PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11922601-4 2001 Op18 phosphorylation is rapidly induced with phorbol myristate acetate (PMA) treatment in a wide range of human cells. Tetradecanoylphorbol Acetate 45-70 stathmin 1 Homo sapiens 0-4 11922601-4 2001 Op18 phosphorylation is rapidly induced with phorbol myristate acetate (PMA) treatment in a wide range of human cells. Tetradecanoylphorbol Acetate 72-75 stathmin 1 Homo sapiens 0-4 7637391-0 1995 The protein kinase C inhibitor H7 blocks phosphorylation of stathmin during TPA-induced growth inhibition of human pre-B leukemia REH6 cells. Tetradecanoylphorbol Acetate 76-79 stathmin 1 Homo sapiens 60-68 8314790-0 1993 Phorbol 12-myristate 13-acetate-induced phosphorylation of Op18 in Jurkat T cells. Tetradecanoylphorbol Acetate 0-31 stathmin 1 Homo sapiens 59-63 7750926-0 1995 Persistent growth of BALB/C mouse plasmacytoma and human myeloma cell lines in the presence of phorbol myristate acetate is associated with continued expression of Lap18 (stathmin). Tetradecanoylphorbol Acetate 95-120 stathmin 1 Homo sapiens 164-169 7750926-0 1995 Persistent growth of BALB/C mouse plasmacytoma and human myeloma cell lines in the presence of phorbol myristate acetate is associated with continued expression of Lap18 (stathmin). Tetradecanoylphorbol Acetate 95-120 stathmin 1 Homo sapiens 171-179 8314790-3 1993 In actively proliferating Jurkat T cells which express Op18 at high level, phorbol 12-myristate 13-acetate (PMA) treatment induces a rapid increase in the level of several Op18 phosphorylated forms. Tetradecanoylphorbol Acetate 75-106 stathmin 1 Homo sapiens 55-59 8314790-3 1993 In actively proliferating Jurkat T cells which express Op18 at high level, phorbol 12-myristate 13-acetate (PMA) treatment induces a rapid increase in the level of several Op18 phosphorylated forms. Tetradecanoylphorbol Acetate 75-106 stathmin 1 Homo sapiens 172-176 8314790-3 1993 In actively proliferating Jurkat T cells which express Op18 at high level, phorbol 12-myristate 13-acetate (PMA) treatment induces a rapid increase in the level of several Op18 phosphorylated forms. Tetradecanoylphorbol Acetate 108-111 stathmin 1 Homo sapiens 55-59 8314790-3 1993 In actively proliferating Jurkat T cells which express Op18 at high level, phorbol 12-myristate 13-acetate (PMA) treatment induces a rapid increase in the level of several Op18 phosphorylated forms. Tetradecanoylphorbol Acetate 108-111 stathmin 1 Homo sapiens 172-176 3015383-2 1986 EGF or TPA induced a 4- to 6-fold increase in the phosphorylation of pp17 and a 2- to 4-fold increase in the phosphorylation of pp27, pp34, and pp80 within 15 min after treatment of subconfluent A431 cells. Tetradecanoylphorbol Acetate 7-10 stathmin 1 Homo sapiens 69-73 1727435-4 1992 In intact striatal neurons grown in primary culture, the cyclic AMP-increasing drug forskolin and the protein kinase C-activating agent 12-O-tetradecanoylphorbol 13-acetate (TPA) induced a potent phosphorylation of stathmin. Tetradecanoylphorbol Acetate 136-172 stathmin 1 Homo sapiens 215-223 1727435-4 1992 In intact striatal neurons grown in primary culture, the cyclic AMP-increasing drug forskolin and the protein kinase C-activating agent 12-O-tetradecanoylphorbol 13-acetate (TPA) induced a potent phosphorylation of stathmin. Tetradecanoylphorbol Acetate 174-177 stathmin 1 Homo sapiens 215-223 1930203-4 1991 Moreover treatment of HL-60 promyelocytic leukemia cells with DMSO or PMA which induced terminal differentiation resulted in a decrease in the level of Op18 RNA and protein. Tetradecanoylphorbol Acetate 70-73 stathmin 1 Homo sapiens 152-156 1903411-3 1991 In the present report we have studied various agents that, like TPA, act as partial or complete mitogens for G0 PBL and have determined their effect on phosphorylation of prosolin and on DNA synthesis in rapidly proliferating (IL-2-dependent) human PBL. Tetradecanoylphorbol Acetate 64-67 stathmin 1 Homo sapiens 171-179 1903411-4 1991 Agents that activate the TCR (OKT3 and PHA), as well as agents that by-pass the receptor but activate biochemical pathways associated with TCR activation (TPA and Ca2(+)-ionophore), all produced rapid phosphorylation of prosolin and prompt down-regulation of DNA synthesis. Tetradecanoylphorbol Acetate 155-158 stathmin 1 Homo sapiens 220-228 2267130-2 1990 Op18 is phosphorylated upon treatment of lymphoid cells with phorbol myristate acetate. Tetradecanoylphorbol Acetate 61-86 stathmin 1 Homo sapiens 0-4 2116478-2 1990 Treatment of growing PBL with phorbol ester (12-O-tetradecanoylphorbol-13-acetate (TPA)) or calcium ionophore (A23187) for 1 h caused phosphorylation of prosolin with the production of up to four prominent phosphorylated forms differing in degree of phosphorylation and/or two-dimensional electrophoretic mobility (peptides B to E). Tetradecanoylphorbol Acetate 45-81 stathmin 1 Homo sapiens 153-161 2116478-2 1990 Treatment of growing PBL with phorbol ester (12-O-tetradecanoylphorbol-13-acetate (TPA)) or calcium ionophore (A23187) for 1 h caused phosphorylation of prosolin with the production of up to four prominent phosphorylated forms differing in degree of phosphorylation and/or two-dimensional electrophoretic mobility (peptides B to E). Tetradecanoylphorbol Acetate 83-86 stathmin 1 Homo sapiens 153-161 2116478-7 1990 The T cell leukemic cells appear to have intact a TPA-activated mechanism for phosphorylating prosolin peptides B and C, but share an impairment of a specific Ca2(+)-activated mechanism, possibly a Ca2(+)-dependent protein kinase, required for phosphorylation of prosolin phosphopeptides D and E. The degree of rapid down-regulation of DNA synthesis was correlated with degree of phosphorylation of peptide E in PBL and in three of four T cell leukemic cell lines. Tetradecanoylphorbol Acetate 50-53 stathmin 1 Homo sapiens 94-102 2116478-8 1990 Thus, rapid phosphorylation of prosolin may mediate responses to TPA and A23187 in normal proliferating PBL, including down-regulation of DNA synthesis. Tetradecanoylphorbol Acetate 65-68 stathmin 1 Homo sapiens 31-39 2745978-3 1989 In our study we examined the expression of prosolin in human peripheral lymphocytes and investigated the effects of TPA treatment on prosolin phosphorylation and on lymphocyte proliferation. Tetradecanoylphorbol Acetate 116-119 stathmin 1 Homo sapiens 133-141 2745978-8 1989 TPA treatment of IL-2-dependent PBL at the peak of their growth caused phosphorylation of about two-thirds of preexisting unphosphorylated prosolin within 1 h. This was accompanied by cessation of cell proliferation, as indicated by measurements of TdR incorporation. Tetradecanoylphorbol Acetate 0-3 stathmin 1 Homo sapiens 139-147 2745978-10 1989 It is suggested that increased phosphorylation of prosolin may be an initiating event in the antiproliferative response to TPA, which would occur only in proliferating lymphocytes expressing prosolin. Tetradecanoylphorbol Acetate 123-126 stathmin 1 Homo sapiens 50-58 2745978-10 1989 It is suggested that increased phosphorylation of prosolin may be an initiating event in the antiproliferative response to TPA, which would occur only in proliferating lymphocytes expressing prosolin. Tetradecanoylphorbol Acetate 123-126 stathmin 1 Homo sapiens 191-199 3464595-1 1986 Treatment of HL-60 promyelocytic leukemia cells with the tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), causes rapid phosphorylation and dephosphorylation of pp17, a 17-20-kDa, pI 5.5 cytosolic protein, as an early event in a response sequence leading to growth arrest and terminal differentiation into monocytes (Feuerstein, N., and Cooper, H. L., (1984) J. Biol. Tetradecanoylphorbol Acetate 126-129 stathmin 1 Homo sapiens 186-190 3464595-9 1986 Upon TPA treatment, pre-existing p17 was rapidly phosphorylated to pp17. Tetradecanoylphorbol Acetate 5-8 stathmin 1 Homo sapiens 67-71 3464595-13 1986 Quantitatively, therefore, the phosphorylation of p17 to pp17 is one of the most prominent early biochemical responses to TPA treatment. Tetradecanoylphorbol Acetate 122-125 stathmin 1 Homo sapiens 57-61 3464595-14 1986 Available data indicate that p17 predominates in rapidly proliferating cells, while phosphorylation to pp17 occurs where cell growth is modified by TPA or other agents. Tetradecanoylphorbol Acetate 148-151 stathmin 1 Homo sapiens 103-107 3161611-9 1985 Also present was a prominent PL-Ca-dependent pp19 which remained unchanged following treatment with DMSO, RA, and 1,25(OH)2D3, but which diminished markedly in TPA-treated cells. Tetradecanoylphorbol Acetate 160-163 stathmin 1 Homo sapiens 45-49