PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12148241-1 2002 By means of cryo-scanning electron microscopy (cryo-SEM) and fluorescent techniques, evidence is provided on how 12-O-tetradecanoylphorbol-13-acetate (TPA) affects Sertoli cell morphology and F-actin and vinculin organization in vitro. Tetradecanoylphorbol Acetate 113-149 vinculin Homo sapiens 204-212 12148241-1 2002 By means of cryo-scanning electron microscopy (cryo-SEM) and fluorescent techniques, evidence is provided on how 12-O-tetradecanoylphorbol-13-acetate (TPA) affects Sertoli cell morphology and F-actin and vinculin organization in vitro. Tetradecanoylphorbol Acetate 151-154 vinculin Homo sapiens 204-212 12148241-6 2002 Thus, the reorganization of actin and vinculin and subsequent changes in cell morphology seem to be brought about by TPA affecting not only actin but also the protein vinculin which interacts with actin. Tetradecanoylphorbol Acetate 117-120 vinculin Homo sapiens 38-46 12148241-6 2002 Thus, the reorganization of actin and vinculin and subsequent changes in cell morphology seem to be brought about by TPA affecting not only actin but also the protein vinculin which interacts with actin. Tetradecanoylphorbol Acetate 117-120 vinculin Homo sapiens 167-175 3048655-5 1988 TPA treatment of HT-29 G+ or G- cells induced early morphological and cytoskeletal alterations: the cells rounded up and lost their stress fibers with the associated caldesmon, alpha-actinin, and vinculin. Tetradecanoylphorbol Acetate 0-3 vinculin Homo sapiens 196-204 11329379-7 2001 Also, the PKC inhibitor GF109203X abolished both the LTD(4)- and the TPA-induced dissociation of vinculin from alpha-catenin. Tetradecanoylphorbol Acetate 69-72 vinculin Homo sapiens 97-105 3099098-7 1986 The changes in PK-C activity in TPA + RA-treated cells were accompanied by Ca2+/phospholipid(PL)-dependent phosphorylation in vitro of pp38 which is characteristic of treatment with RA alone, as well as the Ca2+/PL-independent phosphorylation in vitro of pp82 and pp130 (vinculin) which is prevalent in cells treated continuously with TPA alone and is absent in RA-treated cells. Tetradecanoylphorbol Acetate 32-35 vinculin Homo sapiens 271-279 3130982-1 1988 In response to phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA), HL-60 cells differentiate to macrophage-like cells and exhibit the ability to phosphorylate vinculin in vitro. Tetradecanoylphorbol Acetate 38-74 vinculin Homo sapiens 174-182 3130982-1 1988 In response to phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA), HL-60 cells differentiate to macrophage-like cells and exhibit the ability to phosphorylate vinculin in vitro. Tetradecanoylphorbol Acetate 76-79 vinculin Homo sapiens 174-182 3130982-8 1988 Coincident with these changes after TPA treatment was a reduction in Ca2+ and phospholipid-independent phosphorylation of vinculin in vitro in extracts from HL-60/ADR cells, whereas HL-60 cells exhibited an elevation of this phosphoprotein. Tetradecanoylphorbol Acetate 36-39 vinculin Homo sapiens 122-130 3130982-9 1988 The phosphorylation of vinculin in TPA-treated HL-60 cells or untreated HL-60/ADR cells was blocked by antibodies to protein kinase C. Tetradecanoylphorbol Acetate 35-38 vinculin Homo sapiens 23-31 3319626-5 1987 When the cells were plated in the presence of TPA on pFn or on pFn-fragments, containing the cell binding site, all the cells adhered rapidly, spread extensively, organized prominent F-actin stress fibers and typical ventral plaques of vinculin and alpha-actinin. Tetradecanoylphorbol Acetate 46-49 vinculin Homo sapiens 236-244 3121190-2 1987 Disappearance of vinculin staining from adhesion plaques is also caused by 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 200-400 nM), though the time course of the disappearance of vinculin staining under these conditions takes longer than in cells exposed to PDGF. Tetradecanoylphorbol Acetate 75-112 vinculin Homo sapiens 17-25 3121190-2 1987 Disappearance of vinculin staining from adhesion plaques is also caused by 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 200-400 nM), though the time course of the disappearance of vinculin staining under these conditions takes longer than in cells exposed to PDGF. Tetradecanoylphorbol Acetate 114-117 vinculin Homo sapiens 17-25 3121190-8 1987 Both PDGF (20 ng/ml) and TPA (100 nM) caused cytosolic alkalinization which occurred after PDGF-induced disruption of vinculin from adhesion plaques, as determined using the pH-sensitive indicator BCECF and Digitized Video Microscopy. Tetradecanoylphorbol Acetate 25-28 vinculin Homo sapiens 118-126 3161611-10 1985 On the other hand, TPA-treated cells exhibited a characteristic pp130 which was antigenically related to the actin binding protein, vinculin. Tetradecanoylphorbol Acetate 19-22 vinculin Homo sapiens 132-140 6225775-4 1983 Both calcium and phosphatidylserine were required for vinculin phosphorylation by protein kinase C. In addition, both phorbol 12,13-dibutyrate (10 nM) and phorbol 12-myristate 13-acetate (10 nM) stimulated vinculin phosphorylation by protein kinase C at a limiting calcium concentration (10(-6) M). Tetradecanoylphorbol Acetate 155-186 vinculin Homo sapiens 54-62 6225775-4 1983 Both calcium and phosphatidylserine were required for vinculin phosphorylation by protein kinase C. In addition, both phorbol 12,13-dibutyrate (10 nM) and phorbol 12-myristate 13-acetate (10 nM) stimulated vinculin phosphorylation by protein kinase C at a limiting calcium concentration (10(-6) M). Tetradecanoylphorbol Acetate 155-186 vinculin Homo sapiens 206-214