Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q3V6T2 (ape)
2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mouse monoclonal antibody to HTLV p19 was used to locate HTLV p19 on the surface of cells and virions by immunofluorescence microscopy (IFM) and immunoelectron microscopy (IEM). When HTLV-producing cells HUT 102 (B2 clone), MT-2 and strain A were used as target cells, HTLV p19 was detected on the surface of cells and virions as spots or small sectors by both IFM and IEM. Cells infected with animal type-C retroviruses, e.g., gibbon ape leukemia virus, simian sarcoma virus, feline leukemia virus, and Gross murine leukemia virus, were completely negative for HTLVp19 expression. Other human T cells not producing HTLV, including HUT78 and HSB2-0, immature or pre-T cells (Molt-3) derived from leukemia patients, and fresh peripheral blood T cells from healthy persons, were also negative. In addition, B cells including Rob-B, IM-9, Raji, and BT-1 did not react with the monoclonal antibody to HTLV p19. In the light of the presence of HTLV p19 in the periphery of acetone-fixed HTLV-producing cells as shown by IFM, it seems most likely that HTLV p19 is an internal antigen of HTLV with part of its structure protruding out of the viral and cell membrane. The monoclonal antibody to HTLV p19 did not lyse HTLV-producing cells in the presence of complement, as expected, because the antibody is an IgG1. Antibody-dependent cell-mediated cytotoxicity was also studied by the 51Cr-release assay. No cytotoxicity was observed. Although HTLV p19 does not contribute to the destruction of malignant T cells for treatment and/or virions for prophylaxis, this protein is an important marker for diagnosis of HTLV infection. The patterns of HTLV p19 expression described above were exactly the same for American HTLV-producing HUT 102 (B2 clone), for strain A cells and for Japanese HTLV-producing MT-2 cells. These results further substantiate the close relationship of the Japanese and American HTLV isolates.
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PMID:Location of human T-cell leukemia virus (HTLV) p19 antigen on virus-producing cells. 631 98

This study evaluated the influence of chemical surface treatments in the repair strength of a heat-cured acrylic resin (Lucitone 550, (LU)). A total of 70 specimens were made with LU according to American Dental Association (ADA) specification No. 12. Of these, 14 remained intact and were used as a control group (GI). A total of 56 specimens were selected randomly. These specimens were cut in the middle (10 mm), repaired with a microwave acrylic resin (Acron MC (AC)), and processed in a microwave oven for 3 min at 500 W. Prior to the repair, the surface of the cut ends received different chemical treatments (GIII = AC monomer dipping/30 s; GIV = acetone dipping/30 s; GV = acetone dipping/15 s + blast of air + AC monomer dipping/15 s; GVI = no wetting treatment). However, 14 intact specimens made with AC formed a second control group (GII). The effect of the chemical treatments on the surface texture of LU was observed with scanning electron microscopy. Flexural test results were submitted to paired t-test and showed statistical differences (P < 0.05) only between the pairs GIV-GV and GIV-GVI. Strength mean values of repaired specimens were statistically lower (79-90%) than GII mean values. Strength mean values of GVI and GIV were 93 and 106%, respectively, of GI mean, showing no statistical differences. Scanning electron microscopic observations revealed various effects of the chemical treatments on the denture base resin surface. In conclusion, the wetting surface treatments affected the bond strength between the two acrylic resins, and no statistical differences in strength were observed between intact heat-cured denture base material and the same material repaired with microwave acrylic resin.
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PMID:Heat-cured acrylic resin repaired with microwave-cured one: bond strength and surface texture. 1135 May 91