PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22020547-11 2012 Taken together, we suggest that TPA reciprocally regulates the level of p21 and p53 expression via a MEK/ERK-dependent pathway. Tetradecanoylphorbol Acetate 44-47 tumor protein p53 Homo sapiens 92-95 22020547-0 2012 TPA-induced p21 expression augments G2/M arrest through a p53-independent mechanism in human breast cancer cells. Tetradecanoylphorbol Acetate 0-3 tumor protein p53 Homo sapiens 58-61 24960060-6 2014 In addition, analysis of p53 target genes in TPA-pre-treated TK6 cells revealed a significant modulation of UVC-induced gene expression that supported a shift toward a pro-apoptotic phenotype. Tetradecanoylphorbol Acetate 45-48 tumor protein p53 Homo sapiens 25-28 22020547-4 2012 Our results showed that TPA increased the level of p21 expression in MCF-7 cells with wild-type p53 and MDA-MB-231 cells with mutant p53 in a dose-dependent manner. Tetradecanoylphorbol Acetate 24-27 tumor protein p53 Homo sapiens 108-111 22020547-12 2012 The up-regulation of p21 in response to TPA is mediated through a p53-independent mechanism in breast cancer cells. Tetradecanoylphorbol Acetate 40-43 tumor protein p53 Homo sapiens 78-81 22020547-4 2012 Our results showed that TPA increased the level of p21 expression in MCF-7 cells with wild-type p53 and MDA-MB-231 cells with mutant p53 in a dose-dependent manner. Tetradecanoylphorbol Acetate 24-27 tumor protein p53 Homo sapiens 145-148 22020547-5 2012 In contrast, TPA decreased the expression of p53 in MCF-7 cells, but did not affect MDA-MB-231 cells. Tetradecanoylphorbol Acetate 13-16 tumor protein p53 Homo sapiens 45-48 22299029-1 2012 We have previously shown that TPA activates HTLV-1 LTR in Jurkat T-cells by inducing the binding of Sp1-p53 complex to the Sp1 site residing within the Ets responsive region 1 (ERR-1) of the LTR and that this activation is inhibited by PKCalpha and PKCepsilon. Tetradecanoylphorbol Acetate 30-33 tumor protein p53 Homo sapiens 104-107 22020547-6 2012 We next examined the regulatory mechanism of TPA on p21 and p53 expression. Tetradecanoylphorbol Acetate 45-48 tumor protein p53 Homo sapiens 72-75 22020547-7 2012 Our results showed that the TPA-induced up-regulation of p21 and down-regulation of p53 was reversed by UO126 (a MEK1/2 inhibitor), but not by SP600125 (a JNK inhibitor) or SB203580 (a p38 inhibitor), although TPA increased the phosphorylation of ERK and JNK in MCF-7 cells. Tetradecanoylphorbol Acetate 28-31 tumor protein p53 Homo sapiens 96-99 21705328-6 2011 Our data indicate that TPA-induced MnSOD expression was independent of p53 and most likely mediated by PKC-alpha-, and -epsilon-dependent signaling pathways. Tetradecanoylphorbol Acetate 23-26 tumor protein p53 Homo sapiens 71-74 22911849-9 2012 Over-expression of the dominant negative p53 mutant DeltaTAp53, which inhibits p53 activity, prevented the TPA-induced K14 down-regulation in C9 cells. Tetradecanoylphorbol Acetate 107-110 tumor protein p53 Homo sapiens 41-44 22911849-9 2012 Over-expression of the dominant negative p53 mutant DeltaTAp53, which inhibits p53 activity, prevented the TPA-induced K14 down-regulation in C9 cells. Tetradecanoylphorbol Acetate 107-110 tumor protein p53 Homo sapiens 59-62 22911849-11 2012 Finally, we found that TPA induces the phosphorylation of p53 at residue 378, which enhances the affinity of p53 to bind to Sp1 and repress K14 expression. Tetradecanoylphorbol Acetate 23-26 tumor protein p53 Homo sapiens 58-61 22911849-11 2012 Finally, we found that TPA induces the phosphorylation of p53 at residue 378, which enhances the affinity of p53 to bind to Sp1 and repress K14 expression. Tetradecanoylphorbol Acetate 23-26 tumor protein p53 Homo sapiens 109-112 22009531-6 2011 Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas. Tetradecanoylphorbol Acetate 21-24 tumor protein p53 Homo sapiens 35-38 22009531-6 2011 Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas. Tetradecanoylphorbol Acetate 21-24 tumor protein p53 Homo sapiens 74-77 19366707-4 2009 Within 1 h following TPA treatment of skin epithelial (JB6) cells, p53 accumulated in mitochondria. Tetradecanoylphorbol Acetate 21-24 tumor protein p53 Homo sapiens 67-70 20976134-0 2010 Mitochondrial uncoupling inhibits p53 mitochondrial translocation in TPA-challenged skin epidermal JB6 cells. Tetradecanoylphorbol Acetate 69-72 tumor protein p53 Homo sapiens 34-37 20976134-5 2010 Our results showed that mitochondrial uncoupling blocked p53 mitochondrial translocation induced by 12-O-tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter to induce p53-mediated apoptosis in skin carcinogenesis. Tetradecanoylphorbol Acetate 100-136 tumor protein p53 Homo sapiens 57-60 20976134-5 2010 Our results showed that mitochondrial uncoupling blocked p53 mitochondrial translocation induced by 12-O-tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter to induce p53-mediated apoptosis in skin carcinogenesis. Tetradecanoylphorbol Acetate 100-136 tumor protein p53 Homo sapiens 177-180 20976134-5 2010 Our results showed that mitochondrial uncoupling blocked p53 mitochondrial translocation induced by 12-O-tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter to induce p53-mediated apoptosis in skin carcinogenesis. Tetradecanoylphorbol Acetate 138-141 tumor protein p53 Homo sapiens 57-60 20976134-5 2010 Our results showed that mitochondrial uncoupling blocked p53 mitochondrial translocation induced by 12-O-tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter to induce p53-mediated apoptosis in skin carcinogenesis. Tetradecanoylphorbol Acetate 138-141 tumor protein p53 Homo sapiens 177-180 19541923-12 2009 Ectopic expression of c-Jun/c-Fos or p300 or treatment of cells with phorbol 12-myristate 13-acetate (PMA) stimulated endogenous TFF2 mRNA expression and promoter activity, and p53 inhibited the effects of AP-1 and PMA on TFF2. Tetradecanoylphorbol Acetate 69-100 tumor protein p53 Homo sapiens 177-180 19541923-12 2009 Ectopic expression of c-Jun/c-Fos or p300 or treatment of cells with phorbol 12-myristate 13-acetate (PMA) stimulated endogenous TFF2 mRNA expression and promoter activity, and p53 inhibited the effects of AP-1 and PMA on TFF2. Tetradecanoylphorbol Acetate 102-105 tumor protein p53 Homo sapiens 177-180 19366707-6 2009 The suppressive effect of NPM on p53 mitochondrial localization is also observed in TPA-treated primary epithelial cells and in JB6 cells treated with doxorubicin. Tetradecanoylphorbol Acetate 84-87 tumor protein p53 Homo sapiens 33-36 17108111-0 2006 Mutant p53 protects cells from 12-O-tetradecanoylphorbol-13-acetate-induced death by attenuating activating transcription factor 3 induction. Tetradecanoylphorbol Acetate 31-67 tumor protein p53 Homo sapiens 7-10 18397889-3 2008 Here, we use RNA interference to reduce p53 expression in CHRF cells and show that reduced p53 activity leads to a greater fraction of polyploid cells, higher mean and maximum ploidy, accelerated DNA synthesis, and delayed apoptosis and cell death upon phorbol 12-myristate 13-acetate-induced Mk differentiation. Tetradecanoylphorbol Acetate 253-284 tumor protein p53 Homo sapiens 91-94 18358838-3 2008 Our results demonstrated that CsA and BA blocked TPA-induced p53 translocation, leading to protection against the loss of mitochondrial membrane potential and Complex I activity, and eventually suppression of apoptosis. Tetradecanoylphorbol Acetate 49-52 tumor protein p53 Homo sapiens 61-64 17108111-3 2006 In this study, we explore how the status of p53 affects the immediate response gene activating transcription factor 3 (ATF3) in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-protein kinase C (PKC) pathway. Tetradecanoylphorbol Acetate 132-168 tumor protein p53 Homo sapiens 44-47 17108111-3 2006 In this study, we explore how the status of p53 affects the immediate response gene activating transcription factor 3 (ATF3) in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-protein kinase C (PKC) pathway. Tetradecanoylphorbol Acetate 170-173 tumor protein p53 Homo sapiens 44-47 17108111-4 2006 We show that high doses of TPA induce ATF3 in a WT p53-independent manner correlating with PKCs depletion and cell death. Tetradecanoylphorbol Acetate 27-30 tumor protein p53 Homo sapiens 51-54 17108111-5 2006 We show that cells harboring mutant p53 have attenuated ATF3 induction and are less sensitive to TPA-induced death compared with their p53-null counterparts. Tetradecanoylphorbol Acetate 97-100 tumor protein p53 Homo sapiens 36-39 16267831-6 2006 TPA-induced activation of ERK1/2 was sustained in wild-type p53 cells, while only a transient activation was seen in mutant p53 cells. Tetradecanoylphorbol Acetate 0-3 tumor protein p53 Homo sapiens 124-127 16740634-10 2006 Using ChIP assays and immunoprecipitation, we further demonstrated that p53 interacts with Sp1 to suppress both the constitutive and 12-O-tetradecanoylphorbol-13-acetate-stimulated expression of the MnSOD gene. Tetradecanoylphorbol Acetate 133-169 tumor protein p53 Homo sapiens 72-75 16267831-6 2006 TPA-induced activation of ERK1/2 was sustained in wild-type p53 cells, while only a transient activation was seen in mutant p53 cells. Tetradecanoylphorbol Acetate 0-3 tumor protein p53 Homo sapiens 60-63 16267831-7 2006 Inhibition of MAPK kinase (MEK), an upstream kinase, by U0126, blocked TPA-induced activation of ERK1/2 in wild-type p53 cells and in mutant p53 cells. Tetradecanoylphorbol Acetate 71-74 tumor protein p53 Homo sapiens 117-120 16267831-7 2006 Inhibition of MAPK kinase (MEK), an upstream kinase, by U0126, blocked TPA-induced activation of ERK1/2 in wild-type p53 cells and in mutant p53 cells. Tetradecanoylphorbol Acetate 71-74 tumor protein p53 Homo sapiens 141-144 16267831-8 2006 Treatment of wild-type p53 (SK-Mel 186) cells with small interfering RNA (siRNA) of p53 displayed a transient induction of activation of ERK1/2 following TPA treatment, indicating that p53 has a role in the regulation of the activation of ERK1/2. Tetradecanoylphorbol Acetate 154-157 tumor protein p53 Homo sapiens 23-26 16267831-8 2006 Treatment of wild-type p53 (SK-Mel 186) cells with small interfering RNA (siRNA) of p53 displayed a transient induction of activation of ERK1/2 following TPA treatment, indicating that p53 has a role in the regulation of the activation of ERK1/2. Tetradecanoylphorbol Acetate 154-157 tumor protein p53 Homo sapiens 84-87 16267831-8 2006 Treatment of wild-type p53 (SK-Mel 186) cells with small interfering RNA (siRNA) of p53 displayed a transient induction of activation of ERK1/2 following TPA treatment, indicating that p53 has a role in the regulation of the activation of ERK1/2. Tetradecanoylphorbol Acetate 154-157 tumor protein p53 Homo sapiens 84-87 16267831-10 2006 The expression of either wild-type or mutant p53 had a similar effect on TPA-induced Jun N-terminal kinase (JNK) activation, indicating specificity for the ERK pathway. Tetradecanoylphorbol Acetate 73-76 tumor protein p53 Homo sapiens 45-48 15867370-3 2005 Herein, we show that p53 translocation to mitochondria precedes its translocation to nucleus in JB6 skin epidermal cells treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 153-189 tumor protein p53 Homo sapiens 21-24 15770664-5 2005 Unlike K562 cells, JURL-MK1 cells possess a probably functional p53 protein inducible by TPA (tetradecanoyl phorbol acetate) or UV-B irradiation. Tetradecanoylphorbol Acetate 89-92 tumor protein p53 Homo sapiens 64-67 15770664-5 2005 Unlike K562 cells, JURL-MK1 cells possess a probably functional p53 protein inducible by TPA (tetradecanoyl phorbol acetate) or UV-B irradiation. Tetradecanoylphorbol Acetate 94-123 tumor protein p53 Homo sapiens 64-67 15899818-5 2005 To address the putative mechanisms that underlie resistance to PKC/p53-induced cell death, we generated a phorbol 12-myristate 13-acetate/p53-resistant SW480 subline and compared the gene expression profile of resistant and parental cells by DNA microarray analysis. Tetradecanoylphorbol Acetate 106-137 tumor protein p53 Homo sapiens 67-70 15867370-3 2005 Herein, we show that p53 translocation to mitochondria precedes its translocation to nucleus in JB6 skin epidermal cells treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 191-194 tumor protein p53 Homo sapiens 21-24 15867370-4 2005 Translocation of p53 to mitochondria occurs within 10 minutes after TPA application. Tetradecanoylphorbol Acetate 68-71 tumor protein p53 Homo sapiens 17-20 15867370-6 2005 In contrast to the immediate action on mitochondria, p53 transcriptional activity in the nucleus increases at 1 hour following TPA application, accompanied by an increase in the levels of its target gene bax at 15 hours following TPA treatment. Tetradecanoylphorbol Acetate 127-130 tumor protein p53 Homo sapiens 53-56 15867370-6 2005 In contrast to the immediate action on mitochondria, p53 transcriptional activity in the nucleus increases at 1 hour following TPA application, accompanied by an increase in the levels of its target gene bax at 15 hours following TPA treatment. Tetradecanoylphorbol Acetate 230-233 tumor protein p53 Homo sapiens 53-56 15138488-9 2004 TPA (10(-12)-10(-8) mol l(-1)) treatment of LNCaP cells caused their growth inhibition, cell cycle arrest, upregulation of p53 and p21waf1, and induction of apoptosis. Tetradecanoylphorbol Acetate 0-3 tumor protein p53 Homo sapiens 123-126 12917633-0 2003 Role of protein kinase C and the Sp1-p53 complex in activation of p21(WAF-1) expression by 12-O-tetradecanoylphorbol-13-acetate in human T cells. Tetradecanoylphorbol Acetate 91-127 tumor protein p53 Homo sapiens 37-40 14699137-3 2004 We report here that the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate prevents DNA damage-induced up-regulation of p53 by down-regulating PKC delta. Tetradecanoylphorbol Acetate 54-90 tumor protein p53 Homo sapiens 136-139 14584049-7 2004 Exposure of KCs to IFN-gamma plus TPA reduced total cellular p53 levels and reduced the transcriptional activity of p53. Tetradecanoylphorbol Acetate 34-37 tumor protein p53 Homo sapiens 61-64 14584049-7 2004 Exposure of KCs to IFN-gamma plus TPA reduced total cellular p53 levels and reduced the transcriptional activity of p53. Tetradecanoylphorbol Acetate 34-37 tumor protein p53 Homo sapiens 116-119 14584049-9 2004 Pre-treatment of epidermal equivalents with IFN-gamma plus TPA also blocked UV-light induced increase in p53 levels, and reduced apoptosis. Tetradecanoylphorbol Acetate 59-62 tumor protein p53 Homo sapiens 105-108 11222091-0 2001 Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C. We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1). Tetradecanoylphorbol Acetate 76-112 tumor protein p53 Homo sapiens 4-7 11222091-0 2001 Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C. We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1). Tetradecanoylphorbol Acetate 191-227 tumor protein p53 Homo sapiens 4-7 11222091-0 2001 Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C. We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1). Tetradecanoylphorbol Acetate 229-232 tumor protein p53 Homo sapiens 4-7 11222091-8 2001 Therefore, we speculate that there might be several other PKC-independent biological effects of TPA which result from interaction of such Sp1-p53 complexes with Sp1 recognition sites residing in the promoters of a wide variety of cellular and viral genes. Tetradecanoylphorbol Acetate 96-99 tumor protein p53 Homo sapiens 142-145 10601254-1 1999 The Sp1 transcription factor plays an important role in mediating the p53-independent activation of the p21(WAF1) (WAF1) promoter by phorbol 12-myristate13-acetate (PMA) in hematopoietic cells. Tetradecanoylphorbol Acetate 133-163 tumor protein p53 Homo sapiens 70-73 10601254-1 1999 The Sp1 transcription factor plays an important role in mediating the p53-independent activation of the p21(WAF1) (WAF1) promoter by phorbol 12-myristate13-acetate (PMA) in hematopoietic cells. Tetradecanoylphorbol Acetate 165-168 tumor protein p53 Homo sapiens 70-73 10529369-6 1999 These results may explain how p53 down-regulates the expression of some estrogen-responsive genes such as c-fos, c-jun, TPA, and bcl-2. Tetradecanoylphorbol Acetate 120-123 tumor protein p53 Homo sapiens 30-33 10547071-10 1999 In addition to OM, we showed that the p53 protein expression in MCF-7 cells was also decreased by phorbol 12-myristate 13-acetate treatment (PMA). Tetradecanoylphorbol Acetate 98-129 tumor protein p53 Homo sapiens 38-41 9879997-4 1998 We found up-regulation of p21WAF1 and Bax expressions, however, the expressions of p53 and Bcl-2 genes remained unchanged in TPA-treated cells. Tetradecanoylphorbol Acetate 125-128 tumor protein p53 Homo sapiens 83-86 10543370-5 1999 Activation of protein kinase C by phorbol 12-myristate 13-acetate produced an almost complete inhibition of p53-independent apoptosis following irradiation, whereas no significant effect was observed on the rate of p53-induced apoptosis. Tetradecanoylphorbol Acetate 34-65 tumor protein p53 Homo sapiens 108-111 10543370-6 1999 Although phorbol 12-myristate 13-acetate strongly induced p21 and stabilised p53 in the resting transfected Jurkat cells, neither apoptosis nor cell arrest was observed. Tetradecanoylphorbol Acetate 9-40 tumor protein p53 Homo sapiens 77-80 9879997-8 1998 TPA-induced apoptosis appears to be mediated through a p53-independent pathway, and the up-regulation of p21WAF1 and Bax may be the molecular mechanisms by which TPA induces apoptosis. Tetradecanoylphorbol Acetate 0-3 tumor protein p53 Homo sapiens 55-58 8927716-8 1996 Phorbol 12-myristate 13-acetate (PMA) induced phosphorylation of p53 and pRb1O5 in MCF-7 cells, but EMF exposure had no effect. Tetradecanoylphorbol Acetate 0-31 tumor protein p53 Homo sapiens 65-68 9000576-1 1997 Growth arrest and differentiation of leukemic cells by phorbol 12-myristate 13-acetate (PMA) is accompanied by p53-independent activation of p21WAF1/CIP1 and c-myc down-regulation. Tetradecanoylphorbol Acetate 55-86 tumor protein p53 Homo sapiens 111-114 9000576-1 1997 Growth arrest and differentiation of leukemic cells by phorbol 12-myristate 13-acetate (PMA) is accompanied by p53-independent activation of p21WAF1/CIP1 and c-myc down-regulation. Tetradecanoylphorbol Acetate 88-91 tumor protein p53 Homo sapiens 111-114 21541584-12 1996 The mean TPA percentage was significantly higher in the p53-positive tumors or tumor components (EC and YST) when compared with the mean TPA percentage in those neoplasms that were focally positive or negative for p53 protein (Ki-67, P=0.003; PCNA, P=0.046). Tetradecanoylphorbol Acetate 9-12 tumor protein p53 Homo sapiens 56-59 21541584-13 1996 p53 expression was also associated with histologically aggressive tumors (ECs and YSTs) that also exhibit high TPA. Tetradecanoylphorbol Acetate 111-114 tumor protein p53 Homo sapiens 0-3 9620358-4 1998 After stimulation with anti-CD3 monoclonal antibody (mAb) OKT3 and phorbol myristate acetate (PMA), T cells from young humans exhibited severalfold increases in p53 protein expression compared with resting T cells. Tetradecanoylphorbol Acetate 67-92 tumor protein p53 Homo sapiens 161-164 9620358-4 1998 After stimulation with anti-CD3 monoclonal antibody (mAb) OKT3 and phorbol myristate acetate (PMA), T cells from young humans exhibited severalfold increases in p53 protein expression compared with resting T cells. Tetradecanoylphorbol Acetate 94-97 tumor protein p53 Homo sapiens 161-164 9467850-3 1997 The first of these TPA states is senescence, and several recent studies have shown that abrogation of p53 function permits temporary escape from senescence that ends in a poorly characterized form of arrest (referred to as p53-minus TPA) in which the pRB and p16INK4 genes appear to be involved. Tetradecanoylphorbol Acetate 19-22 tumor protein p53 Homo sapiens 102-105 9467850-3 1997 The first of these TPA states is senescence, and several recent studies have shown that abrogation of p53 function permits temporary escape from senescence that ends in a poorly characterized form of arrest (referred to as p53-minus TPA) in which the pRB and p16INK4 genes appear to be involved. Tetradecanoylphorbol Acetate 233-236 tumor protein p53 Homo sapiens 102-105 8927716-8 1996 Phorbol 12-myristate 13-acetate (PMA) induced phosphorylation of p53 and pRb1O5 in MCF-7 cells, but EMF exposure had no effect. Tetradecanoylphorbol Acetate 33-36 tumor protein p53 Homo sapiens 65-68 8603737-3 1996 We found that phorbol myristate acetate (PMA) activates the src family tyrosine kinases p58c-fgr and p53/56lyn in suspended PMNs. Tetradecanoylphorbol Acetate 14-39 tumor protein p53 Homo sapiens 101-104 8622872-2 1996 Cell type specific differences in p53-independent p21 expression and cell cycle arrest were found following treatment of human tumour cell lines with serum, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or okadaic acid (OA). Tetradecanoylphorbol Acetate 157-194 tumor protein p53 Homo sapiens 34-37 8622872-2 1996 Cell type specific differences in p53-independent p21 expression and cell cycle arrest were found following treatment of human tumour cell lines with serum, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or okadaic acid (OA). Tetradecanoylphorbol Acetate 196-199 tumor protein p53 Homo sapiens 34-37 8603737-3 1996 We found that phorbol myristate acetate (PMA) activates the src family tyrosine kinases p58c-fgr and p53/56lyn in suspended PMNs. Tetradecanoylphorbol Acetate 41-44 tumor protein p53 Homo sapiens 101-104 8603737-4 1996 Moreover, we found that up to about 20% of p58c-fgr and p53/56lyn redistribute to a Triton X-100-insoluble fraction after PMA stimulation, and it is this fraction of the two kinases which diplays an increased activity. Tetradecanoylphorbol Acetate 122-125 tumor protein p53 Homo sapiens 56-59 7560079-6 1995 While p53 was detected in MCF-7 cells, evidence for TPA-induced stimulation of p53 transcriptional activity was not evident. Tetradecanoylphorbol Acetate 52-55 tumor protein p53 Homo sapiens 79-82 7834638-4 1995 We show that p53-independent induction of WAF1/CIP1 occurs in human leukemia cells treated with 12-O-tetradecanoylphorbol-13-acetate, okadaic acid, or IFN-gamma but not with retinoic acid, vitamin D3, or DMSO. Tetradecanoylphorbol Acetate 96-132 tumor protein p53 Homo sapiens 13-16 7727777-7 1995 We show here that TGF-beta treatment of phorbol myristate acetate (PMA) or anti-Ig-activated RL cells results in growth inhibition through a dual effect on Rb and mutant p53. Tetradecanoylphorbol Acetate 40-65 tumor protein p53 Homo sapiens 170-173 7727777-7 1995 We show here that TGF-beta treatment of phorbol myristate acetate (PMA) or anti-Ig-activated RL cells results in growth inhibition through a dual effect on Rb and mutant p53. Tetradecanoylphorbol Acetate 67-70 tumor protein p53 Homo sapiens 170-173 8352891-9 1993 Both p53-hybridizing transcripts were downregulated by prolonged 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment (24 h) regardless of the stage of progression. Tetradecanoylphorbol Acetate 103-106 tumor protein p53 Homo sapiens 5-8 8018565-1 1994 Activation of the protein kinase C signaling pathway by tumor-promoting phorbol esters, such as 4 beta-phorbol 12-myristate 13-acetate (PMA), induced a decrease in the level of p53 mRNA in several serum-starved human cell lines. Tetradecanoylphorbol Acetate 96-134 tumor protein p53 Homo sapiens 177-180 8018565-1 1994 Activation of the protein kinase C signaling pathway by tumor-promoting phorbol esters, such as 4 beta-phorbol 12-myristate 13-acetate (PMA), induced a decrease in the level of p53 mRNA in several serum-starved human cell lines. Tetradecanoylphorbol Acetate 136-139 tumor protein p53 Homo sapiens 177-180 8018565-7 1994 PMA induced a similar transient decrease in the level of p53 protein in the A549 cell line. Tetradecanoylphorbol Acetate 0-3 tumor protein p53 Homo sapiens 57-60 8352891-9 1993 Both p53-hybridizing transcripts were downregulated by prolonged 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment (24 h) regardless of the stage of progression. Tetradecanoylphorbol Acetate 65-101 tumor protein p53 Homo sapiens 5-8 8108142-5 1994 Mutant p53 specifically increases TPA induction of VEGF without affecting the expression of other TPA inducible genes. Tetradecanoylphorbol Acetate 34-37 tumor protein p53 Homo sapiens 7-10 8108142-6 1994 TPA dependent VEGF expression is also enhanced by human p53 mutated at amino acid 175. Tetradecanoylphorbol Acetate 0-3 tumor protein p53 Homo sapiens 56-59 8352891-10 1993 We conclude from this study that in JB6 variants (1) mutational activation of Ha-ras and inactivation of p53 are unlikely to be involved in preneoplastic progression; (2) increased amounts of p53 protein may be involved in a subset of transformed cells, possibly reflecting a longer half-life, as demonstrated in other systems; and (3) late downregulation of p53 mRNA but not protein expression may be a secondary response in the TPA-mediated signal transduction pathway. Tetradecanoylphorbol Acetate 430-433 tumor protein p53 Homo sapiens 192-195 8352891-10 1993 We conclude from this study that in JB6 variants (1) mutational activation of Ha-ras and inactivation of p53 are unlikely to be involved in preneoplastic progression; (2) increased amounts of p53 protein may be involved in a subset of transformed cells, possibly reflecting a longer half-life, as demonstrated in other systems; and (3) late downregulation of p53 mRNA but not protein expression may be a secondary response in the TPA-mediated signal transduction pathway. Tetradecanoylphorbol Acetate 430-433 tumor protein p53 Homo sapiens 192-195 33791017-11 2021 Perp and phorbol-12-myristate-13-acetate-induced protein 1 were demonstrated to have vital roles in the p53 signaling pathway which was indicated in the interaction network. Tetradecanoylphorbol Acetate 9-40 tumor protein p53 Homo sapiens 104-107 1868448-6 1991 Similarly, p53 levels increased and DNA synthesis decreased during 12-O-tetradecanoylphorbol-13-acetate-induced differentiation of ML-1 myeloblastic leukemia cells. Tetradecanoylphorbol Acetate 67-103 tumor protein p53 Homo sapiens 11-14 29660338-7 2018 It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA. Tetradecanoylphorbol Acetate 18-21 tumor protein p53 Homo sapiens 86-89 32705219-8 2020 Moreover, by using western blot analysis, we determined that EA increased the protein expression of the p53 target proteins p21, p53 upregulated modulator of apoptosis (PUMA) [also known as Bcl-2-binding component 3 (BBC3)] and Phorbol-12-myristate-13-acetate-induced protein 1 (NOXA). Tetradecanoylphorbol Acetate 228-259 tumor protein p53 Homo sapiens 104-107 32705219-8 2020 Moreover, by using western blot analysis, we determined that EA increased the protein expression of the p53 target proteins p21, p53 upregulated modulator of apoptosis (PUMA) [also known as Bcl-2-binding component 3 (BBC3)] and Phorbol-12-myristate-13-acetate-induced protein 1 (NOXA). Tetradecanoylphorbol Acetate 228-259 tumor protein p53 Homo sapiens 129-132 31726940-6 2019 In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1. Tetradecanoylphorbol Acetate 478-509 tumor protein p53 Homo sapiens 47-50 31726940-6 2019 In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1. Tetradecanoylphorbol Acetate 478-509 tumor protein p53 Homo sapiens 215-218 31726940-6 2019 In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1. Tetradecanoylphorbol Acetate 478-509 tumor protein p53 Homo sapiens 215-218 31726940-6 2019 In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1. Tetradecanoylphorbol Acetate 478-509 tumor protein p53 Homo sapiens 215-218 31726940-6 2019 In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1. Tetradecanoylphorbol Acetate 478-509 tumor protein p53 Homo sapiens 215-218 31726940-6 2019 In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1. Tetradecanoylphorbol Acetate 478-509 tumor protein p53 Homo sapiens 215-218 29660338-7 2018 It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA. Tetradecanoylphorbol Acetate 18-21 tumor protein p53 Homo sapiens 104-107 29660338-7 2018 It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA. Tetradecanoylphorbol Acetate 182-185 tumor protein p53 Homo sapiens 86-89 29660338-7 2018 It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA. Tetradecanoylphorbol Acetate 182-185 tumor protein p53 Homo sapiens 104-107 29660338-8 2018 In addition, TPA treatment highly induced the expression of CREB which attached to the Sp1-p53 complex mainly after a long exposure to TPA. Tetradecanoylphorbol Acetate 13-16 tumor protein p53 Homo sapiens 91-94 29660338-8 2018 In addition, TPA treatment highly induced the expression of CREB which attached to the Sp1-p53 complex mainly after a long exposure to TPA. Tetradecanoylphorbol Acetate 135-138 tumor protein p53 Homo sapiens 91-94 29660338-9 2018 A strong binding of sp1, p53 and CREB proteins with HTLV-1 LTR and strong binding of NF-kappaB with HIV-1 LTR were observed after long (24 h) and short (6 h) exposures to TPA respectively by Chip assay. Tetradecanoylphorbol Acetate 171-174 tumor protein p53 Homo sapiens 25-28 29660338-10 2018 These results support the possibility that sp1, p53 and CREB are involved in the TPA induced HTLV-1 LTR expression while TPA activation of HIV-1 LTR seems to be dependent on PKC activity through the NF-kappaB pathway. Tetradecanoylphorbol Acetate 81-84 tumor protein p53 Homo sapiens 48-51 28765903-5 2017 To examine the mechanism underlying the relationship between p53 and FN expression, we treated MCF7 breast cancer cells with the tumor promoter TPA (12-O-tetradecanoylphorbol-13-acetate). Tetradecanoylphorbol Acetate 144-147 tumor protein p53 Homo sapiens 61-64 28765903-7 2017 In contrast, the level of p53 expression was decreased by TPA treatment. Tetradecanoylphorbol Acetate 58-61 tumor protein p53 Homo sapiens 26-29 28765903-9 2017 Furthermore, the alterations in FN and p53 expression in response to TPA were prevented by a specific MEK inhibitor, UO126. Tetradecanoylphorbol Acetate 69-72 tumor protein p53 Homo sapiens 39-42 28765903-10 2017 Finally, we demonstrated that TPA triggers degradation of p53 through the proteasomal pathway in MCF7 cells. Tetradecanoylphorbol Acetate 30-33 tumor protein p53 Homo sapiens 58-61 27409664-6 2016 Furthermore, downregulation of CTBP1 by miR-644a upregulates wild type- or mutant-p53 which acts as a "molecular switch" between G1-arrest and apoptosis by inducing cyclin-dependent kinase inhibitor 1 (p21, CDKN1A, CIP1) or pro-apoptotic phorbol-12-myristate-13-acetate-induced protein 1 (Noxa, PMAIP1), respectively. Tetradecanoylphorbol Acetate 238-269 tumor protein p53 Homo sapiens 82-85 26231140-7 2015 These compounds appeared the most effective inducers of p53 in the TPA-challenged neutrophils, what may suggest that pro-apoptotic activity of these stilbenes might be related to p53 activation. Tetradecanoylphorbol Acetate 67-70 tumor protein p53 Homo sapiens 56-59 26581877-6 2016 Our results indicate that confinement of p53 in the cytoplasm is one of the potential mechanisms by which TPA interferes with the process of radiation-induced apoptosis in human lymphocytes. Tetradecanoylphorbol Acetate 106-109 tumor protein p53 Homo sapiens 41-44 26431317-7 2015 Further analysis revealed that TPA+UVC co-exposure caused synergistic perturbation of specific genes associated with p53, AP-1 and inflammatory pathways important in carcinogenesis. Tetradecanoylphorbol Acetate 31-34 tumor protein p53 Homo sapiens 117-120 26231140-7 2015 These compounds appeared the most effective inducers of p53 in the TPA-challenged neutrophils, what may suggest that pro-apoptotic activity of these stilbenes might be related to p53 activation. Tetradecanoylphorbol Acetate 67-70 tumor protein p53 Homo sapiens 179-182