13 research outputs found

    Additional file 2: of The HCV care continuum among people who use drugs: protocol for a systematic review and meta-analysis

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    Search strategy for CINAHL (via EBSCO), Embase (via Ovid), PsycInfo (via Ovid), and PubMed (via Medline)

    Additional file 3: Figure S3. of Cryptic protein-protein interaction motifs in the cytoplasmic domain of MHCI proteins

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    Frequency of occurrence of specific class 2 and 3 PDZ ligand motifs in the cytoplasmic domains of 99 MHCI proteins from 21 species. A. Class 2 PDZ ligand motifs ([ΦXΦ], where Φ = V, I, L, M, F, W, or C), or B. class 3 PDZ ligand motifs ([D/E X Φ) [46]) in the cytoplasmic domains of 99 MHCI proteins from 21 species (data used to create pie charts in Fig. 2e and f, respectively). Shown are the number of occurrences of each motif as well as the fraction they represent of the total motifs observed in each domain. Class 2 PDZ ligand forms that were never observed in either domain are not shown. (PPTX 73 kb

    Additional file 2: Figure S2. of Cryptic protein-protein interaction motifs in the cytoplasmic domain of MHCI proteins

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    PDZ ligand motifs identified in the cytoplasmic domains of 16 mouse MHCI and MHCI-like proteins. Putative PDZ ligand motifs are highlighted in red, and previously noted conserved serines and tyrosine (see text) are underlined in bold. Consensus motifs: class 1 PDZ, [S/T X Φ]; class 2 PDZ, [ΦXΦ]; class 3 PDZ, [D/E X Φ]; Φ = Y, F, W, C, M, V, I, L, or A [44]. H2-T23 is also known as Qa-1. No ligand motifs were found in the cytoplasmic domain of H2-M2 or -M9, and therefore they are omitted. Soluble MHCI proteins including H2-Q10 lack a cytoplasmic domain and were not considered in this analysis. (PPTX 37 kb

    Additional file 1: Figure S1. of Cryptic protein-protein interaction motifs in the cytoplasmic domain of MHCI proteins

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    Categorization of PDZ ligands. The current study made use of forms of Lenfant et al.’s [44] and Nourry et al.’s [46] criteria to identify potential PDZ ligand motifs in MHCI proteins. Related rules were proposed in [45]. (PPTX 35 kb

    Demographic and drug use characteristics of people with injecting drug use who started injecting in 1995 or later New York City Mount Sinai Beth Israel drug treatment programs.

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    <p># Significant difference (p<0.05) across race/ethnicity groups by one-way analysis-of- variance.</p><p>* Significant difference (p<0.05) across race/ethnicity groups by chi-square test.</p><p>Demographic and drug use characteristics of people with injecting drug use who started injecting in 1995 or later New York City Mount Sinai Beth Israel drug treatment programs.</p

    (A) Western blot analysis of phospho-Akt and S6K1 in the absence or presence of the PI3K inhibitor wortmannin (WT) in response to control fibroblast attachment to monomeric collagen in the absence of serum

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    One representative example is shown. (B) Western blot analysis of phospho-Akt in control fibroblasts preincubated with the indicated integrin blocking antibody and plated on monomeric collagen. (C) Fibroblasts were plated on tissue culture plates coated with monomeric collagen and blocked by BSA. Cells were allowed to spread for 30 min. Cell areas of a random 150 cells were quantified by tracing the cell border using ImageJ software (available at ). (D) Western blot analysis of phospho-Akt and S6K1 in response to control fibroblast attachment to polymerized collagen in the absence of serum. (E) Western blot analysis of phospho-Akt and S6K1 in control fibroblasts cultured on monomeric or polymerized collagen in growth factor–replete media. One representative example is shown. (F) GD25, GD25 β1, and GD25 α2β1 fibroblasts were cultured on monomeric (left) or polymerized (right) collagen in the presence of serum, and cell numbers were quantified. (G) Proliferation assay of control fibroblasts expressing dominant-negative Akt (Ad-DN-Akt; left) or constitutively active p110 subunit of PI3K (Ad-PI3Kp110; right) and cultured on monomeric or polymerized collagen in growth factor–replete media, respectively. (top left) Western blot analyses of phospho- and total Akt. (bottom left) Shown is the percent change in cell growth. *, P < 0.01 and 0.001 for the percent change in fibroblast growth on monomeric collagen that was significantly less in control fibroblasts expressing dominant-negative Akt compared with cells expressing control vector at days 3 and 6, respectively. (top right) Western blot analyses of phospho- and total Akt. (bottom right) Shown is the percent change in cell growth. *, P < 0.01 and 0.0001 for the percent change in fibroblast growth on polymerized collagen that was significantly greater in control cells expressing constitutively active p110 subunit of PI3K compared with control vector at days 3 and 6, respectively. Error bars represent SEM. Data are representative of three independent experiments.<p><b>Copyright information:</b></p><p>Taken from "Pathological integrin signaling enhances proliferation of primary lung fibroblasts from patients with idiopathic pulmonary fibrosis"</p><p></p><p>The Journal of Experimental Medicine 2008;205(7):1659-1672.</p><p>Published online 7 Jul 2008</p><p>PMCID:PMC2442643.</p><p></p

    (A) Western blot analysis of total PTEN and phospho-Akt and S6K1 in IPF fibroblasts expressing wild-type PTEN (Ad-wtPTEN) or empty vector (Ad-GFP) and cultured on polymerized collagen in growth factor–replete media

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    (B) eIF4F activity (RLUC luminescence) in IPF fibroblasts expressing wild-type PTEN or control vector and cultured for 3 d on polymerized collagen. *, P < 0.0001 for significantly less eIF4F activity in IPF fibroblasts expressing wild-type PTEN compared with control. (C) Quantification of DNA synthesis by BrdU incorporation in IPF fibroblasts expressing wild-type PTEN or empty vector and cultured on polymerized collagen in growth factor–replete media for 3 d. Shown is the percentage of BrdU-positive IPF fibroblasts. *, P < 0.0001 for the percentage of BrdU-positive IPF fibroblasts expressing wild-type PTEN that was significantly less compared with control. Error bars represent SEM. Data are representative of three independent experiments from one IPF cell line.<p><b>Copyright information:</b></p><p>Taken from "Pathological integrin signaling enhances proliferation of primary lung fibroblasts from patients with idiopathic pulmonary fibrosis"</p><p></p><p>The Journal of Experimental Medicine 2008;205(7):1659-1672.</p><p>Published online 7 Jul 2008</p><p>PMCID:PMC2442643.</p><p></p
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