells and Western blot for gB (rabbit serum 746-868), gE (mAb 8612), and phosphorylated tyrosine (pY; mAbs 4G10/pY20). Arrowheads indicate the 66- and 124-kDa gB species that are tyrosine-phosphorylated. (D) Coomassie blue staining (Upper) and Western blot (Lower; mAb 4G10) of the same membrane to detect phosphorylated tyrosine on purified GST (negative control) and the GST-tagged cytoplasmic domains of the proteins FcRγ (GST-FcRγ; positive control) and gBcyt (GST-gB) expressed in BL21 or BL21 E. coli expressing the tyrosine kinase Elk-1. Molecular mass standards (kDa) are indicated.

Stefan L. Oliver, et al. Proc Natl Acad Sci U S A. 2013 January 29;110(5):1911-1916.

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