PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9547581-1 1997 The sphingosine analog L-threo-dihydrosphingosine has been shown to inhibit protein kinase C (PKC) isoenzymes in mixed micelle and vesicle assays. safingol 23-49 proline rich transmembrane protein 2 Homo sapiens 76-92 9186373-4 1997 RESULTS: Triamcinolone (TA) and sphinganine synergized to inhibit the proliferation rate of PA III prostate tumor cells by converging through separate mechanisms to inhibit protein kinase C. safingol 32-43 proline rich transmembrane protein 2 Homo sapiens 173-189 9186373-6 1997 Exogenous sphinganine, a competitive inhibitor at the regulatory domain of PKC had no anti-proliferative effect at 1 microM, but in combination with TA synergized to reduce proliferation 80-90%, three days in advance of any detectable inhibitory effect of TA alone on cell number. safingol 10-21 proline rich transmembrane protein 2 Homo sapiens 75-78 9186373-13 1997 CONCLUSIONS: TA-induced reduction of PKC concentration coupled with sphinganine antagonism of PKC activation contributed to in a synergistic growth inhibition of an androgen resistant prostatic carcinoma. safingol 68-79 proline rich transmembrane protein 2 Homo sapiens 94-97 9147607-8 1997 While adequate PKC modulation might offer an attractive concept to modulate MDR, other potential mechanisms of PKC interaction with anticancer drugs exist and have been documented, such as the enhancement of chemotherapy-induced apoptosis by safingol, a specific PKC inhibitor. safingol 242-250 proline rich transmembrane protein 2 Homo sapiens 111-114 9147607-8 1997 While adequate PKC modulation might offer an attractive concept to modulate MDR, other potential mechanisms of PKC interaction with anticancer drugs exist and have been documented, such as the enhancement of chemotherapy-induced apoptosis by safingol, a specific PKC inhibitor. safingol 242-250 proline rich transmembrane protein 2 Homo sapiens 111-114 10665476-7 1999 Such chemosensitizing strategies can involve either (a) direct inhibition of PKC (e.g., following acute treatment with relatively specific inhibitors such as the synthetic sphingoid base analog safingol, or the novel staurosporine derivatives UCN-01 and CGP-41251) or (b) down-regulation (e.g., following chronic treatment with the non-tumor-promoting PKC activator bryostatin 1). safingol 194-202 proline rich transmembrane protein 2 Homo sapiens 77-80 9186373-0 1997 Protein kinase C mediated anti-proliferative glucocorticoid-sphinganine synergism in cultured Pollard III prostate tumor cells. safingol 60-71 proline rich transmembrane protein 2 Homo sapiens 0-16 9547581-1 1997 The sphingosine analog L-threo-dihydrosphingosine has been shown to inhibit protein kinase C (PKC) isoenzymes in mixed micelle and vesicle assays. safingol 23-49 proline rich transmembrane protein 2 Homo sapiens 94-97 8440177-7 1993 The PKC inhibitors H7 (1 microM), tamoxifen (10 microM), and sphinganine (5 microM) inhibited PTH release at low Ca2+e (0.1 and 0.2 mM) and decreased cell recruitment over the physiological range of Ca2+e. safingol 61-72 proline rich transmembrane protein 2 Homo sapiens 4-7 7658500-0 1995 Potentiation of apoptosis by treatment with the protein kinase C-specific inhibitor safingol in mitomycin C-treated gastric cancer cells. safingol 84-92 proline rich transmembrane protein 2 Homo sapiens 48-64 7658500-2 1995 Safingol, an optical isomer (the L-threo enantiomer) of dihydrosphingosine, is a specific inhibitor of PKC and might represent a novel agent for anticancer therapy. safingol 0-8 proline rich transmembrane protein 2 Homo sapiens 103-106 7658500-2 1995 Safingol, an optical isomer (the L-threo enantiomer) of dihydrosphingosine, is a specific inhibitor of PKC and might represent a novel agent for anticancer therapy. safingol 56-74 proline rich transmembrane protein 2 Homo sapiens 103-106 7658500-15 1995 CONCLUSIONS: The PKC inhibitor safingol enhances the cytotoxic effect of the chemotherapeutic agent MMC in gastric cancer cells by promoting drug-induced apoptosis. safingol 31-39 proline rich transmembrane protein 2 Homo sapiens 17-20 1379255-7 1992 The transient PKC activator diC8 had no effect, while studies with the PKC inhibitors sphinganine and H-7 were limited by solvent vehicle cytotoxicity. safingol 86-97 proline rich transmembrane protein 2 Homo sapiens 71-74 1635422-0 1992 Protein kinase C activity during sphinganine potentiation of retinoic acid-induced differentiation in a human leukemia cell line (HL-60). safingol 33-44 proline rich transmembrane protein 2 Homo sapiens 0-16 1635422-2 1992 The enhancement of RA-induced differentiation and the potentiation of the decrease of PKC activity by sphinganine (SP) seemed to correlate with each other. safingol 102-113 proline rich transmembrane protein 2 Homo sapiens 86-89 1635422-2 1992 The enhancement of RA-induced differentiation and the potentiation of the decrease of PKC activity by sphinganine (SP) seemed to correlate with each other. safingol 115-117 proline rich transmembrane protein 2 Homo sapiens 86-89 1635422-3 1992 Kinetically, PKC activity during RA-induced differentiation without SP decreased to its lowest (75% of the control) after 48h; about 50% of the reduction was observed at 24h. safingol 68-70 proline rich transmembrane protein 2 Homo sapiens 13-16 1635422-4 1992 In the presence of SP, PKC activity decreased more rapidly to its lowest (60% of the control) within 24h of incubation of RA. safingol 19-21 proline rich transmembrane protein 2 Homo sapiens 23-26 1635422-5 1992 SP, added 24h before or concomitantly with the addition of RA, could potentiate the RA-induced differentiation and the reduction of PKC activity. safingol 0-2 proline rich transmembrane protein 2 Homo sapiens 132-135 11914646-7 2002 Using the colorimetric MTT assay, PKC inhibitors Saf and Che showed comparable dose-dependent growth inhibition. safingol 49-52 proline rich transmembrane protein 2 Homo sapiens 34-37 19098447-0 2009 Safingol (L-threo-sphinganine) induces autophagy in solid tumor cells through inhibition of PKC and the PI3-kinase pathway. safingol 0-8 proline rich transmembrane protein 2 Homo sapiens 92-95 19098447-5 2009 Conversely, activation of PKCs with phorbol 12,13-dibutyrate (PDBu) or transient transfection of a constitutively active form of Akt each reduced safingol"s autophagic induction, but not completely, indicating that Akt- and PKC-dependent pathways both contribute partially and independently to safingol-induced autophagy. safingol 146-154 proline rich transmembrane protein 2 Homo sapiens 26-29 19098447-5 2009 Conversely, activation of PKCs with phorbol 12,13-dibutyrate (PDBu) or transient transfection of a constitutively active form of Akt each reduced safingol"s autophagic induction, but not completely, indicating that Akt- and PKC-dependent pathways both contribute partially and independently to safingol-induced autophagy. safingol 294-302 proline rich transmembrane protein 2 Homo sapiens 26-29 15929099-7 2005 Following safingol treatment, several genes showed marked downregulation and PKC-related proteins demonstrated decreased hybridization signals. safingol 10-18 proline rich transmembrane protein 2 Homo sapiens 77-80 11914646-9 2002 Combinations of cisplatin (IC50 = 0.4-5.8 microg/ml) and either PKC inhibitor (5 microM Saf, 10 microM Che) led to a significant decrease of cisplatin IC50 values in most cell lines. safingol 88-91 proline rich transmembrane protein 2 Homo sapiens 64-67