PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27520485-7 2016 At the molecular level, the expression of several key TPA-induced pro-survival and pro-proliferative genes (Bcl2, Cyclin D1, and c-Myc) decreased rapidly after BET inhibition. Tetradecanoylphorbol Acetate 54-57 MYC proto-oncogene, bHLH transcription factor Homo sapiens 129-134 25908095-6 2015 Conversely, MAPK/p38 inactivation or REGgamma deletion prevents the increase of cyclinD1 and c-Myc by TPA. Tetradecanoylphorbol Acetate 102-105 MYC proto-oncogene, bHLH transcription factor Homo sapiens 93-98 15949478-5 2005 METHODS AND RESULTS: Downregulation of PKC by phorbol 12-myristate 13-acetate (PMA) inhibited bFGF-induced DNA synthesis, the activation of MAPK, and the expression of c-myc, demonstrating the involvement of PMA-sensitive PKC isoforms in growth factor-induced proliferation and the MAPK pathway. Tetradecanoylphorbol Acetate 46-77 MYC proto-oncogene, bHLH transcription factor Homo sapiens 168-173 23562609-7 2013 During SIRPalpha induction, levels of these 3 miRNAs were all reduced, and their downregulation by retinoic acid or phorbol 12-myristate 13-acetate occurred through suppression of the c-Myc signaling pathway. Tetradecanoylphorbol Acetate 116-147 MYC proto-oncogene, bHLH transcription factor Homo sapiens 184-189 19526458-8 2009 Subsequent biological network analysis suggests that many of the differentially expressed genes that are common to bFGF- and TPA-dependent AIG are regulated by c-Myc, SP-1, and HNF-4 transcription factors. Tetradecanoylphorbol Acetate 125-128 MYC proto-oncogene, bHLH transcription factor Homo sapiens 160-165 15949478-5 2005 METHODS AND RESULTS: Downregulation of PKC by phorbol 12-myristate 13-acetate (PMA) inhibited bFGF-induced DNA synthesis, the activation of MAPK, and the expression of c-myc, demonstrating the involvement of PMA-sensitive PKC isoforms in growth factor-induced proliferation and the MAPK pathway. Tetradecanoylphorbol Acetate 79-82 MYC proto-oncogene, bHLH transcription factor Homo sapiens 168-173 14757441-5 2004 Furthermore, when HL-60 myeloid leukemic cells were differentiated with phorbol ester (TPA), PBK/TOPK protein expression was strongly down-regulated by 24 h. Under these same conditions, phosphorylated c-Myc was rapidly down-regulated (by 4 h), while the levels of cyclin D1 and phosphorylated p38 were constant. Tetradecanoylphorbol Acetate 87-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 202-207 15479821-9 2004 Our present study demonstrates for the first time that either p38 or c-myc siRNA can efficiently inhibit TPA-induced EBV reactivation in GT38 cells, indicating that p38- and/or c-myc-associated signaling pathways may play critical roles in the disruption of EBV latency by TPA. Tetradecanoylphorbol Acetate 105-108 MYC proto-oncogene, bHLH transcription factor Homo sapiens 177-182 15479821-2 2004 In this study, we found that TPA up-regulated phosphorylation of p38, a mitogen-activated protein kinase, and activated c-myc mRNA in EBV-positive epithelial GT38 cells. Tetradecanoylphorbol Acetate 29-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 120-125 15479821-6 2004 Pretreatment of GT38 cells with the nitric oxide (NO) donor S-nitroso-N-acetylpenicillamine inhibited p38 phosphorylation and c-Myc activation by TPA, suggesting that NO may inhibit EBV reactivation via both p38 and c-Myc. Tetradecanoylphorbol Acetate 146-149 MYC proto-oncogene, bHLH transcription factor Homo sapiens 126-131 15479821-9 2004 Our present study demonstrates for the first time that either p38 or c-myc siRNA can efficiently inhibit TPA-induced EBV reactivation in GT38 cells, indicating that p38- and/or c-myc-associated signaling pathways may play critical roles in the disruption of EBV latency by TPA. Tetradecanoylphorbol Acetate 105-108 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-74 12910377-7 2003 In vitro, terminal differentiation towards a megakaryocyte-like phenotype could be induced by phorbol myristate acetate (PMA), with typical morphological features, upregulation of platelet-specific and downregulation of erythroid antigens, going along with downregulation of c-myc. Tetradecanoylphorbol Acetate 94-119 MYC proto-oncogene, bHLH transcription factor Homo sapiens 275-280 12910377-7 2003 In vitro, terminal differentiation towards a megakaryocyte-like phenotype could be induced by phorbol myristate acetate (PMA), with typical morphological features, upregulation of platelet-specific and downregulation of erythroid antigens, going along with downregulation of c-myc. Tetradecanoylphorbol Acetate 121-124 MYC proto-oncogene, bHLH transcription factor Homo sapiens 275-280 12091391-5 2002 When expression of c-myc was reduced in human promyelocytic leukemia HL60 cells by phorbol 12-myristate 13-acetate, the expression of mina53 mRNA and protein was reduced. Tetradecanoylphorbol Acetate 83-114 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-24 12688321-3 2003 Pretreatment with phorbol 12-myristate 13-acetate (PMA), an activator of PKC, prevented TNF-alpha-induced rapid onset of apoptosis, which occurs at 3 h culture with TNF-alpha, concomitantly with the up-regulation of c-Myc protein expression. Tetradecanoylphorbol Acetate 18-49 MYC proto-oncogene, bHLH transcription factor Homo sapiens 216-221 12688321-3 2003 Pretreatment with phorbol 12-myristate 13-acetate (PMA), an activator of PKC, prevented TNF-alpha-induced rapid onset of apoptosis, which occurs at 3 h culture with TNF-alpha, concomitantly with the up-regulation of c-Myc protein expression. Tetradecanoylphorbol Acetate 51-54 MYC proto-oncogene, bHLH transcription factor Homo sapiens 216-221 12688321-7 2003 Up-regulation of c-Myc protein evoked by pretreatment with PMA for a short time could disturb the signaling pathway of the ceramide and sphingosine, which are known to function as the endogenous modulators mediating the apoptotic signal of TNF-alpha. Tetradecanoylphorbol Acetate 59-62 MYC proto-oncogene, bHLH transcription factor Homo sapiens 17-22 11710937-6 2001 This study also involves the first investigation of the effects of aging on c-myc expression by 12-O-tetradecanoyl-phorbol-13-acetate treatment. Tetradecanoylphorbol Acetate 96-133 MYC proto-oncogene, bHLH transcription factor Homo sapiens 76-81 12118374-12 2002 Taken together, our data demonstrate that PMA-mediated inhibition of apoptosis is a complex process that is integrated at both the transcriptional and post-transcriptional level and point out to the potential role of Mcl-1, Bcl-x, c-Myc and survivin in this process. Tetradecanoylphorbol Acetate 42-45 MYC proto-oncogene, bHLH transcription factor Homo sapiens 231-236 10849366-8 2000 The levels of c-Myc and Mad1 mRNAs and proteins increased within 3 h of anti-mu stimulation, and the levels were further enhanced by TPA. Tetradecanoylphorbol Acetate 133-136 MYC proto-oncogene, bHLH transcription factor Homo sapiens 14-19 10931849-5 2000 TPA-induced differentiation of K562 cells causes rapid down-regulation of c-myc expression, due in part to an mRNA decay rate that is 4-fold faster compared with dividing cells. Tetradecanoylphorbol Acetate 0-3 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-79 10931849-6 2000 A cell-free mRNA decay system reconstitutes TPA-induced destabilization of c-myc mRNA, but it requires at least two components for reconstitution. Tetradecanoylphorbol Acetate 44-47 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-80 10918054-1 2000 Treatment of human promyelocytic leukemia cells (HL-60) with phorbol 12-myristate 13-acetate (PMA) is known to decrease c-myc mRNA by blocking transcription elongation at sites near the first exon/intron border. Tetradecanoylphorbol Acetate 61-92 MYC proto-oncogene, bHLH transcription factor Homo sapiens 120-125 10918054-1 2000 Treatment of human promyelocytic leukemia cells (HL-60) with phorbol 12-myristate 13-acetate (PMA) is known to decrease c-myc mRNA by blocking transcription elongation at sites near the first exon/intron border. Tetradecanoylphorbol Acetate 94-97 MYC proto-oncogene, bHLH transcription factor Homo sapiens 120-125 10918054-4 2000 Treatment with PMA or bryostatin 1 increased nuclear protein binding to MIE1, a c-myc intron 1 element that defines an RFX1-binding X box. Tetradecanoylphorbol Acetate 15-18 MYC proto-oncogene, bHLH transcription factor Homo sapiens 80-85 11598794-3 2001 Indeed starved cells undergo apoptosis in the presence of constitutively elevated c-myc expression and the phorbol ester, phorbol 12-miristate 13-acetate (PMA), which rescues cells from apoptosis, induces complete c-myc down-regulation. Tetradecanoylphorbol Acetate 155-158 MYC proto-oncogene, bHLH transcription factor Homo sapiens 214-219 10849366-9 2000 Furthermore, the expressions of both c-Myc and Mad1 were reduced by forskolin, which also inhibited the anti-mu + TPA driven growth and differentiation of the B lymphocytes. Tetradecanoylphorbol Acetate 114-117 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-42 10511314-1 1999 We have studied the regulation and role of c-Myc and Max in the differentiation pathways induced in K562 cells by 12-O-tetradecanoyl phorbol-13 acetate (TPA) and staurosporine, an activator and inhibitor, respectively, of protein kinase C (PKC). Tetradecanoylphorbol Acetate 114-151 MYC proto-oncogene, bHLH transcription factor Homo sapiens 43-48 10511314-4 1999 c-myc expression was down-regulated in K562 differentiated by both TPA and staurosporine, whereas max expression did not change in either case. Tetradecanoylphorbol Acetate 67-70 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 10397677-6 1999 The inhibition of PKC by chelerythrine or its downregulation by phorbol 12-myristate 13-acetate (PMA) inhibited bFGF-induced DNA synthesis and blocked the phosphorylation of MAPK and c-myc expression in response to bFGF. Tetradecanoylphorbol Acetate 64-95 MYC proto-oncogene, bHLH transcription factor Homo sapiens 183-188 10397677-6 1999 The inhibition of PKC by chelerythrine or its downregulation by phorbol 12-myristate 13-acetate (PMA) inhibited bFGF-induced DNA synthesis and blocked the phosphorylation of MAPK and c-myc expression in response to bFGF. Tetradecanoylphorbol Acetate 97-100 MYC proto-oncogene, bHLH transcription factor Homo sapiens 183-188 10339499-2 1999 Constitutive expression of v-Myc blocks phorbol ester (TPA)-induced differentiation of human U-937 monoblasts. Tetradecanoylphorbol Acetate 55-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 29-32 10339499-3 1999 However, costimulation with interferon-gamma (IFN-gamma) and TPA restores terminal differentiation and G1 cell-cycle arrest despite continuous expression of v-Myc. Tetradecanoylphorbol Acetate 61-64 MYC proto-oncogene, bHLH transcription factor Homo sapiens 159-162 10339499-4 1999 The mechanism by which TPA + IFN-gamma counteract v-Myc activity has not been unravelled. Tetradecanoylphorbol Acetate 23-26 MYC proto-oncogene, bHLH transcription factor Homo sapiens 52-55 10339499-5 1999 Our results show that TPA + IFN-gamma treatment led to an inhibition of v-Myc- and c-Myc-dependent transcription, and a specific reduction of v-Myc:Max complexes and associated DNA-binding activity, whereas the steady state level of the v-Myc protein was only marginally affected. Tetradecanoylphorbol Acetate 22-25 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-77 10339499-5 1999 Our results show that TPA + IFN-gamma treatment led to an inhibition of v-Myc- and c-Myc-dependent transcription, and a specific reduction of v-Myc:Max complexes and associated DNA-binding activity, whereas the steady state level of the v-Myc protein was only marginally affected. Tetradecanoylphorbol Acetate 22-25 MYC proto-oncogene, bHLH transcription factor Homo sapiens 83-88 10339499-5 1999 Our results show that TPA + IFN-gamma treatment led to an inhibition of v-Myc- and c-Myc-dependent transcription, and a specific reduction of v-Myc:Max complexes and associated DNA-binding activity, whereas the steady state level of the v-Myc protein was only marginally affected. Tetradecanoylphorbol Acetate 22-25 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-88 10339499-5 1999 Our results show that TPA + IFN-gamma treatment led to an inhibition of v-Myc- and c-Myc-dependent transcription, and a specific reduction of v-Myc:Max complexes and associated DNA-binding activity, whereas the steady state level of the v-Myc protein was only marginally affected. Tetradecanoylphorbol Acetate 22-25 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-88 10339499-8 1999 Phosphatase treatment of Myc:Max complexes lead to their dissociation, thus mimicking the effect of TPA + IFN-gamma. Tetradecanoylphorbol Acetate 100-103 MYC proto-oncogene, bHLH transcription factor Homo sapiens 25-28 9341140-4 1997 Reporter gene assays also demonstrated that gastrin and PMA stimulated Elk-1- and c-Myc-dependent transactivation, consistent with gastrin- and PMA-induced activation of ERKs. Tetradecanoylphorbol Acetate 56-59 MYC proto-oncogene, bHLH transcription factor Homo sapiens 82-87 10319992-0 1999 Overexpression of c-Myc inhibits p21WAF1/CIP1 expression and induces S-phase entry in 12-O-tetradecanoylphorbol-13-acetate (TPA)-sensitive human cancer cells. Tetradecanoylphorbol Acetate 86-122 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23 10319992-0 1999 Overexpression of c-Myc inhibits p21WAF1/CIP1 expression and induces S-phase entry in 12-O-tetradecanoylphorbol-13-acetate (TPA)-sensitive human cancer cells. Tetradecanoylphorbol Acetate 124-127 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23 10319992-5 1999 A time course after infection of TPA-arrested cells using a c-Myc-expressing adenovirus revealed that the inhibition of p21 expression preceded entry into S-phase. Tetradecanoylphorbol Acetate 33-36 MYC proto-oncogene, bHLH transcription factor Homo sapiens 60-65 10027304-11 1999 Overexpression of c-myc was inhibited by TPA and p21waf1/cip1 mRNA increased. Tetradecanoylphorbol Acetate 41-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23 9615391-8 1998 In addition, bryostatin 1 was less effective than PMA in dephosphorylating pRb, modifying E2F complexes, and downregulating c-Myc. Tetradecanoylphorbol Acetate 50-53 MYC proto-oncogene, bHLH transcription factor Homo sapiens 124-129 9615391-9 1998 Co-administration of bryostatin 1 with PMA antagonized the latter"s differentiation-inducing capacity and anti-proliferative effects, actions that were accompanied by a reduction in PMA-mediated p21CIP1/WAF1 induction, CDK2 inhibition, pRb dephosphorylation, and c-Myc downregulation. Tetradecanoylphorbol Acetate 39-42 MYC proto-oncogene, bHLH transcription factor Homo sapiens 263-268 9514905-4 1998 The regulation of the c-myc mRNA by TPA correlated inversely with activation of cell death being down-regulated in LNCaP cells, and slightly increased in the androgen-independent cell lines. Tetradecanoylphorbol Acetate 36-39 MYC proto-oncogene, bHLH transcription factor Homo sapiens 22-27 9341140-4 1997 Reporter gene assays also demonstrated that gastrin and PMA stimulated Elk-1- and c-Myc-dependent transactivation, consistent with gastrin- and PMA-induced activation of ERKs. Tetradecanoylphorbol Acetate 144-147 MYC proto-oncogene, bHLH transcription factor Homo sapiens 82-87 10322942-4 1997 On the other hand, the expression level of c-myc gene in HL-60 cells decreased apparently after the preincubation of TA. Tetradecanoylphorbol Acetate 117-119 MYC proto-oncogene, bHLH transcription factor Homo sapiens 43-48 9378547-7 1997 c-myc can also form transcriptionally active heterodimeric complexes with the nuclear phosphoproteins p20/p22 max: thus, TPA treatment resulted in down-regulation of the p20 form of max in TUR cells. Tetradecanoylphorbol Acetate 121-124 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 9202001-7 1997 This differential substrate specificity of MKP-1 can be functionally extended to nuclear transcriptional events in that PMA-induced c-Jun transcriptional activity was more sensitive to inhibition by MKP-1 than either Elk-1 or c-Myc. Tetradecanoylphorbol Acetate 120-123 MYC proto-oncogene, bHLH transcription factor Homo sapiens 226-231 9301678-5 1997 Expression of the c-myc gene was down-regulated and c-jun and c-fms transcripts increased following exposure to 5-500 nM TPA. Tetradecanoylphorbol Acetate 121-124 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23 9301678-6 1997 In contrast, exposure to 0.5 nM TPA decreased c-myc expression and increased c-jun transcripts only transiently between 4 and 8 h while little if any effect was detectable on c-fms mRNA expression and subsequent differentiation. Tetradecanoylphorbol Acetate 32-35 MYC proto-oncogene, bHLH transcription factor Homo sapiens 46-51 9057647-5 1997 Surprisingly, all RU clones resisted the suppressing effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on c-myc oncogene expression and cell proliferation. Tetradecanoylphorbol Acetate 63-99 MYC proto-oncogene, bHLH transcription factor Homo sapiens 109-114 9057647-5 1997 Surprisingly, all RU clones resisted the suppressing effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on c-myc oncogene expression and cell proliferation. Tetradecanoylphorbol Acetate 101-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 109-114 8870649-4 1996 c-myc, which was induced strongly in response to PMA treatment, was only marginally up-regulated by bryostatin. Tetradecanoylphorbol Acetate 49-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 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 MYC proto-oncogene, bHLH transcription factor Homo sapiens 158-163 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 MYC proto-oncogene, bHLH transcription factor Homo sapiens 158-163 9000576-7 1997 Our findings suggest that induction of p21 and down-regulation of c-myc may be necessary steps in a PMA-induced growth-inhibitory pathway in cancer cells. Tetradecanoylphorbol Acetate 100-103 MYC proto-oncogene, bHLH transcription factor Homo sapiens 66-71 8870649-6 1996 Finally, an anti-sense oligonucleotide blockade of c-myc inhibited PMA-induced proliferation but not the differentiation of BCLL cells, implicating this nuclear oncogene as an important determinant distinguishing PMA from bryostatin-coupled biological responses and also as a candidate third-messenger effector target for the anti-tumour effects of bryostatin. Tetradecanoylphorbol Acetate 67-70 MYC proto-oncogene, bHLH transcription factor Homo sapiens 51-56 7794791-2 1995 HL60 cells are able to differentiate into a granulocytic lineage by prolonged exposure to retinoids and into a macrophage-like lineage by exposure to tumor promoter 12-O-tetradecanoylphorbol 13-acetate, with a rapid decrease of c-myc gene expression. Tetradecanoylphorbol Acetate 165-201 MYC proto-oncogene, bHLH transcription factor Homo sapiens 228-233 8778231-4 1996 Adrenocorticotropin (ACTH) treatment increased c-myc mRNA accumulation dose- and time-dependently up to more than 5-fold (on average), with the maximal effect at 2 h. (Bu)2cAMP and 12-O-tetradecanoyl phorbol 13-acetate (TPA) also induced c-myc gene expression. Tetradecanoylphorbol Acetate 181-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 8778231-4 1996 Adrenocorticotropin (ACTH) treatment increased c-myc mRNA accumulation dose- and time-dependently up to more than 5-fold (on average), with the maximal effect at 2 h. (Bu)2cAMP and 12-O-tetradecanoyl phorbol 13-acetate (TPA) also induced c-myc gene expression. Tetradecanoylphorbol Acetate 220-223 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 8778231-7 1996 H-7 totally abolished ACTH-, TPA- and (Bu)2cAMP-induced c-myc expression, while staurosporine inhibited the stimulatory effects of ACTH and TPA, and HA1004 weakly inhibited the effects of ACTH and (Bu)2cAMP. Tetradecanoylphorbol Acetate 29-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 56-61 7554401-5 1995 Importantly, the levels of mRNA encoding c-myc, IL-2R alpha, IL-2 and IFN-gamma were markedly decreased in patient lymphocytes stimulated with PMA+ionomycin as compared to control lymphocytes. Tetradecanoylphorbol Acetate 143-146 MYC proto-oncogene, bHLH transcription factor Homo sapiens 41-46 7500645-2 1995 Treatment of U-937 cells with 12-O-tetradecanoyl phorbol-13-acetate (TPA) which is associated with the induction of a monocytic differentiation program and growth arrest, revealed an initial up-regulation of c-myc, c-max, and mxi1 mRNAs after 1-6 h. Thereafter expression of these genes significantly declined to barely detectable levels when the cells ceased to grow after 12-24 h of TPA treatment. Tetradecanoylphorbol Acetate 30-67 MYC proto-oncogene, bHLH transcription factor Homo sapiens 208-213 7500645-2 1995 Treatment of U-937 cells with 12-O-tetradecanoyl phorbol-13-acetate (TPA) which is associated with the induction of a monocytic differentiation program and growth arrest, revealed an initial up-regulation of c-myc, c-max, and mxi1 mRNAs after 1-6 h. Thereafter expression of these genes significantly declined to barely detectable levels when the cells ceased to grow after 12-24 h of TPA treatment. Tetradecanoylphorbol Acetate 69-72 MYC proto-oncogene, bHLH transcription factor Homo sapiens 208-213 21043585-6 1995 C-myc expression was turned off by TPA (16 nM) stimulation of cells within 2-4 h. This TPA-mediated effect likely occurred at the transcriptional level since the half life of c-myc mRN A induced by GM-CSF was less than 30 min. Tetradecanoylphorbol Acetate 35-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 175-180 21043585-6 1995 C-myc expression was turned off by TPA (16 nM) stimulation of cells within 2-4 h. This TPA-mediated effect likely occurred at the transcriptional level since the half life of c-myc mRN A induced by GM-CSF was less than 30 min. Tetradecanoylphorbol Acetate 35-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 21043585-6 1995 C-myc expression was turned off by TPA (16 nM) stimulation of cells within 2-4 h. This TPA-mediated effect likely occurred at the transcriptional level since the half life of c-myc mRN A induced by GM-CSF was less than 30 min. Tetradecanoylphorbol Acetate 87-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 21043585-6 1995 C-myc expression was turned off by TPA (16 nM) stimulation of cells within 2-4 h. This TPA-mediated effect likely occurred at the transcriptional level since the half life of c-myc mRN A induced by GM-CSF was less than 30 min. Tetradecanoylphorbol Acetate 87-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 175-180 21043585-10 1995 These studies suggest a link between PKC stimulation by TPA and AP-1 activation with downregulation of c-myc transcription on a molecular level. Tetradecanoylphorbol Acetate 56-59 MYC proto-oncogene, bHLH transcription factor Homo sapiens 103-108 7849624-0 1994 Regulation of cell growth and the c-myc proto-oncogene expression by phorbol ester 12-0-tetradecanoyl phorbol-13-acetate (TPA) in the androgen-independent human prostatic JCA-1 cells. Tetradecanoylphorbol Acetate 122-125 MYC proto-oncogene, bHLH transcription factor Homo sapiens 34-39 7847852-7 1994 Flow immunocytometry revealed reduced levels of c-myc and bcl-2 oncoproteins in RA and PMA treated cells. Tetradecanoylphorbol Acetate 87-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 48-53 8183547-2 1994 Addition of the tumor promoter, phorbol myristate acetate (PMA), prevents apoptotic cell death induced by low serum concentrations in NIH3T3 cells that constitutively express and are transformed by v-myc. Tetradecanoylphorbol Acetate 32-57 MYC proto-oncogene, bHLH transcription factor Homo sapiens 200-203 7849624-4 1994 Following a 24h, 48h, and 72h treatment, with 16 nM TPA, c-myc mRNA was suppressed by 91%, 83%, and 78%, respectively, in good agreement with the extent of growth reduction observed. Tetradecanoylphorbol Acetate 52-55 MYC proto-oncogene, bHLH transcription factor Homo sapiens 57-62 7849624-5 1994 At the low dose of TPA (0.16 nM), however, the c-myc mRNA expression remained inhibited by 85% even though cell growth was only reduced by 10-14%. Tetradecanoylphorbol Acetate 19-22 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 7694866-10 1993 Treatment with tetradecanoyl phorbol acetate (TPA), a potent activator of protein kinase C (PKC), in combination with IL-7 induced a level of c-myc expression greater than that elicited by either factor alone, suggesting that TPA and IL-7 utilize cooperative signaling pathways to increase c-myc gene expression. Tetradecanoylphorbol Acetate 15-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 142-147 7841543-6 1994 A time course study showed that both hKLK2 and c-myc mRNAs were repressed by TPA as early as four hours. Tetradecanoylphorbol Acetate 77-80 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 9397949-6 1994 In addition to estrogen, epidermal growth factor (EGF) and tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) can also induce c-myc expression with no effect on c-fos or lactoferrin expression. Tetradecanoylphorbol Acetate 74-110 MYC proto-oncogene, bHLH transcription factor Homo sapiens 133-138 9397949-6 1994 In addition to estrogen, epidermal growth factor (EGF) and tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) can also induce c-myc expression with no effect on c-fos or lactoferrin expression. Tetradecanoylphorbol Acetate 112-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 133-138 7864662-8 1994 Treatment with 10 nM TPA, which also induces keratinocyte differentiation, reduced c-myc RNA levels to 70% of control levels during the first 4 h, but thereafter c-myc levels remained approximately constant for a further 20 h. TGF beta (2 ng/ml), which inhibits keratinocyte growth without inducing differentiation, did not alter c-myc RNA levels over a 4-day period. Tetradecanoylphorbol Acetate 21-24 MYC proto-oncogene, bHLH transcription factor Homo sapiens 83-88 7864662-8 1994 Treatment with 10 nM TPA, which also induces keratinocyte differentiation, reduced c-myc RNA levels to 70% of control levels during the first 4 h, but thereafter c-myc levels remained approximately constant for a further 20 h. TGF beta (2 ng/ml), which inhibits keratinocyte growth without inducing differentiation, did not alter c-myc RNA levels over a 4-day period. Tetradecanoylphorbol Acetate 21-24 MYC proto-oncogene, bHLH transcription factor Homo sapiens 162-167 7864662-8 1994 Treatment with 10 nM TPA, which also induces keratinocyte differentiation, reduced c-myc RNA levels to 70% of control levels during the first 4 h, but thereafter c-myc levels remained approximately constant for a further 20 h. TGF beta (2 ng/ml), which inhibits keratinocyte growth without inducing differentiation, did not alter c-myc RNA levels over a 4-day period. Tetradecanoylphorbol Acetate 21-24 MYC proto-oncogene, bHLH transcription factor Homo sapiens 162-167 7694866-10 1993 Treatment with tetradecanoyl phorbol acetate (TPA), a potent activator of protein kinase C (PKC), in combination with IL-7 induced a level of c-myc expression greater than that elicited by either factor alone, suggesting that TPA and IL-7 utilize cooperative signaling pathways to increase c-myc gene expression. Tetradecanoylphorbol Acetate 15-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 290-295 7694866-10 1993 Treatment with tetradecanoyl phorbol acetate (TPA), a potent activator of protein kinase C (PKC), in combination with IL-7 induced a level of c-myc expression greater than that elicited by either factor alone, suggesting that TPA and IL-7 utilize cooperative signaling pathways to increase c-myc gene expression. Tetradecanoylphorbol Acetate 46-49 MYC proto-oncogene, bHLH transcription factor Homo sapiens 142-147 7694866-10 1993 Treatment with tetradecanoyl phorbol acetate (TPA), a potent activator of protein kinase C (PKC), in combination with IL-7 induced a level of c-myc expression greater than that elicited by either factor alone, suggesting that TPA and IL-7 utilize cooperative signaling pathways to increase c-myc gene expression. Tetradecanoylphorbol Acetate 46-49 MYC proto-oncogene, bHLH transcription factor Homo sapiens 290-295 8231250-5 1993 In contrast, c-myc expression decreased when cells underwent terminal differentiation, either along the myelomonocytic (by 12-O-tetradecanoylphorbol-13-acetate) or erythroid (by 1-beta-D-arabinofuranosylcytosine) lineages. Tetradecanoylphorbol Acetate 123-159 MYC proto-oncogene, bHLH transcription factor Homo sapiens 13-18 8352523-3 1993 The results showed that TPA down-modulated the constitutive expression of c-myc, c-myb, and c-fms, mRNA to low but still detectable levels. Tetradecanoylphorbol Acetate 24-27 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-79 8518229-2 1993 Expression of the endogenous c-myc gene has now been monitored during the differentiation, and associated loss of proliferation, of ML-1 human myeloblastic leukemia cells: c-myc mRNA remains detectable, at decreased levels, during differentiation along the monocyte/macrophage pathway induced with 12-O-tetradecanoylphorbol-13-acetate. Tetradecanoylphorbol Acetate 298-334 MYC proto-oncogene, bHLH transcription factor Homo sapiens 29-34 8100719-4 1993 When stimulated with anti-CD3 and phorbol 12-myristate 13-acetate, purified patient CD8+ T cells exhibited significantly decreased proliferation, c-myc expression, and interleukin-2 (IL-2) production compared with that of normal CD8+ T cells. Tetradecanoylphorbol Acetate 34-65 MYC proto-oncogene, bHLH transcription factor Homo sapiens 146-151 8518229-6 1993 These findings suggest that, during the 12-O-tetradecanoylphorbol-13-acetate-induced differentiation and loss of proliferation of ML-1 cells, c-myc protein is regulated through alterations that affect its cytoplasmic/nuclear distribution rather than its total cellular content. Tetradecanoylphorbol Acetate 40-76 MYC proto-oncogene, bHLH transcription factor Homo sapiens 142-147 1450490-4 1992 Thus, treatment of cells with TPA results in a reduction in the levels of c-myb and c-myc mRNA, while the expression of c-fos, c-jun, and junB is greatly enhanced. Tetradecanoylphorbol Acetate 30-33 MYC proto-oncogene, bHLH transcription factor Homo sapiens 84-89 1501891-3 1992 In addition, constitutive expression of exogenous myc inhibited induced differentiation of these cells by a variety of treatments including addition to the medium of lipopolysaccharide (LPS) or the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA) as well as complete withdrawal of serum from the medium. Tetradecanoylphorbol Acetate 212-249 MYC proto-oncogene, bHLH transcription factor Homo sapiens 50-53 1501891-3 1992 In addition, constitutive expression of exogenous myc inhibited induced differentiation of these cells by a variety of treatments including addition to the medium of lipopolysaccharide (LPS) or the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA) as well as complete withdrawal of serum from the medium. Tetradecanoylphorbol Acetate 251-254 MYC proto-oncogene, bHLH transcription factor Homo sapiens 50-53 1639858-5 1992 The c-myc proto-oncogene, known to have a high constitutive expression in actively proliferating cells, was strongly downregulated by TPA, but calcium had no effect over a 32 hour period, consistent with the greater growth inhibition of TPA in this system. Tetradecanoylphorbol Acetate 134-137 MYC proto-oncogene, bHLH transcription factor Homo sapiens 4-9 1639858-5 1992 The c-myc proto-oncogene, known to have a high constitutive expression in actively proliferating cells, was strongly downregulated by TPA, but calcium had no effect over a 32 hour period, consistent with the greater growth inhibition of TPA in this system. Tetradecanoylphorbol Acetate 237-240 MYC proto-oncogene, bHLH transcription factor Homo sapiens 4-9 8097865-4 1993 In contrast, TPA treatment inhibited the expression of c-myc mRNA. Tetradecanoylphorbol Acetate 13-16 MYC proto-oncogene, bHLH transcription factor Homo sapiens 55-60 1472905-3 1992 This report describes the sequential changes in the expression of four proto-oncogenes, c-fos, c-myc, c-sis and H-ras in DMEC following PMA exposure. Tetradecanoylphorbol Acetate 136-139 MYC proto-oncogene, bHLH transcription factor Homo sapiens 95-100 1506773-10 1992 The down-regulation of the differentiation-related oncogenes c-myc and c-myb was the same in cells treated with TPA in the presence or absence of glucocorticoids. Tetradecanoylphorbol Acetate 112-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 61-66 1755845-3 1991 Both thrombin and phorbol-12-myristate-13-acetate (PMA) induced mRNA for the c-myc oncogene; peak levels of expression were found 4-5 h after exposure to either agent. Tetradecanoylphorbol Acetate 18-49 MYC proto-oncogene, bHLH transcription factor Homo sapiens 77-82 1755845-3 1991 Both thrombin and phorbol-12-myristate-13-acetate (PMA) induced mRNA for the c-myc oncogene; peak levels of expression were found 4-5 h after exposure to either agent. Tetradecanoylphorbol Acetate 51-54 MYC proto-oncogene, bHLH transcription factor Homo sapiens 77-82 1743296-2 1991 Previous work has suggested that the activation of protein kinase C by TPA contributes to the decrease in c-myc expression during differentiation of these cells. Tetradecanoylphorbol Acetate 71-74 MYC proto-oncogene, bHLH transcription factor Homo sapiens 106-111 1743296-3 1991 The present studies demonstrate that the decline in c-myc mRNA levels following exposure of HL-60 cells to TPA is preceded by an increase in expression of this gene. Tetradecanoylphorbol Acetate 107-110 MYC proto-oncogene, bHLH transcription factor Homo sapiens 52-57 1774959-8 1991 Augmented TPA dependent vector derived c-myc expression was accompanied by enhanced mitogenesis of the cell line FDMT myc.A1 compared with FDC-P1. Tetradecanoylphorbol Acetate 10-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 39-44 1774959-9 1991 In addition, TPA mediated expression of the transfected c-myc gene in FDMT myc.A1 was accompanied by augmented transcription of c-jun and c-fos in response to TPA. Tetradecanoylphorbol Acetate 13-16 MYC proto-oncogene, bHLH transcription factor Homo sapiens 56-61 1774959-6 1991 However, stable transfection of FDC-P1 with a c-myc expression vector driven by a human methallothionein IIA promoter containing the TPA responsive element (TRE), led to a cell clone, FDMT myc.A1, in which TPA mediated selective transcription of the transfected TRE driven c-myc vector and down-regulated expression of the endogenous c-myc gene. Tetradecanoylphorbol Acetate 206-209 MYC proto-oncogene, bHLH transcription factor Homo sapiens 46-51 2011401-3 1991 In unstimulated proliferating JURKAT cells, high levels of C-MYC, N-RAS, and BCL2 mRNAs were found that diminished rapidly following TPA-induced cessation of growth. Tetradecanoylphorbol Acetate 133-136 MYC proto-oncogene, bHLH transcription factor Homo sapiens 59-64 1774959-9 1991 In addition, TPA mediated expression of the transfected c-myc gene in FDMT myc.A1 was accompanied by augmented transcription of c-jun and c-fos in response to TPA. Tetradecanoylphorbol Acetate 159-162 MYC proto-oncogene, bHLH transcription factor Homo sapiens 56-61 1774959-4 1991 On the other hand, the protein kinase C agonist, TPA, strongly activated c-jun expression but poorly promoted expression (transcription) of c-myc in FDC-P1. Tetradecanoylphorbol Acetate 49-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 140-145 1774959-6 1991 However, stable transfection of FDC-P1 with a c-myc expression vector driven by a human methallothionein IIA promoter containing the TPA responsive element (TRE), led to a cell clone, FDMT myc.A1, in which TPA mediated selective transcription of the transfected TRE driven c-myc vector and down-regulated expression of the endogenous c-myc gene. Tetradecanoylphorbol Acetate 133-136 MYC proto-oncogene, bHLH transcription factor Homo sapiens 46-51 2011401-8 1991 Thus, although C-MYC and BCL2 proto-oncogene expression correlated with proliferation in TPA-treated JURKAT cells, continuous over-expression of even the combination of these oncogenes was insufficient for abrogating the effects of TPA in these leukemic T cells. Tetradecanoylphorbol Acetate 89-92 MYC proto-oncogene, bHLH transcription factor Homo sapiens 15-20 1997162-4 1991 Phorbol myristate acetate reduced expression of c-myc, c-myb, and heat shock protein 70 and enhanced those of macrophage-colony-stimulating factor and c-fms. Tetradecanoylphorbol Acetate 0-25 MYC proto-oncogene, bHLH transcription factor Homo sapiens 48-53 1705899-3 1991 This inhibitor selectively blocks the mRNA expression of the proto-oncogene c-myc in response to the phorbol ester, PMA. Tetradecanoylphorbol Acetate 116-119 MYC proto-oncogene, bHLH transcription factor Homo sapiens 61-81 2278884-4 1990 Both p120 mRNA and c-myc mRNA levels were significantly decreased in 12-O-tetradecanoyl-phorbol-13-acetate-differentiated HL-60 leukemic cells and in confluent normal immortalized human fibroblasts (WSI). Tetradecanoylphorbol Acetate 69-106 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-24 2201557-7 1990 In contrast, after 2 h of exposure to 8 nM PMA, a statistically significant increase (p less than 0.001) in c-myc and beta-actin mRNA expression was observed, whereas FV mRNA expression appeared to be unchanged (p = 0.207). Tetradecanoylphorbol Acetate 43-46 MYC proto-oncogene, bHLH transcription factor Homo sapiens 108-113 2127692-1 1990 We show that in the human T lymphoblastic tumor cell line Molt4 c-myc mRNA and protein expression is down-regulated after exposure to dimethyl sulfoxide, to phorbol myristate acetate, or to the calcium ionophore A23187, which raises the intracellular calcium concentration. Tetradecanoylphorbol Acetate 157-182 MYC proto-oncogene, bHLH transcription factor Homo sapiens 64-69 1688464-0 1990 Platelet-derived growth factor-stimulated c-myc RNA accumulation in MG-63 human osteosarcoma cells is independent of both protein kinase A and protein kinase C. Treatment of quiescent MG-63 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) or platelet-derived growth factor (PDGF) stimulates the rapid accumulation of c-myc RNA. Tetradecanoylphorbol Acetate 201-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 42-47 1688464-8 1990 We had previously shown that PDGF action is not affected by prior treatment of MG-63 cells with TPA, a treatment which desensitizes the c-myc response to TPA. Tetradecanoylphorbol Acetate 154-157 MYC proto-oncogene, bHLH transcription factor Homo sapiens 136-141 2529540-4 1989 Loss of MYC seems to be associated with granulocytic differentiation because the time course of its loss was similar to that of appearance of nitroblue tetrazolium-positive cells, mature granulocytes, and its loss was not observed on differentiation of HL-60 cells into macrophages induced by phorbol 12-myristate 13-acetate or teleocidin. Tetradecanoylphorbol Acetate 293-324 MYC proto-oncogene, bHLH transcription factor Homo sapiens 8-11 2670202-7 1989 In this paper, we show that exposing phorbol ester-sensitive (S) HL-60 cells to TPA caused the disappearance of the c-myc protein antigen (detected on Western blots) in 4 h, whereas TPA had no effect on the c-myc protein content of PET cells. Tetradecanoylphorbol Acetate 80-83 MYC proto-oncogene, bHLH transcription factor Homo sapiens 116-121 2670202-7 1989 In this paper, we show that exposing phorbol ester-sensitive (S) HL-60 cells to TPA caused the disappearance of the c-myc protein antigen (detected on Western blots) in 4 h, whereas TPA had no effect on the c-myc protein content of PET cells. Tetradecanoylphorbol Acetate 80-83 MYC proto-oncogene, bHLH transcription factor Homo sapiens 207-212 2670202-11 1989 TPA induced the down-regulation of c-myc mRNA in S cells to a greater extent than in PET cells. Tetradecanoylphorbol Acetate 0-3 MYC proto-oncogene, bHLH transcription factor Homo sapiens 35-40 2558432-6 1989 In addition, EGF, insulin, and TPA, like hCG, elevated mRNA levels of competence oncogenes (c-fos and c-myc), albeit to different extents. Tetradecanoylphorbol Acetate 31-34 MYC proto-oncogene, bHLH transcription factor Homo sapiens 102-107 2551669-2 1989 Here we demonstrate that the normal c-myc allele can be induced in BL cells by 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 79-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 36-41 2551669-2 1989 Here we demonstrate that the normal c-myc allele can be induced in BL cells by 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 117-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 36-41 2551669-3 1989 TPA did activate the normal c-myc alleles in Raji(P207), BL36, P3HR1, Jijoye and LY91 cells, but not in Raji(DE88), BL41, BL67, LY47 and KK124 cells. Tetradecanoylphorbol Acetate 0-3 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 2551669-4 1989 C-myc RNA derived from the normal allele appeared 6 h after treatment with TPA and showed the characteristic preferential usage of the second promoter. Tetradecanoylphorbol Acetate 75-78 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 2551669-8 1989 Expression of the translocated c-myc alleles was also affected by TPA; however, only if cycloheximide was simultaneously present. Tetradecanoylphorbol Acetate 66-69 MYC proto-oncogene, bHLH transcription factor Homo sapiens 31-36 2551669-9 1989 TPA plus cycloheximide induced a rapid decrease of c-myc RNA derived from the translocated allele within 6 h, whereas cycloheximide alone led to abolition of c-myc RNA after 16-24 h. This rapid decline of c-myc RNA was observed in Raji and BL41 cells, but not in three cell lines with variant t(2;8) and t(8;22) translocations. Tetradecanoylphorbol Acetate 0-3 MYC proto-oncogene, bHLH transcription factor Homo sapiens 51-56 2551669-9 1989 TPA plus cycloheximide induced a rapid decrease of c-myc RNA derived from the translocated allele within 6 h, whereas cycloheximide alone led to abolition of c-myc RNA after 16-24 h. This rapid decline of c-myc RNA was observed in Raji and BL41 cells, but not in three cell lines with variant t(2;8) and t(8;22) translocations. Tetradecanoylphorbol Acetate 0-3 MYC proto-oncogene, bHLH transcription factor Homo sapiens 158-163 2551669-9 1989 TPA plus cycloheximide induced a rapid decrease of c-myc RNA derived from the translocated allele within 6 h, whereas cycloheximide alone led to abolition of c-myc RNA after 16-24 h. This rapid decline of c-myc RNA was observed in Raji and BL41 cells, but not in three cell lines with variant t(2;8) and t(8;22) translocations. Tetradecanoylphorbol Acetate 0-3 MYC proto-oncogene, bHLH transcription factor Homo sapiens 158-163 2463169-1 1988 An extracellular signal, such as phorbol-12-myristate-13-acetate (PMA), was found to reduce the c-myc expression in Burkitt lymphoma (BL) cells but augment the expression of the same gene in a B-lymphoblastoid cell line (B-LCL). Tetradecanoylphorbol Acetate 33-64 MYC proto-oncogene, bHLH transcription factor Homo sapiens 96-101 2467914-3 1988 Both interferons and TPA down-regulate expression of the c-myc oncogene in these cells. Tetradecanoylphorbol Acetate 21-24 MYC proto-oncogene, bHLH transcription factor Homo sapiens 57-62 2467914-7 1988 This agent induces a higher level of c-myc mRNA in the cells and stimulates the incorporation of [3H]thymidine into DNA; although these effects are partially counteracted by interferon or TPA treatment, the elevated expression of the c-myc gene may be sufficient to prevent terminal differentiation and allow cell proliferation to continue. Tetradecanoylphorbol Acetate 188-191 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-42 2467914-7 1988 This agent induces a higher level of c-myc mRNA in the cells and stimulates the incorporation of [3H]thymidine into DNA; although these effects are partially counteracted by interferon or TPA treatment, the elevated expression of the c-myc gene may be sufficient to prevent terminal differentiation and allow cell proliferation to continue. Tetradecanoylphorbol Acetate 188-191 MYC proto-oncogene, bHLH transcription factor Homo sapiens 234-239 2463169-1 1988 An extracellular signal, such as phorbol-12-myristate-13-acetate (PMA), was found to reduce the c-myc expression in Burkitt lymphoma (BL) cells but augment the expression of the same gene in a B-lymphoblastoid cell line (B-LCL). Tetradecanoylphorbol Acetate 66-69 MYC proto-oncogene, bHLH transcription factor Homo sapiens 96-101 3053165-4 1988 These two pathways, which can be activated by phorbol myristate acetate (PMA) and ionomycin respectively, appear to play complementary roles in the transcriptional induction of c-myc gene expression by the antigen receptor complex. Tetradecanoylphorbol Acetate 46-71 MYC proto-oncogene, bHLH transcription factor Homo sapiens 177-182 3169138-1 1988 The induction of differentiation in SH-SY5Y human neuroblastoma cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is accompanied by a rapid and a transient expression of c-fos mRNA and a down-regulation of c-myc mRNA. Tetradecanoylphorbol Acetate 75-111 MYC proto-oncogene, bHLH transcription factor Homo sapiens 210-215 3169138-1 1988 The induction of differentiation in SH-SY5Y human neuroblastoma cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is accompanied by a rapid and a transient expression of c-fos mRNA and a down-regulation of c-myc mRNA. Tetradecanoylphorbol Acetate 113-116 MYC proto-oncogene, bHLH transcription factor Homo sapiens 210-215 3053165-4 1988 These two pathways, which can be activated by phorbol myristate acetate (PMA) and ionomycin respectively, appear to play complementary roles in the transcriptional induction of c-myc gene expression by the antigen receptor complex. Tetradecanoylphorbol Acetate 73-76 MYC proto-oncogene, bHLH transcription factor Homo sapiens 177-182 3422230-1 1988 Treatment of human promyelocytic leukemia cells (HL-60) with phorbol 12-myristate 13-acetate or phorbol 12,13-dibutyrate (PDBu) caused a rapid decrease in transcription of the c-myc protooncogene. Tetradecanoylphorbol Acetate 61-92 MYC proto-oncogene, bHLH transcription factor Homo sapiens 176-181 3152600-8 1988 The extent and kinetics of c-myc oncoprotein induction have been determined following phorbol ester, 12-O tetradecanoylphorbol 13 acetate (TPA) and interferon-gamma (IFN-gamma) exposure of both HL-60 and Daudi cells. Tetradecanoylphorbol Acetate 101-137 MYC proto-oncogene, bHLH transcription factor Homo sapiens 27-32 3152600-8 1988 The extent and kinetics of c-myc oncoprotein induction have been determined following phorbol ester, 12-O tetradecanoylphorbol 13 acetate (TPA) and interferon-gamma (IFN-gamma) exposure of both HL-60 and Daudi cells. Tetradecanoylphorbol Acetate 139-142 MYC proto-oncogene, bHLH transcription factor Homo sapiens 27-32 3152600-9 1988 TPA produced a gradual reduction in the level of c-myc protein and arrested the cells in G0/G1 phase in HL-60 cells. Tetradecanoylphorbol Acetate 0-3 MYC proto-oncogene, bHLH transcription factor Homo sapiens 49-54 2449430-3 1988 Treatment of quiescent cells with 12-O-tetradecanoyl phorbol-13-acetate (TPA) to down-regulate protein kinase C inhibited TPA-stimulated c-myc expression but did not affect the PDGF-modulated process. Tetradecanoylphorbol Acetate 34-71 MYC proto-oncogene, bHLH transcription factor Homo sapiens 137-142 2449430-3 1988 Treatment of quiescent cells with 12-O-tetradecanoyl phorbol-13-acetate (TPA) to down-regulate protein kinase C inhibited TPA-stimulated c-myc expression but did not affect the PDGF-modulated process. Tetradecanoylphorbol Acetate 73-76 MYC proto-oncogene, bHLH transcription factor Homo sapiens 137-142 2449430-3 1988 Treatment of quiescent cells with 12-O-tetradecanoyl phorbol-13-acetate (TPA) to down-regulate protein kinase C inhibited TPA-stimulated c-myc expression but did not affect the PDGF-modulated process. Tetradecanoylphorbol Acetate 122-125 MYC proto-oncogene, bHLH transcription factor Homo sapiens 137-142 3127645-4 1988 The tumor promoter tetradecanoyl phorbol acetate (TPA) was found to selectively induce the transcription of c-myc without observable effect on the transcription of the other oncogenes studied, and without inducing cell division. Tetradecanoylphorbol Acetate 19-48 MYC proto-oncogene, bHLH transcription factor Homo sapiens 108-113 3257396-13 1988 Taken together these results and previous work on the induction of the protooncogene c-myc and c-fos suggest that this B-CLL clone represents GO cells that undergo differentiation without concomitant proliferation when exposed to TPA. Tetradecanoylphorbol Acetate 230-233 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-90 3127645-4 1988 The tumor promoter tetradecanoyl phorbol acetate (TPA) was found to selectively induce the transcription of c-myc without observable effect on the transcription of the other oncogenes studied, and without inducing cell division. Tetradecanoylphorbol Acetate 50-53 MYC proto-oncogene, bHLH transcription factor Homo sapiens 108-113 2948635-5 1987 Nuclear run-on assays showed that E1 transcription, as well as transcription of c-fos, c-myc, and beta-actin was stimulated in 293 cells within 30 min of TPA exposure and returned to basal levels by 60 min. Tetradecanoylphorbol Acetate 154-157 MYC proto-oncogene, bHLH transcription factor Homo sapiens 87-92 3115797-3 1987 The phorbol ester TPA and the adenylate cyclase activator forskolin reduced the c-myc RNA, levels and after 3 days of treatment a proportion of the cells accumulated in G1. Tetradecanoylphorbol Acetate 18-21 MYC proto-oncogene, bHLH transcription factor Homo sapiens 80-85 3495533-2 1987 PMA, carbachol, and EGF all stimulated rapid accumulation of mRNA for the proto-oncogenes c-fos and c-myc in the normal cells; in the protein kinase C-deficient cells, carbachol and EGF, but not PMA, retained this effect, which was not mimicked by the calcium ionophore A23187. Tetradecanoylphorbol Acetate 0-3 MYC proto-oncogene, bHLH transcription factor Homo sapiens 100-105 3306603-5 1987 In contrast, c-myc mRNA expression is both in TPA- and DMSO-induced differentiation reduced to less then 5% of its initial level within 4h. Tetradecanoylphorbol Acetate 46-49 MYC proto-oncogene, bHLH transcription factor Homo sapiens 13-18 3306603-6 1987 Nuclear run-on analysis revealed that the reduction of c-myc-mRNA expression during both TPA- and DMSO-induced differentiation could be ascribed to the abolition of transcription of the third exon, whereas no change in the transcription of the first exon could be observed. Tetradecanoylphorbol Acetate 89-92 MYC proto-oncogene, bHLH transcription factor Homo sapiens 55-60 3597558-0 1987 Differential induction of transcription of c-myc and c-fos proto-oncogenes by 12-O-tetradecanoylphorbol-13-acetate in mortal and immortal human urothelial cells. Tetradecanoylphorbol Acetate 78-114 MYC proto-oncogene, bHLH transcription factor Homo sapiens 43-48 3597558-2 1987 A single treatment with TPA (1 microgram/ml) increased the transcription of c-fos and c-myc proto-oncogenes at least 20-fold in the mortal cell line HU 1752. Tetradecanoylphorbol Acetate 24-27 MYC proto-oncogene, bHLH transcription factor Homo sapiens 86-91 3597558-4 1987 When immortalized cell lines were treated with TPA a similar rapid and transient morphological response was observed, but the TPA treatment only increased the level of c-fos mRNA, suggesting that the normal regulation of c-myc transcription is altered in immortalized cells irrespective of their tumorigenic properties. Tetradecanoylphorbol Acetate 47-50 MYC proto-oncogene, bHLH transcription factor Homo sapiens 221-226 3597558-4 1987 When immortalized cell lines were treated with TPA a similar rapid and transient morphological response was observed, but the TPA treatment only increased the level of c-fos mRNA, suggesting that the normal regulation of c-myc transcription is altered in immortalized cells irrespective of their tumorigenic properties. Tetradecanoylphorbol Acetate 126-129 MYC proto-oncogene, bHLH transcription factor Homo sapiens 221-226 3495445-5 1987 Stimulation of B lymphocytes with TPA plus ionomycin resulted in increased magnitude and a shift in the kinetics of c-fos and c-myc expression compared with either agent used alone. Tetradecanoylphorbol Acetate 34-37 MYC proto-oncogene, bHLH transcription factor Homo sapiens 126-131 3022291-7 1986 Serum and the phorbol ester tumor promoter phorbol 12-myristate 13-acetate also enhanced c-myc expression in cardiac myocyte cultures. Tetradecanoylphorbol Acetate 43-74 MYC proto-oncogene, bHLH transcription factor Homo sapiens 89-94 3099293-5 1987 The expression of MYC and FOS was rapidly induced by the phorbol 12-myristate 13-acetate treatment. Tetradecanoylphorbol Acetate 57-88 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-21 3159569-8 1985 We observed strong induction of c-fos and to a lesser extent of c-myc also by TPA, and by the calcium ionophore A23187, indicating an important role for kinase C in proto-oncogene activation by growth factors. Tetradecanoylphorbol Acetate 78-81 MYC proto-oncogene, bHLH transcription factor Homo sapiens 64-69 3948318-1 1986 The effect of a single treatment with the skin tumor-promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) on the expression of the cellular proto-oncogenes, c-myc, c-rasHa, c-rasKi and c-fos was examined in the non-tumorigenic human bladder epithelial cell line HCV 29. Tetradecanoylphorbol Acetate 62-98 MYC proto-oncogene, bHLH transcription factor Homo sapiens 156-161 3096504-1 1986 After stimulation of human lymphocytes by 12-0 tetradecanoyl phorbol acetate (TPA) and by the calcium ionophore A23187 an early transient expression of proto-oncogene fos followed by an expression of c-myc is observed, as has been described in rodent fibroblast stimulated by growth factors. Tetradecanoylphorbol Acetate 78-81 MYC proto-oncogene, bHLH transcription factor Homo sapiens 200-205 3933820-3 1985 It is shown in the present study that treatments of the myeloid leukemia HL60 cells with various inducers of cell differentiation (dimethyl sulfoxide, retinoic acid, mezerein, 12-O-tetradecanoylphorbol-13-acetate, teleocidin) caused a dose-dependent reduction of the level of TaDNA transcripts, correlated with the diminution of c-myc transcripts. Tetradecanoylphorbol Acetate 176-212 MYC proto-oncogene, bHLH transcription factor Homo sapiens 329-334 2578312-3 1985 Five days after the addition of either 180 mM dimethyl sulfoxide or 60 nM 12-O-tetradecanoylphorbol-13-acetate to HL-60 cultures, transcription of the c-myc gene was markedly reduced when compared with control cultures. Tetradecanoylphorbol Acetate 74-110 MYC proto-oncogene, bHLH transcription factor Homo sapiens 151-156 3855302-4 1985 We found that the phorbol esters, 12-O-tetradecanoyl phorbol 13-acetate and phorbol 12,13-dibutyrate 1) altered the morphology of the TT cells towards that of high-calcitonin-containing cells; 2) enhanced calcitonin secretion 7-fold; 3) increased calcitonin production at the transcriptional level by 2-fold; 4) inhibited cellular proliferation; and 5) decreased, by 80%, the levels of the c-myc gene mRNA. Tetradecanoylphorbol Acetate 34-71 MYC proto-oncogene, bHLH transcription factor Homo sapiens 390-395