PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11298136-9 2001 The results obtained during a three year period in the proliferation assays show an impaired PMA (phorbol myristate acetate) activation in specific T lymphocyte activation pathways (CD69, CD26, CD28, CD3, PHA, PWM and Con A mediated) but not in others (CD2, ionomycin, and Ig surface receptor). Tetradecanoylphorbol Acetate 98-123 dipeptidyl peptidase 4 Homo sapiens 188-192 9758695-8 1998 The data presented here suggest that the inhibition of DPIV enzymatic activity induces a inhibitory signal transmitted by tyrosine kinases which leads to a block in a PMA-induced downstream pathway. Tetradecanoylphorbol Acetate 167-170 dipeptidyl peptidase 4 Homo sapiens 55-59 10634965-3 1999 METHODS: Basal, concanavalin A (Con A)-, and phorbol-12-myristate-13-acetate (PMA)-stimulated lymphocyte PC-1, aminopeptidase N (APN), and dipeptidylpeptidase IV (DPP IV) activities were determined in 16 patients with Type 2 diabetes before and after 3 months of metformin treatment. Tetradecanoylphorbol Acetate 45-76 dipeptidyl peptidase 4 Homo sapiens 139-161 10634965-3 1999 METHODS: Basal, concanavalin A (Con A)-, and phorbol-12-myristate-13-acetate (PMA)-stimulated lymphocyte PC-1, aminopeptidase N (APN), and dipeptidylpeptidase IV (DPP IV) activities were determined in 16 patients with Type 2 diabetes before and after 3 months of metformin treatment. Tetradecanoylphorbol Acetate 45-76 dipeptidyl peptidase 4 Homo sapiens 163-169 8104537-10 1993 On preactivating the same cells, using phorbol myristate acetate (PMA)/ionomycin on concanavalin A (ConA) or especially PHA, levels of CD26 were upregulated and the immunotoxin effectively inhibited the ability to provide help for B-cell Ig synthesis while leaving intact the CD4-CD26+ and CD4+CD26- populations; an effect observed both functionally and by phenotype. Tetradecanoylphorbol Acetate 39-64 dipeptidyl peptidase 4 Homo sapiens 280-284 7590918-0 1995 Enzymatic activity of DPIV/CD26 is involved in PMA-induced hyperphosphorylation of p56lck. Tetradecanoylphorbol Acetate 47-50 dipeptidyl peptidase 4 Homo sapiens 27-31 8104537-10 1993 On preactivating the same cells, using phorbol myristate acetate (PMA)/ionomycin on concanavalin A (ConA) or especially PHA, levels of CD26 were upregulated and the immunotoxin effectively inhibited the ability to provide help for B-cell Ig synthesis while leaving intact the CD4-CD26+ and CD4+CD26- populations; an effect observed both functionally and by phenotype. Tetradecanoylphorbol Acetate 39-64 dipeptidyl peptidase 4 Homo sapiens 135-139 8104537-10 1993 On preactivating the same cells, using phorbol myristate acetate (PMA)/ionomycin on concanavalin A (ConA) or especially PHA, levels of CD26 were upregulated and the immunotoxin effectively inhibited the ability to provide help for B-cell Ig synthesis while leaving intact the CD4-CD26+ and CD4+CD26- populations; an effect observed both functionally and by phenotype. Tetradecanoylphorbol Acetate 39-64 dipeptidyl peptidase 4 Homo sapiens 280-284 8104537-10 1993 On preactivating the same cells, using phorbol myristate acetate (PMA)/ionomycin on concanavalin A (ConA) or especially PHA, levels of CD26 were upregulated and the immunotoxin effectively inhibited the ability to provide help for B-cell Ig synthesis while leaving intact the CD4-CD26+ and CD4+CD26- populations; an effect observed both functionally and by phenotype. Tetradecanoylphorbol Acetate 66-69 dipeptidyl peptidase 4 Homo sapiens 135-139 8104537-10 1993 On preactivating the same cells, using phorbol myristate acetate (PMA)/ionomycin on concanavalin A (ConA) or especially PHA, levels of CD26 were upregulated and the immunotoxin effectively inhibited the ability to provide help for B-cell Ig synthesis while leaving intact the CD4-CD26+ and CD4+CD26- populations; an effect observed both functionally and by phenotype. Tetradecanoylphorbol Acetate 66-69 dipeptidyl peptidase 4 Homo sapiens 280-284 8104537-10 1993 On preactivating the same cells, using phorbol myristate acetate (PMA)/ionomycin on concanavalin A (ConA) or especially PHA, levels of CD26 were upregulated and the immunotoxin effectively inhibited the ability to provide help for B-cell Ig synthesis while leaving intact the CD4-CD26+ and CD4+CD26- populations; an effect observed both functionally and by phenotype. Tetradecanoylphorbol Acetate 66-69 dipeptidyl peptidase 4 Homo sapiens 280-284 8099849-7 1993 When CD26+ T cells were cultured in the presence of PMA, which depletes pkC activity, CD26 antigen expression was down-regulated. Tetradecanoylphorbol Acetate 52-55 dipeptidyl peptidase 4 Homo sapiens 5-9 8099849-6 1993 When activated through the TCR/CD3 pathway, the CD2 pathway, or directly by the phorbol ester, PMA, the memory (CD26+) T cells showed an increased proliferative response that was inhibited by the pkC inhibitor, staurosporine. Tetradecanoylphorbol Acetate 95-98 dipeptidyl peptidase 4 Homo sapiens 112-116 8099849-7 1993 When CD26+ T cells were cultured in the presence of PMA, which depletes pkC activity, CD26 antigen expression was down-regulated. Tetradecanoylphorbol Acetate 52-55 dipeptidyl peptidase 4 Homo sapiens 86-90 8227206-3 1993 TPA prevented the accumulation of differentiation markers such as dipeptidylpeptidase IV, villin or mucins, down-regulated the expression of these molecules in post-confluent differentiated cell cultures and induced the loss of the functional integrity of the tight junction in the monolayer (i.e. decreased transepithelial resistance and inhibited dome formation). Tetradecanoylphorbol Acetate 0-3 dipeptidyl peptidase 4 Homo sapiens 66-88 25022544-7 2014 To determine the role of PKC activation in the effects of DPP-4 inhibitors, cells were treated with PMA- which blocked the effect of DPP-4 inhibitors on NLRP3 and IL-1beta as well as TLR4 and GLP-1R. Tetradecanoylphorbol Acetate 100-103 dipeptidyl peptidase 4 Homo sapiens 58-63 2891591-0 1987 Dipeptidyl peptidase IV activity in cells of T-lymphoid origin is decreased in cultures with 12-0-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 131-134 dipeptidyl peptidase 4 Homo sapiens 0-23 2891591-2 1987 It has been attempted to induce DPP IV activity in DPP IV negative T-lymphoid leukaemias by 12-o-tetradecanoylphrobol-13-acetate (TPA). Tetradecanoylphorbol Acetate 130-133 dipeptidyl peptidase 4 Homo sapiens 32-38 2891591-2 1987 It has been attempted to induce DPP IV activity in DPP IV negative T-lymphoid leukaemias by 12-o-tetradecanoylphrobol-13-acetate (TPA). Tetradecanoylphorbol Acetate 130-133 dipeptidyl peptidase 4 Homo sapiens 51-57 2891591-4 1987 The percentage of DPP IV positive lymphocytes from blood donors remained unchanged in control and HPCM cultures, but decreased significantly in TPA cultures. Tetradecanoylphorbol Acetate 144-147 dipeptidyl peptidase 4 Homo sapiens 18-24 2891591-5 1987 Leukemic cells from three DPP IV positive cases of acute T-lymphoblastic leukaemia (T-ALL) reacted to the TPA treatment in a similar manner. Tetradecanoylphorbol Acetate 106-109 dipeptidyl peptidase 4 Homo sapiens 26-32 27887857-10 2017 In vitro studies demonstrated that the inhibition of DPP-4 promoted PMA-induced monocytic cells differentiation, with increased CD68 and p21 expression, regulated by extracellular signal-regulated protein kinase 1/2 activation. Tetradecanoylphorbol Acetate 68-71 dipeptidyl peptidase 4 Homo sapiens 53-58 25022544-7 2014 To determine the role of PKC activation in the effects of DPP-4 inhibitors, cells were treated with PMA- which blocked the effect of DPP-4 inhibitors on NLRP3 and IL-1beta as well as TLR4 and GLP-1R. Tetradecanoylphorbol Acetate 100-103 dipeptidyl peptidase 4 Homo sapiens 133-138