PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
6284358-10	1982	EGF receptors are clearly not necessary for TPA promotion of anchorage independence in JB6 cells but may mediate mitogenic stimulation of these cells by TPA.	Tetradecanoylphorbol Acetate	153-156	epidermal growth factor	Homo sapiens	0-3	
11272120-7	1980	Taken together, our results suggest that TPA inhibition of EGF-receptor binding results from TPA-induced changes in the membrane microenvironment of EGF receptors.	Tetradecanoylphorbol Acetate	41-44	epidermal growth factor	Homo sapiens	59-62	
6259217-5	1981	Like EGF, the potent phorbol ester 12-O-tetradecanoyl-13-phorbol acetate (TPA) stimulates protein synthesis as indicated by a twofold increase in [(3)H]leucine incorporation into protein after 24 h in TPA.	Tetradecanoylphorbol Acetate	74-77	epidermal growth factor	Homo sapiens	5-8	
6259217-9	1981	Furthermore, TPA inhibits cell division in media with or without serum, and prevents growth stimulation by EGF.	Tetradecanoylphorbol Acetate	13-16	epidermal growth factor	Homo sapiens	107-110	
6265908-3	1981	12-O-Tetradecanoylphorbol 13-acetate also produced an increase in enzyme activity in these cells and exhibited an additive effect with EGF.	Tetradecanoylphorbol Acetate	0-36	epidermal growth factor	Homo sapiens	135-138	
11272120-1	1980	This study analyzes the mechanism by which the tumor promoter 12-0-tetradecanoyl-phorbol 13-acetate (TPA) inhibits binding of epidermal growth factor (EGF) to its membrane receptors in HeLa cells.	Tetradecanoylphorbol Acetate	101-104	epidermal growth factor	Homo sapiens	126-149	
11272120-1	1980	This study analyzes the mechanism by which the tumor promoter 12-0-tetradecanoyl-phorbol 13-acetate (TPA) inhibits binding of epidermal growth factor (EGF) to its membrane receptors in HeLa cells.	Tetradecanoylphorbol Acetate	101-104	epidermal growth factor	Homo sapiens	151-154	
11272120-2	1980	Kinetic studies indicate that inhibition of EGF binding occurs within a few minutes after exposure of cells to TPA; delayed addition of TPA causes a reduction in previously bound EGF.	Tetradecanoylphorbol Acetate	111-114	epidermal growth factor	Homo sapiens	44-47	
11272120-2	1980	Kinetic studies indicate that inhibition of EGF binding occurs within a few minutes after exposure of cells to TPA; delayed addition of TPA causes a reduction in previously bound EGF.	Tetradecanoylphorbol Acetate	136-139	epidermal growth factor	Homo sapiens	179-182	
11272120-3	1980	With prolonged exposure to TPA, the cells become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	27-30	epidermal growth factor	Homo sapiens	81-84	
11272120-7	1980	Taken together, our results suggest that TPA inhibition of EGF-receptor binding results from TPA-induced changes in the membrane microenvironment of EGF receptors.	Tetradecanoylphorbol Acetate	41-44	epidermal growth factor	Homo sapiens	149-152	
11272120-3	1980	With prolonged exposure to TPA, the cells become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	63-66	epidermal growth factor	Homo sapiens	81-84	
11272120-4	1980	Evidence was obtained that TPA acts by causing the dissociation of EGF-receptor complexes present on the cell surface and not by increasing the proteolytic degradation or internalization of EGF.	Tetradecanoylphorbol Acetate	27-30	epidermal growth factor	Homo sapiens	67-70	
11272120-5	1980	Evidence that the TPA inhibition of EGF-receptor binding is not a direct consequence of TPA binding to the "active site" of EGF receptors was obtained by the differential effects of pH, temperature or exposure time and that TPA does not inhibit EGF binding when added to isolated plasma membrane fragments.	Tetradecanoylphorbol Acetate	18-21	epidermal growth factor	Homo sapiens	36-39	
11272120-7	1980	Taken together, our results suggest that TPA inhibition of EGF-receptor binding results from TPA-induced changes in the membrane microenvironment of EGF receptors.	Tetradecanoylphorbol Acetate	93-96	epidermal growth factor	Homo sapiens	59-62	
11272120-6	1980	Studies with a variety of inhibitors suggest that the TPA inhibition of EGF-receptor binding does not require macromolecular synthesis, energy metabolism, or cytoskeletal changes.	Tetradecanoylphorbol Acetate	54-57	epidermal growth factor	Homo sapiens	72-75	
11272120-7	1980	Taken together, our results suggest that TPA inhibition of EGF-receptor binding results from TPA-induced changes in the membrane microenvironment of EGF receptors.	Tetradecanoylphorbol Acetate	93-96	epidermal growth factor	Homo sapiens	149-152	
315558-1	1979	In previous studies we demonstrated that the tumor-promoting agent 12-O-tetradecanoyl phorbol 13-acetate (TPA) and related macrocyclic diterpenes are potent inhibitors of the binding of epidermal growth factor (EGF) to its cell surface receptors in HeLa cells.	Tetradecanoylphorbol Acetate	67-104	epidermal growth factor	Homo sapiens	186-209	
315558-1	1979	In previous studies we demonstrated that the tumor-promoting agent 12-O-tetradecanoyl phorbol 13-acetate (TPA) and related macrocyclic diterpenes are potent inhibitors of the binding of epidermal growth factor (EGF) to its cell surface receptors in HeLa cells.	Tetradecanoylphorbol Acetate	106-109	epidermal growth factor	Homo sapiens	211-214	
315558-4	1979	In HeLa cells TPA inhibits the initial binding of EGF and also accelerates the loss of previously bound EGF from cells.	Tetradecanoylphorbol Acetate	14-17	epidermal growth factor	Homo sapiens	50-53	
315558-1	1979	In previous studies we demonstrated that the tumor-promoting agent 12-O-tetradecanoyl phorbol 13-acetate (TPA) and related macrocyclic diterpenes are potent inhibitors of the binding of epidermal growth factor (EGF) to its cell surface receptors in HeLa cells.	Tetradecanoylphorbol Acetate	67-104	epidermal growth factor	Homo sapiens	211-214	
315558-4	1979	In HeLa cells TPA inhibits the initial binding of EGF and also accelerates the loss of previously bound EGF from cells.	Tetradecanoylphorbol Acetate	14-17	epidermal growth factor	Homo sapiens	104-107	
315558-1	1979	In previous studies we demonstrated that the tumor-promoting agent 12-O-tetradecanoyl phorbol 13-acetate (TPA) and related macrocyclic diterpenes are potent inhibitors of the binding of epidermal growth factor (EGF) to its cell surface receptors in HeLa cells.	Tetradecanoylphorbol Acetate	106-109	epidermal growth factor	Homo sapiens	186-209	
22505246-3	2012	The results showed that TPA- and endothelial growth factor (EGF)-induced anchorage-independent colony formation were suppressed in a dose-dependent manner by treatment of JB6 CI41 mouse skin epidermal cells with juglone (2.5 and 5 microM).	Tetradecanoylphorbol Acetate	24-27	epidermal growth factor	Homo sapiens	60-63	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	4-7	epidermal growth factor	Homo sapiens	18-21	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	4-7	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	4-7	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	4-7	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	18-21	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	18-21	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	18-21	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	18-21	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-6	1979	The TPA effect on EGF receptors is mediated by a highly temperature-dependent process because TPA inhibition of EGF binding, and TPA-induced release of prebound EGF, are much greater at 37 degrees C or 22 degrees C than at 4 degrees C. A curious feature is that when cells are grown in TPA for one or more days they escape or become refractory to TPA inhibition of EGF binding.	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	112-115	
315558-7	1979	Taken together, these results suggest that TPA inhibits EGF binding not by binding directly to the "active site" of the EGF receptor but by indirectly altering the conformation or inducing the clustering of EGF receptors.	Tetradecanoylphorbol Acetate	43-46	epidermal growth factor	Homo sapiens	56-59	
315558-7	1979	Taken together, these results suggest that TPA inhibits EGF binding not by binding directly to the "active site" of the EGF receptor but by indirectly altering the conformation or inducing the clustering of EGF receptors.	Tetradecanoylphorbol Acetate	43-46	epidermal growth factor	Homo sapiens	120-123	
315558-7	1979	Taken together, these results suggest that TPA inhibits EGF binding not by binding directly to the "active site" of the EGF receptor but by indirectly altering the conformation or inducing the clustering of EGF receptors.	Tetradecanoylphorbol Acetate	43-46	epidermal growth factor	Homo sapiens	120-123	
26786102-3	2016	Here we show that androgens (5alpha-dihydrotestosterone and R1881) suppress c-Fos protein and mRNA expression induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) or EGF in human prostate cancer (PCa) cell lines.	Tetradecanoylphorbol Acetate	159-162	epidermal growth factor	Homo sapiens	167-170	
15542774-6	2004	Activation of PKC by phorbol ester (phorbol 12-myristate 13-acetate) enhanced EGF action on ERK1/2 phosphorylation without significantly altering p53 phosphorylation by resveratrol.	Tetradecanoylphorbol Acetate	36-67	epidermal growth factor	Homo sapiens	78-81	
17928641-9	2007	After the addition of EGF to acini incubated previously with phorbol ester TPA, strong decrease in pY-ERK level was also observed.	Tetradecanoylphorbol Acetate	75-78	epidermal growth factor	Homo sapiens	22-25	
17617058-8	2007	In cells, the IGF-1-stimulated phosphorylations, and certain EGF-stimulated phosphorylations, were inhibited by PI3K (phosphoinositide 3-kinase) inhibitors, whereas the RSK inhibitor BI-D1870 inhibited the PMA-induced phosphorylations.	Tetradecanoylphorbol Acetate	206-209	epidermal growth factor	Homo sapiens	61-64	
12801607-7	2003	Furthermore, stimulation of PKC, using short-term 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment, markedly inhibited the stimulatory effects of EGF on Akt phosphorylation.	Tetradecanoylphorbol Acetate	50-86	epidermal growth factor	Homo sapiens	150-153	
12878187-2	2003	Here, we demonstrate that PKC activation via phorbol 12-myristate 13-acetate (PMA) treatment of MDA-MB-231 cells inhibits EGF-induced cell spreading, the initial event of motility and chemotaxis.	Tetradecanoylphorbol Acetate	45-76	epidermal growth factor	Homo sapiens	122-125	
12878187-2	2003	Here, we demonstrate that PKC activation via phorbol 12-myristate 13-acetate (PMA) treatment of MDA-MB-231 cells inhibits EGF-induced cell spreading, the initial event of motility and chemotaxis.	Tetradecanoylphorbol Acetate	78-81	epidermal growth factor	Homo sapiens	122-125	
12801607-7	2003	Furthermore, stimulation of PKC, using short-term 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment, markedly inhibited the stimulatory effects of EGF on Akt phosphorylation.	Tetradecanoylphorbol Acetate	88-91	epidermal growth factor	Homo sapiens	150-153	
9666308-2	1998	In fact, epidermal growth factor was an excellent mitogen, even after prolonged pretreatment of cells with TPA, suggesting that the PKC isoform implicated in proliferation is not down-regulated by 12-O-tetradecanoyl phorbol-13-acetate (TPA).	Tetradecanoylphorbol Acetate	107-110	epidermal growth factor	Homo sapiens	9-32	
11267936-5	2001	Upon differentiation-induction with 12-O-tetradecanoylphorbol-13-acetate (TPA), in TTC549, showing an expression of TGF-alpha but not EGF initially, de novo expression of EGF mRNA appeared abruptly on day 2 of TPA treatment.	Tetradecanoylphorbol Acetate	36-72	epidermal growth factor	Homo sapiens	171-174	
11267936-5	2001	Upon differentiation-induction with 12-O-tetradecanoylphorbol-13-acetate (TPA), in TTC549, showing an expression of TGF-alpha but not EGF initially, de novo expression of EGF mRNA appeared abruptly on day 2 of TPA treatment.	Tetradecanoylphorbol Acetate	74-77	epidermal growth factor	Homo sapiens	134-137	
11267936-5	2001	Upon differentiation-induction with 12-O-tetradecanoylphorbol-13-acetate (TPA), in TTC549, showing an expression of TGF-alpha but not EGF initially, de novo expression of EGF mRNA appeared abruptly on day 2 of TPA treatment.	Tetradecanoylphorbol Acetate	74-77	epidermal growth factor	Homo sapiens	171-174	
11267936-5	2001	Upon differentiation-induction with 12-O-tetradecanoylphorbol-13-acetate (TPA), in TTC549, showing an expression of TGF-alpha but not EGF initially, de novo expression of EGF mRNA appeared abruptly on day 2 of TPA treatment.	Tetradecanoylphorbol Acetate	210-213	epidermal growth factor	Homo sapiens	171-174	
11160957-4	2001	METHODS: The authors assessed endogenous CREB phosphorylation in a CLS fibroblast line by Western blotting and found impaired CREB phosphorylation in response to stimulation by EGF and the protein kinase C (PKC) agonist phorbol 12-myristate 13-acetate (PMA).	Tetradecanoylphorbol Acetate	220-251	epidermal growth factor	Homo sapiens	177-180	
11160957-4	2001	METHODS: The authors assessed endogenous CREB phosphorylation in a CLS fibroblast line by Western blotting and found impaired CREB phosphorylation in response to stimulation by EGF and the protein kinase C (PKC) agonist phorbol 12-myristate 13-acetate (PMA).	Tetradecanoylphorbol Acetate	253-256	epidermal growth factor	Homo sapiens	177-180	
9612280-4	1998	However, TPA-induced alkalosis is not blocked by tyrosine kinase inhibitors; and 3) the stimulatory effect of EGF on the Na(+)-H+ exchanger acts via stimulation of tyrosine kinase-receptor activity because it is inhibited by tyrosine kinase inhibitors (genistein, lavendustin A, and herbimycin A).	Tetradecanoylphorbol Acetate	9-12	epidermal growth factor	Homo sapiens	110-113	
11082532-3	2000	Daunorubicin, as well as sphingomyelinase (SMase) and the exogenous cell-permeable ceramide analogue C(2)-ceramide, inhibited phospholipase D activity stimulated by phorbol 12-myristate 13-acetate or epidermal growth factor (EGF).	Tetradecanoylphorbol Acetate	165-196	epidermal growth factor	Homo sapiens	200-223	
11082532-3	2000	Daunorubicin, as well as sphingomyelinase (SMase) and the exogenous cell-permeable ceramide analogue C(2)-ceramide, inhibited phospholipase D activity stimulated by phorbol 12-myristate 13-acetate or epidermal growth factor (EGF).	Tetradecanoylphorbol Acetate	165-196	epidermal growth factor	Homo sapiens	225-228	
9666308-2	1998	In fact, epidermal growth factor was an excellent mitogen, even after prolonged pretreatment of cells with TPA, suggesting that the PKC isoform implicated in proliferation is not down-regulated by 12-O-tetradecanoyl phorbol-13-acetate (TPA).	Tetradecanoylphorbol Acetate	236-239	epidermal growth factor	Homo sapiens	9-32	
9345355-1	1997	Previous studies from this laboratory have shown that epidermal growth factor (EGF) and the tumor promoter, phorbol myristate acetate (PMA), are mitogenic in the endometrial cancer cell line HEC-1-A.	Tetradecanoylphorbol Acetate	108-133	epidermal growth factor	Homo sapiens	54-77	
9177393-5	1997	The c-jun and c-fos mRNA stimulation elicited by TPA was reduced by the PKC inhibitors, chelerythrine and staurosporine, and could not be mimicked by 4alpha-phorbol 12,13-didecanoate (a phorbol ester that fails to activate PKC), whereas the stimulation induced by EGF was diminished by the PTK inhibitor, genistein.	Tetradecanoylphorbol Acetate	49-52	epidermal growth factor	Homo sapiens	264-267	
9048588-4	1997	On the other hand, epidermal growth factor (EGF), Ca ionophore, the protein kinase C activator 12-O-tetradecanoylphorbol-13-acetate (TPA), and cAMP elevated 17HSD type 1 expression only in JEG-3 cells.	Tetradecanoylphorbol Acetate	133-136	epidermal growth factor	Homo sapiens	19-42	
8912706-0	1996	Phorbol 12-myristate 13-acetate inhibits epidermal growth factor signalling in human keratinocytes, leading to decreased ornithine decarboxylase activity.	Tetradecanoylphorbol Acetate	0-31	epidermal growth factor	Homo sapiens	41-64	
8912706-8	1996	To explore the mechanism whereby PMA interfered with EGF signalling, the effect of PMA on EGF binding to its cell-surface receptor was studied; acute treatment with PMA (within 7 h) decreased EGF binding to 41-57% of the baseline level.	Tetradecanoylphorbol Acetate	33-36	epidermal growth factor	Homo sapiens	53-56	
8912706-12	1996	Additionally, PMA inhibited the induction of ODC by EGF through decreased EGF binding, possibly mediated by PKC activation.	Tetradecanoylphorbol Acetate	14-17	epidermal growth factor	Homo sapiens	52-55	
8912706-12	1996	Additionally, PMA inhibited the induction of ODC by EGF through decreased EGF binding, possibly mediated by PKC activation.	Tetradecanoylphorbol Acetate	14-17	epidermal growth factor	Homo sapiens	74-77	
8913498-0	1996	Translational augmentation of pro-matrix metalloproteinase 3 (prostromelysin 1) and a tissue inhibitor of metalloproteinases (TIMP)-1 mRNAs by epidermal growth factor and transforming growth factor alpha, but not by interleukin 1 alpha or 12-O-tetradecanoylphorbol 13-acetate in human uterine cervical fibroblasts: the possible involvement of an atypical protein kinase C. We have previously reported that epidermal growth factor (EGF) augments the translation of pro-matrix metalloproteinase 3 (proMMP-3/prostromelysin 1) and tissue inhibitor of metalloproteinases (TIMP)-1 mRNAs during the first 1-h treatment of human uterine cervical fibroblasts (Hosono, T. et al., FEBS Lett., 381, 115-118, (1996)).	Tetradecanoylphorbol Acetate	239-275	epidermal growth factor	Homo sapiens	143-166	
8816913-1	1996	Studies on the link between cellular signalling and cell cycle control at the G2 checkpoint have shown that, in HeLa cells, epidermal growth factor (EGF) and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) rapidly inhibit the G2-M transition by preventing the key component of mitosis-promoting factor (MPF), p34cdc2, from expressing protein kinase activity.	Tetradecanoylphorbol Acetate	214-217	epidermal growth factor	Homo sapiens	124-147	
8816913-1	1996	Studies on the link between cellular signalling and cell cycle control at the G2 checkpoint have shown that, in HeLa cells, epidermal growth factor (EGF) and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) rapidly inhibit the G2-M transition by preventing the key component of mitosis-promoting factor (MPF), p34cdc2, from expressing protein kinase activity.	Tetradecanoylphorbol Acetate	214-217	epidermal growth factor	Homo sapiens	149-152	
8593248-4	1995	Here we investigate the effect of well-known PKC activator 12-O-tetradecanoyl-2 phorbol-13-acetate (TPA), on the levels of 32P incorporation into EGF induced phosphatidylinositols (PI, PI4P, PI4, 5P2) and different phospholipids (PC, PA, PS) as well as on induced tyrosine kinase activity.	Tetradecanoylphorbol Acetate	100-103	epidermal growth factor	Homo sapiens	146-149	
8631300-1	1996	Overexpression of a TPA-insensitive PKC member, an atypical protein kinase C (aPKClambda), results in an enhancement of the transcriptional activation of TPA response element (TRE) in cells stimulated with epidermal growth factor (EGF) or platelet-derived growth factor (PDGF).	Tetradecanoylphorbol Acetate	20-23	epidermal growth factor	Homo sapiens	206-229	
8631300-1	1996	Overexpression of a TPA-insensitive PKC member, an atypical protein kinase C (aPKClambda), results in an enhancement of the transcriptional activation of TPA response element (TRE) in cells stimulated with epidermal growth factor (EGF) or platelet-derived growth factor (PDGF).	Tetradecanoylphorbol Acetate	20-23	epidermal growth factor	Homo sapiens	231-234	
8631300-1	1996	Overexpression of a TPA-insensitive PKC member, an atypical protein kinase C (aPKClambda), results in an enhancement of the transcriptional activation of TPA response element (TRE) in cells stimulated with epidermal growth factor (EGF) or platelet-derived growth factor (PDGF).	Tetradecanoylphorbol Acetate	154-157	epidermal growth factor	Homo sapiens	206-229	
8631300-1	1996	Overexpression of a TPA-insensitive PKC member, an atypical protein kinase C (aPKClambda), results in an enhancement of the transcriptional activation of TPA response element (TRE) in cells stimulated with epidermal growth factor (EGF) or platelet-derived growth factor (PDGF).	Tetradecanoylphorbol Acetate	154-157	epidermal growth factor	Homo sapiens	231-234	
8843340-1	1996	Effects of p110, the catalytic subunit of PI-3 kinase, on induction of TPA response element-driven promoter by EGF was examined.	Tetradecanoylphorbol Acetate	71-74	epidermal growth factor	Homo sapiens	111-114	
8593248-5	1995	TPA significantly decreased the effects of EGF and it had the biggest inhibitory effect on EGF induced PC level.	Tetradecanoylphorbol Acetate	0-3	epidermal growth factor	Homo sapiens	43-46	
8593248-5	1995	TPA significantly decreased the effects of EGF and it had the biggest inhibitory effect on EGF induced PC level.	Tetradecanoylphorbol Acetate	0-3	epidermal growth factor	Homo sapiens	91-94	
7523156-8	1994	EGF and TNF-alpha could enhance c-fos gene expression when protein kinase C was down-regulated by phorbol ester myristate (PMA).	Tetradecanoylphorbol Acetate	123-126	epidermal growth factor	Homo sapiens	0-3	
7534073-5	1995	However, when protein kinase C (PKC) was either inhibited by the PKC inhibitor GF 109203X or depleted by a prolonged TPA treatment, the stimulation of MBP phosphorylation by EGF was strongly inhibited.	Tetradecanoylphorbol Acetate	117-120	epidermal growth factor	Homo sapiens	174-177	
7860643-11	1995	The role of protein kinase C (PKC) in the EGF-stimulated ERK signaling pathway was further examined by inhibition of PKC with the staurosporine analog, CGP41251, and by down-regulation of PKC via chronic treatment with PMA.	Tetradecanoylphorbol Acetate	219-222	epidermal growth factor	Homo sapiens	42-45	
7835292-11	1995	EGF, on the other hand, only enhanced cell proliferation at a late stage (coincident with the TPA-mitogenic effect).	Tetradecanoylphorbol Acetate	94-97	epidermal growth factor	Homo sapiens	0-3	
21153151-10	1995	Treatment of PCOS theca cells with EGF, FGF, TGFbeta and TPA resulted in the inhibition of forskolin-stimulated 17alpha-hydroxyprogesterone production.	Tetradecanoylphorbol Acetate	57-60	epidermal growth factor	Homo sapiens	35-38	
7988452-7	1994	Furthermore, phorbol 12-myristate 13-acetate potentiated the stimulatory effect of EGF.	Tetradecanoylphorbol Acetate	13-44	epidermal growth factor	Homo sapiens	83-86	
7927239-7	1994	Phorbol ester PMA (phorbol 12-myristate 13-acetate), a potent activator of protein kinase C, induced a slight intracellular pH increase significantly smaller than that with epidermal growth factor, whereas this effect was completely blocked by pretreatment with H-7, indicating that PMA-induced intracellular pH increase is mediated by protein kinase C pathways, unlike epidermal growth factor.	Tetradecanoylphorbol Acetate	19-50	epidermal growth factor	Homo sapiens	370-393	
7927239-7	1994	Phorbol ester PMA (phorbol 12-myristate 13-acetate), a potent activator of protein kinase C, induced a slight intracellular pH increase significantly smaller than that with epidermal growth factor, whereas this effect was completely blocked by pretreatment with H-7, indicating that PMA-induced intracellular pH increase is mediated by protein kinase C pathways, unlike epidermal growth factor.	Tetradecanoylphorbol Acetate	14-17	epidermal growth factor	Homo sapiens	173-196	
7927239-7	1994	Phorbol ester PMA (phorbol 12-myristate 13-acetate), a potent activator of protein kinase C, induced a slight intracellular pH increase significantly smaller than that with epidermal growth factor, whereas this effect was completely blocked by pretreatment with H-7, indicating that PMA-induced intracellular pH increase is mediated by protein kinase C pathways, unlike epidermal growth factor.	Tetradecanoylphorbol Acetate	14-17	epidermal growth factor	Homo sapiens	370-393	
8083760-6	1994	Treatment with either TGF alpha or its structural homolog, epidermal growth factor (EGF), increased TGF alpha mRNA levels within 8 hr of exposure; the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was similarly effective.	Tetradecanoylphorbol Acetate	165-202	epidermal growth factor	Homo sapiens	59-82	
8083760-6	1994	Treatment with either TGF alpha or its structural homolog, epidermal growth factor (EGF), increased TGF alpha mRNA levels within 8 hr of exposure; the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was similarly effective.	Tetradecanoylphorbol Acetate	165-202	epidermal growth factor	Homo sapiens	84-87	
8083760-6	1994	Treatment with either TGF alpha or its structural homolog, epidermal growth factor (EGF), increased TGF alpha mRNA levels within 8 hr of exposure; the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was similarly effective.	Tetradecanoylphorbol Acetate	204-207	epidermal growth factor	Homo sapiens	59-82	
8083760-6	1994	Treatment with either TGF alpha or its structural homolog, epidermal growth factor (EGF), increased TGF alpha mRNA levels within 8 hr of exposure; the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was similarly effective.	Tetradecanoylphorbol Acetate	204-207	epidermal growth factor	Homo sapiens	84-87	
8081876-3	1993	EGF-induced phosphorylation and communication inhibition were retained in cells pretreated with phorbol 12-myristate 13-acetate (PMA) to deplete protein kinase C. These results show that the EGF inhibition of communication is tightly linked to protein kinase C-independent phosphorylation of Cx43.	Tetradecanoylphorbol Acetate	96-127	epidermal growth factor	Homo sapiens	0-3	
8045498-5	1994	Interleukin-1 beta and phorbol myristate acetate were also shown to induce in a dose-dependent fashion a threefold to fivefold increase of interleukin-6 production as measured by enzyme-linked immunosorbent assay in human primary biliary duct epithelium cultures, when compared with hepatocyte growth factor, epidermal growth factor, insulin-like growth factor, phytohemagglutinin, tumor necrosis factor-alpha or platelet-derived growth factor.	Tetradecanoylphorbol Acetate	23-48	epidermal growth factor	Homo sapiens	309-332	
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	epidermal growth factor	Homo sapiens	25-48	
8175715-5	1994	The sequence at position -52 to -40 (mLF-CRE) of the gene conferred transcriptional activation in the presence of forskolin, cyclic AMP, and 12-O-tetradecanoylphorbol-13-acetate in transiently transfected human endometrium carcinoma RL95-2 cells, whereas the region at -80 to -60 responded to EGF/TGF-alpha stimulation.	Tetradecanoylphorbol Acetate	141-177	epidermal growth factor	Homo sapiens	293-296	
8224278-8	1993	The stimulation by EGF was attenuated by the treatment with genistein, 12-O-tetradecanoylphorbol-13-acetate, or thapsigargin.	Tetradecanoylphorbol Acetate	71-107	epidermal growth factor	Homo sapiens	19-22	
7932377-9	1994	12-O-Tetradecanoylphorbol-13-acetate decreased the affinity of the receptor for EGF changing the dissociation constant from 1.8 to 3.9 nmol l-1.	Tetradecanoylphorbol Acetate	0-36	epidermal growth factor	Homo sapiens	80-83	
8188084-2	1994	EGF (10 ng/ml) and the tumor promoter, protein kinase C agonist, phorbol 12-myristate 13-acetate (PMA) were potent stimulators (P < 0.01) of DNA synthesis in this cell line as determined by [3H]thymidine incorporation into DNA.	Tetradecanoylphorbol Acetate	98-101	epidermal growth factor	Homo sapiens	0-3	
8081876-3	1993	EGF-induced phosphorylation and communication inhibition were retained in cells pretreated with phorbol 12-myristate 13-acetate (PMA) to deplete protein kinase C. These results show that the EGF inhibition of communication is tightly linked to protein kinase C-independent phosphorylation of Cx43.	Tetradecanoylphorbol Acetate	96-127	epidermal growth factor	Homo sapiens	191-194	
8081876-3	1993	EGF-induced phosphorylation and communication inhibition were retained in cells pretreated with phorbol 12-myristate 13-acetate (PMA) to deplete protein kinase C. These results show that the EGF inhibition of communication is tightly linked to protein kinase C-independent phosphorylation of Cx43.	Tetradecanoylphorbol Acetate	129-132	epidermal growth factor	Homo sapiens	0-3	
8312133-4	1993	The Ca2+ signal induced by fluoride as well as one induced by EGF was inhibited by the pretreatment of cells with protein kinase C activator, phorbol myristate acetate (PMA).	Tetradecanoylphorbol Acetate	142-167	epidermal growth factor	Homo sapiens	62-65	
8312133-4	1993	The Ca2+ signal induced by fluoride as well as one induced by EGF was inhibited by the pretreatment of cells with protein kinase C activator, phorbol myristate acetate (PMA).	Tetradecanoylphorbol Acetate	169-172	epidermal growth factor	Homo sapiens	62-65	
8241569-9	1993	Two-dimensional tryptic and chymotryptic phosphopeptide mapping demonstrated that the in vitro phosphopeptides represented a specific subset of the in vivo phosphopeptides produced in response to EGF after chronic TPA treatment.	Tetradecanoylphorbol Acetate	214-217	epidermal growth factor	Homo sapiens	196-199	
8081876-3	1993	EGF-induced phosphorylation and communication inhibition were retained in cells pretreated with phorbol 12-myristate 13-acetate (PMA) to deplete protein kinase C. These results show that the EGF inhibition of communication is tightly linked to protein kinase C-independent phosphorylation of Cx43.	Tetradecanoylphorbol Acetate	129-132	epidermal growth factor	Homo sapiens	191-194	
1707036-4	1991	Addition of fetuin or epidermal growth factor (EGF) to incubates with serum-deprived cells increased the ability of TPA to affect growth, but addition of platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-beta) or retinoic acid (RA) was without effect.	Tetradecanoylphorbol Acetate	116-119	epidermal growth factor	Homo sapiens	22-45	
1445344-5	1992	IGF-I and EGF stimulated the transcriptional activity dependent on the phorbol 12-myristate 13-acetate-responsive element (TRE) to the same extent, when measured by the chloramphenicol acetyl transferase activity of a transiently transfected multiple TRE construct.	Tetradecanoylphorbol Acetate	71-102	epidermal growth factor	Homo sapiens	10-13	
1427596-10	1992	However, this effect of EGF was counteracted by the pretreatment with TPA or H-7.	Tetradecanoylphorbol Acetate	70-73	epidermal growth factor	Homo sapiens	24-27	
1915667-3	1991	In this paper we show that epidermal growth factor (EGF)- and 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced expression of the c-fos and c-jun protooncogenes is decreased in microgravity, while no effect of gravity changes was observed on A23187- and forskolin-induced expression of these genes.	Tetradecanoylphorbol Acetate	101-104	epidermal growth factor	Homo sapiens	27-50	
1915667-3	1991	In this paper we show that epidermal growth factor (EGF)- and 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced expression of the c-fos and c-jun protooncogenes is decreased in microgravity, while no effect of gravity changes was observed on A23187- and forskolin-induced expression of these genes.	Tetradecanoylphorbol Acetate	101-104	epidermal growth factor	Homo sapiens	52-55	
8424125-6	1993	Like 12-O-Tetradecanoly phorbol-13-acetate (TPA), a PK-C activator which also enhances EGF-stimulated growth of MEC, linoleate can phosphorylate a 40-42 KD protein.	Tetradecanoylphorbol Acetate	44-47	epidermal growth factor	Homo sapiens	87-90	
11537644-4	1992	In addition, we have investigated signalling pathways as induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), forskolin, and A23187 that bypass the EGF receptor, but mimic the partial activation of signal transduction pathways.	Tetradecanoylphorbol Acetate	68-104	epidermal growth factor	Homo sapiens	150-153	
11537644-11	1992	These observations demonstrate that gravity affects specific components in the EGF-induced signal transduction circuitry, in particular the protein kinase C pathway which is common to EGF and TPA activated intracellular signalling.	Tetradecanoylphorbol Acetate	192-195	epidermal growth factor	Homo sapiens	79-82	
1738590-4	1992	Induction of jun B can be mimicked in wild type P19 EC cells by the synergistic action of the phorbol ester TPA and the calcium ionophore A23187, through activation of signal transduction pathways, that are activated simultaneously by EGF.	Tetradecanoylphorbol Acetate	108-111	epidermal growth factor	Homo sapiens	235-238	
1850101-7	1991	After both 1 and 24 h, tyrphostin was a less effective inhibitor of tyrosine kinase activity than the potent tumor promoter 12-O-tetradecanoyl phorbol-13-acetate, which almost completely blocked EGF receptor autophosphorylation.	Tetradecanoylphorbol Acetate	124-161	epidermal growth factor	Homo sapiens	195-198	
1707036-4	1991	Addition of fetuin or epidermal growth factor (EGF) to incubates with serum-deprived cells increased the ability of TPA to affect growth, but addition of platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-beta) or retinoic acid (RA) was without effect.	Tetradecanoylphorbol Acetate	116-119	epidermal growth factor	Homo sapiens	47-50	
2283681-5	1990	Low concentrations of TPA (2 x 10(-10) M) had no effect on Ca2+ release due to EGF, TGR-alpha or bradykinin but resulted in a rapid return of [Ca2+]i to baseline levels for EGF or TGF-alpha.	Tetradecanoylphorbol Acetate	22-25	epidermal growth factor	Homo sapiens	173-176	
2171499-3	1990	Both the Ca2+ ionophore ionomycin and the tumour promotor tetradecanoylphorbol acetate (TPA), added shortly before EGF, inhibit EGF receptor protein tyrosine kinase activity in intact cells.	Tetradecanoylphorbol Acetate	58-86	epidermal growth factor	Homo sapiens	115-118	
2171499-3	1990	Both the Ca2+ ionophore ionomycin and the tumour promotor tetradecanoylphorbol acetate (TPA), added shortly before EGF, inhibit EGF receptor protein tyrosine kinase activity in intact cells.	Tetradecanoylphorbol Acetate	88-91	epidermal growth factor	Homo sapiens	115-118	
1985972-4	1991	The study of EGF binding to only low affinity receptors was performed with cells pretreated with the phorbol ester phorbol 12-myristate 13-acetate, which induces a conversion of high affinity receptors to low affinity receptors.	Tetradecanoylphorbol Acetate	115-146	epidermal growth factor	Homo sapiens	13-16	
1701695-6	1990	The EGF-dependent growth stimulation in ER11 cells was inhibited by 12-O-tetradecanoylphorbol 13-acetate (TPA).	Tetradecanoylphorbol Acetate	68-104	epidermal growth factor	Homo sapiens	4-7	
1701695-6	1990	The EGF-dependent growth stimulation in ER11 cells was inhibited by 12-O-tetradecanoylphorbol 13-acetate (TPA).	Tetradecanoylphorbol Acetate	106-109	epidermal growth factor	Homo sapiens	4-7	
1701695-7	1990	Exposure of NA and ER11 cells to TPA for 30 h resulted in the down-regulation of protein kinase C. In these protein kinase C-deficient cells, EGF was able to activate autophosphorylation of the EGF receptor.	Tetradecanoylphorbol Acetate	33-36	epidermal growth factor	Homo sapiens	142-145	
1701695-7	1990	Exposure of NA and ER11 cells to TPA for 30 h resulted in the down-regulation of protein kinase C. In these protein kinase C-deficient cells, EGF was able to activate autophosphorylation of the EGF receptor.	Tetradecanoylphorbol Acetate	33-36	epidermal growth factor	Homo sapiens	194-197	
2637248-1	1989	Tumor promoting phorbol esters, 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu), significantly enhanced the growth of human gastric cancer cell line TMK-1, whilst activating protein kinase C. The time course of 125I-epidermal growth factor (EGF) binding to TMK-1 cells after TPA treatment showed a decrease in the number of EGF receptors on TMK-1 cells within 3 hr.	Tetradecanoylphorbol Acetate	32-68	epidermal growth factor	Homo sapiens	242-270	
2283681-6	1990	Addition of the PKC inhibitor staurosporine (1 and 10 nM) completely inhibited the action of TPA on EGF-induced [Ca2+]i changes.	Tetradecanoylphorbol Acetate	93-96	epidermal growth factor	Homo sapiens	100-103	
2283681-8	1990	Down-regulation of PKC by overnight incubation with 0.1 or 1 microM TPA produced the converse effect, namely prolonged Ca2+ entry following stimulation with EGF or TGF-alpha.	Tetradecanoylphorbol Acetate	68-71	epidermal growth factor	Homo sapiens	157-160	
2283681-13	1990	A431 cells treated with higher concentrations of TPA (5 x 10(-8) M) inhibited not only Ca2+ entry but also Ca2+ release due to EGF/TGF-alpha but had no effect on bradykinin-mediated Ca2+ release, suggesting differences in the regulation of the intracellular stores responsive to these two classes of agonists.	Tetradecanoylphorbol Acetate	49-52	epidermal growth factor	Homo sapiens	127-130	
2107492-0	1990	2-Aminopurine abolishes EGF- and TPA-stimulated pp33 phosphorylation and c-fos induction without affecting the activation of protein kinase C. Epidermal Growth Factor (EGF) and Tetradecanoyl Phorbol Acetate (TPA) initiate signalling cascades in C3H 10T1/2 fibroblasts by primarily activating distinct protein kinases, the EGF receptor tyrosine kinase and protein kinase C respectively; there is no signal crossover at the initiation of signalling.	Tetradecanoylphorbol Acetate	33-36	epidermal growth factor	Homo sapiens	143-166	
2107492-0	1990	2-Aminopurine abolishes EGF- and TPA-stimulated pp33 phosphorylation and c-fos induction without affecting the activation of protein kinase C. Epidermal Growth Factor (EGF) and Tetradecanoyl Phorbol Acetate (TPA) initiate signalling cascades in C3H 10T1/2 fibroblasts by primarily activating distinct protein kinases, the EGF receptor tyrosine kinase and protein kinase C respectively; there is no signal crossover at the initiation of signalling.	Tetradecanoylphorbol Acetate	33-36	epidermal growth factor	Homo sapiens	168-171	
2107492-0	1990	2-Aminopurine abolishes EGF- and TPA-stimulated pp33 phosphorylation and c-fos induction without affecting the activation of protein kinase C. Epidermal Growth Factor (EGF) and Tetradecanoyl Phorbol Acetate (TPA) initiate signalling cascades in C3H 10T1/2 fibroblasts by primarily activating distinct protein kinases, the EGF receptor tyrosine kinase and protein kinase C respectively; there is no signal crossover at the initiation of signalling.	Tetradecanoylphorbol Acetate	33-36	epidermal growth factor	Homo sapiens	168-171	
2107492-0	1990	2-Aminopurine abolishes EGF- and TPA-stimulated pp33 phosphorylation and c-fos induction without affecting the activation of protein kinase C. Epidermal Growth Factor (EGF) and Tetradecanoyl Phorbol Acetate (TPA) initiate signalling cascades in C3H 10T1/2 fibroblasts by primarily activating distinct protein kinases, the EGF receptor tyrosine kinase and protein kinase C respectively; there is no signal crossover at the initiation of signalling.	Tetradecanoylphorbol Acetate	177-206	epidermal growth factor	Homo sapiens	24-27	
2107492-0	1990	2-Aminopurine abolishes EGF- and TPA-stimulated pp33 phosphorylation and c-fos induction without affecting the activation of protein kinase C. Epidermal Growth Factor (EGF) and Tetradecanoyl Phorbol Acetate (TPA) initiate signalling cascades in C3H 10T1/2 fibroblasts by primarily activating distinct protein kinases, the EGF receptor tyrosine kinase and protein kinase C respectively; there is no signal crossover at the initiation of signalling.	Tetradecanoylphorbol Acetate	208-211	epidermal growth factor	Homo sapiens	24-27	
2107492-0	1990	2-Aminopurine abolishes EGF- and TPA-stimulated pp33 phosphorylation and c-fos induction without affecting the activation of protein kinase C. Epidermal Growth Factor (EGF) and Tetradecanoyl Phorbol Acetate (TPA) initiate signalling cascades in C3H 10T1/2 fibroblasts by primarily activating distinct protein kinases, the EGF receptor tyrosine kinase and protein kinase C respectively; there is no signal crossover at the initiation of signalling.	Tetradecanoylphorbol Acetate	208-211	epidermal growth factor	Homo sapiens	143-166	
2107492-5	1990	Further, we show here that although EGF- and TPA-stimulated induction of c-fos is abolished by 2-aminopurine, the appearance of TRE-binding activity in nuclear extracts of stimulated cells is unaffected, suggesting that EGF- and TPA-stimulated induction of TRE-binding activity utilises existing proteins and is not dependent on fresh c-FOS synthesis.	Tetradecanoylphorbol Acetate	45-48	epidermal growth factor	Homo sapiens	220-223	
2169292-3	1990	Downmodulation of EGF receptors by 12-O-tetradecanoylphorbol 13-acetate (TPA) is also observed.	Tetradecanoylphorbol Acetate	35-71	epidermal growth factor	Homo sapiens	18-21	
2169292-3	1990	Downmodulation of EGF receptors by 12-O-tetradecanoylphorbol 13-acetate (TPA) is also observed.	Tetradecanoylphorbol Acetate	73-76	epidermal growth factor	Homo sapiens	18-21	
2637248-1	1989	Tumor promoting phorbol esters, 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu), significantly enhanced the growth of human gastric cancer cell line TMK-1, whilst activating protein kinase C. The time course of 125I-epidermal growth factor (EGF) binding to TMK-1 cells after TPA treatment showed a decrease in the number of EGF receptors on TMK-1 cells within 3 hr.	Tetradecanoylphorbol Acetate	32-68	epidermal growth factor	Homo sapiens	272-275	
2637248-1	1989	Tumor promoting phorbol esters, 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu), significantly enhanced the growth of human gastric cancer cell line TMK-1, whilst activating protein kinase C. The time course of 125I-epidermal growth factor (EGF) binding to TMK-1 cells after TPA treatment showed a decrease in the number of EGF receptors on TMK-1 cells within 3 hr.	Tetradecanoylphorbol Acetate	32-68	epidermal growth factor	Homo sapiens	355-358	
2637248-1	1989	Tumor promoting phorbol esters, 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu), significantly enhanced the growth of human gastric cancer cell line TMK-1, whilst activating protein kinase C. The time course of 125I-epidermal growth factor (EGF) binding to TMK-1 cells after TPA treatment showed a decrease in the number of EGF receptors on TMK-1 cells within 3 hr.	Tetradecanoylphorbol Acetate	70-73	epidermal growth factor	Homo sapiens	242-270	
2637248-1	1989	Tumor promoting phorbol esters, 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu), significantly enhanced the growth of human gastric cancer cell line TMK-1, whilst activating protein kinase C. The time course of 125I-epidermal growth factor (EGF) binding to TMK-1 cells after TPA treatment showed a decrease in the number of EGF receptors on TMK-1 cells within 3 hr.	Tetradecanoylphorbol Acetate	70-73	epidermal growth factor	Homo sapiens	272-275	
2637248-1	1989	Tumor promoting phorbol esters, 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu), significantly enhanced the growth of human gastric cancer cell line TMK-1, whilst activating protein kinase C. The time course of 125I-epidermal growth factor (EGF) binding to TMK-1 cells after TPA treatment showed a decrease in the number of EGF receptors on TMK-1 cells within 3 hr.	Tetradecanoylphorbol Acetate	70-73	epidermal growth factor	Homo sapiens	355-358	
2637248-2	1989	Autophosphorylation of EGF receptor decreased in accordance with the decrease of EGF binding by TPA treatment.	Tetradecanoylphorbol Acetate	96-99	epidermal growth factor	Homo sapiens	23-26	
2637248-2	1989	Autophosphorylation of EGF receptor decreased in accordance with the decrease of EGF binding by TPA treatment.	Tetradecanoylphorbol Acetate	96-99	epidermal growth factor	Homo sapiens	81-84	
2637248-3	1989	Scatchard plot analysis of TMK-1 cells after TPA treatment showed that high affinity EGF receptor disappeared at 3hr but the number of EGF receptors increased at 24 hr.	Tetradecanoylphorbol Acetate	45-48	epidermal growth factor	Homo sapiens	85-88	
2851595-6	1988	Potentiation of the action of EGF by the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA), indicates that activation of protein kinase C and an influx of Ca2+ share a common mechanism for initiating DNA synthesis.	Tetradecanoylphorbol Acetate	56-93	epidermal growth factor	Homo sapiens	30-33	
2549060-7	1989	Desensitization to EGF was observed in cells in which protein kinase C had been down-regulated by prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate, implying that EGF receptor desensitization is independent of protein kinase C. The desensitizing effects of EGF on growth factor-induced phosphatidylinositol turnover could be prevented by pretreatment of the cells with the calmodulin antagonist trifluoperazine, suggesting that calmodulin may be involved in the regulation of EGF receptor sensitivity.	Tetradecanoylphorbol Acetate	123-159	epidermal growth factor	Homo sapiens	19-22	
2588913-5	1989	However, in the case of 7402 cells, while the number of receptors, like 7721 cells, remained unchanged, the affinity of EGF receptors displayed a time dependent modulation after PMA treatment.	Tetradecanoylphorbol Acetate	178-181	epidermal growth factor	Homo sapiens	120-123	
2495278-1	1989	In this study we report that pretreatment of human amniotic (WISH) cells with interferon gamma (IFN-gamma) in the presence of 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in the down-modulation of epidermal growth factor (EGF) receptors with respect to both receptor number and affinity.	Tetradecanoylphorbol Acetate	126-162	epidermal growth factor	Homo sapiens	204-227	
2495278-1	1989	In this study we report that pretreatment of human amniotic (WISH) cells with interferon gamma (IFN-gamma) in the presence of 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in the down-modulation of epidermal growth factor (EGF) receptors with respect to both receptor number and affinity.	Tetradecanoylphorbol Acetate	126-162	epidermal growth factor	Homo sapiens	229-232	
2495278-1	1989	In this study we report that pretreatment of human amniotic (WISH) cells with interferon gamma (IFN-gamma) in the presence of 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in the down-modulation of epidermal growth factor (EGF) receptors with respect to both receptor number and affinity.	Tetradecanoylphorbol Acetate	164-167	epidermal growth factor	Homo sapiens	204-227	
2495278-1	1989	In this study we report that pretreatment of human amniotic (WISH) cells with interferon gamma (IFN-gamma) in the presence of 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in the down-modulation of epidermal growth factor (EGF) receptors with respect to both receptor number and affinity.	Tetradecanoylphorbol Acetate	164-167	epidermal growth factor	Homo sapiens	229-232	
2495278-3	1989	Pretreatment with IFN-gamma for 24 h enhanced the TPA-induced inhibition of EGF binding whereas IFN-gamma alone had no effect on binding.	Tetradecanoylphorbol Acetate	50-53	epidermal growth factor	Homo sapiens	76-79	
2521857-1	1989	We have previously reported that both 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) can stimulate the synthesis rate of EGF receptors.	Tetradecanoylphorbol Acetate	38-74	epidermal growth factor	Homo sapiens	151-154	
2521857-1	1989	We have previously reported that both 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) can stimulate the synthesis rate of EGF receptors.	Tetradecanoylphorbol Acetate	76-79	epidermal growth factor	Homo sapiens	151-154	
2521857-2	1989	We now show that the MDA468 breast cancer cells express the mRNA for the EGF-like molecule, transforming growth factor-alpha (TGF-alpha), and demonstrate that TPA or EGF cause an accumulation of both EGF receptor and TGF-alpha mRNA.	Tetradecanoylphorbol Acetate	159-162	epidermal growth factor	Homo sapiens	73-76	
2521857-3	1989	The levels of EGF receptor mRNA paralleled our earlier protein data, with peak accumulations of 2-3-fold with 10(-9) M EGF and 3-5-fold with 100 ng/ml TPA seen between 6 and 8 h. A 7-fold accumulation of TGF-alpha mRNA was seen following 4 h of treatment with TPA, and a 2-fold accumulation was seen after 8 h with EGF.	Tetradecanoylphorbol Acetate	151-154	epidermal growth factor	Homo sapiens	14-17	
2521857-3	1989	The levels of EGF receptor mRNA paralleled our earlier protein data, with peak accumulations of 2-3-fold with 10(-9) M EGF and 3-5-fold with 100 ng/ml TPA seen between 6 and 8 h. A 7-fold accumulation of TGF-alpha mRNA was seen following 4 h of treatment with TPA, and a 2-fold accumulation was seen after 8 h with EGF.	Tetradecanoylphorbol Acetate	260-263	epidermal growth factor	Homo sapiens	14-17	
2851595-6	1988	Potentiation of the action of EGF by the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA), indicates that activation of protein kinase C and an influx of Ca2+ share a common mechanism for initiating DNA synthesis.	Tetradecanoylphorbol Acetate	95-98	epidermal growth factor	Homo sapiens	30-33	
3138977-9	1988	Treatment of the cells with 12-O-tetradecanoylphorbol 13-acetate completely abolishes the response to EGF and to sub-optimal doses of bradykinin, suggesting a negative-feedback function of protein kinase C. Pretreatment of the cells with pertussis toxin has no effect on inositol phosphate formation induced by either EGF or bradykinin.	Tetradecanoylphorbol Acetate	28-64	epidermal growth factor	Homo sapiens	102-105	
3138977-9	1988	Treatment of the cells with 12-O-tetradecanoylphorbol 13-acetate completely abolishes the response to EGF and to sub-optimal doses of bradykinin, suggesting a negative-feedback function of protein kinase C. Pretreatment of the cells with pertussis toxin has no effect on inositol phosphate formation induced by either EGF or bradykinin.	Tetradecanoylphorbol Acetate	28-64	epidermal growth factor	Homo sapiens	318-321	
3260374-1	1988	Expression of the epidermal growth factor (EGF) receptor gene is stimulated by EGF and the phorbol ester, 4 beta-phorbol 12-myristate 13-acetate (PMA).	Tetradecanoylphorbol Acetate	106-144	epidermal growth factor	Homo sapiens	43-46	
3260374-1	1988	Expression of the epidermal growth factor (EGF) receptor gene is stimulated by EGF and the phorbol ester, 4 beta-phorbol 12-myristate 13-acetate (PMA).	Tetradecanoylphorbol Acetate	146-149	epidermal growth factor	Homo sapiens	43-46	
3258542-8	1988	It was also determined that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate reduces EGF binding to the high affinity receptors of A-431R-1 cells; whereas, transforming growth factor type beta did not significantly affect EGF binding.	Tetradecanoylphorbol Acetate	46-82	epidermal growth factor	Homo sapiens	91-94	
3259583-3	1988	Using fibroblastic cells depleted of protein kinase C by chronic treatment with the tumor promoter tetradecanoyl phorbol acetate (TPA), we now show that protein kinase C is required for the tyrosine phosphorylation of the 42-kD protein, even when epidermal growth factor (EGF), whose receptor is a tyrosine-specific protein kinase, provides the initial stimulus.	Tetradecanoylphorbol Acetate	99-128	epidermal growth factor	Homo sapiens	247-270	
3259583-3	1988	Using fibroblastic cells depleted of protein kinase C by chronic treatment with the tumor promoter tetradecanoyl phorbol acetate (TPA), we now show that protein kinase C is required for the tyrosine phosphorylation of the 42-kD protein, even when epidermal growth factor (EGF), whose receptor is a tyrosine-specific protein kinase, provides the initial stimulus.	Tetradecanoylphorbol Acetate	99-128	epidermal growth factor	Homo sapiens	272-275	
3259583-3	1988	Using fibroblastic cells depleted of protein kinase C by chronic treatment with the tumor promoter tetradecanoyl phorbol acetate (TPA), we now show that protein kinase C is required for the tyrosine phosphorylation of the 42-kD protein, even when epidermal growth factor (EGF), whose receptor is a tyrosine-specific protein kinase, provides the initial stimulus.	Tetradecanoylphorbol Acetate	130-133	epidermal growth factor	Homo sapiens	247-270	
3259583-3	1988	Using fibroblastic cells depleted of protein kinase C by chronic treatment with the tumor promoter tetradecanoyl phorbol acetate (TPA), we now show that protein kinase C is required for the tyrosine phosphorylation of the 42-kD protein, even when epidermal growth factor (EGF), whose receptor is a tyrosine-specific protein kinase, provides the initial stimulus.	Tetradecanoylphorbol Acetate	130-133	epidermal growth factor	Homo sapiens	272-275	
3260332-0	1988	Independent transcriptional regulation of a single VL30 element by epidermal growth factor and activators of protein kinase C. A single VL30 element present in the RVL-3 cell line was transcriptionally induced by both epidermal growth factor (EGF) and the protein kinase C (pkC) activators 12-O-tetradecanoylphorbol-13-acetate (TPA) and sn-1,2-dioctanoylglycerol within 5 min of stimulation.	Tetradecanoylphorbol Acetate	290-326	epidermal growth factor	Homo sapiens	67-90	
3260332-0	1988	Independent transcriptional regulation of a single VL30 element by epidermal growth factor and activators of protein kinase C. A single VL30 element present in the RVL-3 cell line was transcriptionally induced by both epidermal growth factor (EGF) and the protein kinase C (pkC) activators 12-O-tetradecanoylphorbol-13-acetate (TPA) and sn-1,2-dioctanoylglycerol within 5 min of stimulation.	Tetradecanoylphorbol Acetate	290-326	epidermal growth factor	Homo sapiens	218-241	
3260332-0	1988	Independent transcriptional regulation of a single VL30 element by epidermal growth factor and activators of protein kinase C. A single VL30 element present in the RVL-3 cell line was transcriptionally induced by both epidermal growth factor (EGF) and the protein kinase C (pkC) activators 12-O-tetradecanoylphorbol-13-acetate (TPA) and sn-1,2-dioctanoylglycerol within 5 min of stimulation.	Tetradecanoylphorbol Acetate	290-326	epidermal growth factor	Homo sapiens	243-246	
3260332-0	1988	Independent transcriptional regulation of a single VL30 element by epidermal growth factor and activators of protein kinase C. A single VL30 element present in the RVL-3 cell line was transcriptionally induced by both epidermal growth factor (EGF) and the protein kinase C (pkC) activators 12-O-tetradecanoylphorbol-13-acetate (TPA) and sn-1,2-dioctanoylglycerol within 5 min of stimulation.	Tetradecanoylphorbol Acetate	328-331	epidermal growth factor	Homo sapiens	67-90	
3260332-0	1988	Independent transcriptional regulation of a single VL30 element by epidermal growth factor and activators of protein kinase C. A single VL30 element present in the RVL-3 cell line was transcriptionally induced by both epidermal growth factor (EGF) and the protein kinase C (pkC) activators 12-O-tetradecanoylphorbol-13-acetate (TPA) and sn-1,2-dioctanoylglycerol within 5 min of stimulation.	Tetradecanoylphorbol Acetate	328-331	epidermal growth factor	Homo sapiens	218-241	
3260332-0	1988	Independent transcriptional regulation of a single VL30 element by epidermal growth factor and activators of protein kinase C. A single VL30 element present in the RVL-3 cell line was transcriptionally induced by both epidermal growth factor (EGF) and the protein kinase C (pkC) activators 12-O-tetradecanoylphorbol-13-acetate (TPA) and sn-1,2-dioctanoylglycerol within 5 min of stimulation.	Tetradecanoylphorbol Acetate	328-331	epidermal growth factor	Homo sapiens	243-246	
3260332-1	1988	Following TPA-induced depletion of protein kinase C activity, EGF stimulation of VL30 transcription and accumulation was unaffected while TPA effects were inhibited, implying that EGF and TPA act by separable pathways.	Tetradecanoylphorbol Acetate	10-13	epidermal growth factor	Homo sapiens	180-183	
2897079-5	1988	However, in contrast to TPA, EGF increased the phosphorylation of the c-erbB-2 protein in cells whose protein kinase C had been down-regulated by long-term pretreatment with TPA, suggesting that EGF and TPA induce phosphorylation by different mechanisms.	Tetradecanoylphorbol Acetate	174-177	epidermal growth factor	Homo sapiens	29-32	
2897079-5	1988	However, in contrast to TPA, EGF increased the phosphorylation of the c-erbB-2 protein in cells whose protein kinase C had been down-regulated by long-term pretreatment with TPA, suggesting that EGF and TPA induce phosphorylation by different mechanisms.	Tetradecanoylphorbol Acetate	174-177	epidermal growth factor	Homo sapiens	195-198	
2897079-5	1988	However, in contrast to TPA, EGF increased the phosphorylation of the c-erbB-2 protein in cells whose protein kinase C had been down-regulated by long-term pretreatment with TPA, suggesting that EGF and TPA induce phosphorylation by different mechanisms.	Tetradecanoylphorbol Acetate	174-177	epidermal growth factor	Homo sapiens	29-32	
2897079-5	1988	However, in contrast to TPA, EGF increased the phosphorylation of the c-erbB-2 protein in cells whose protein kinase C had been down-regulated by long-term pretreatment with TPA, suggesting that EGF and TPA induce phosphorylation by different mechanisms.	Tetradecanoylphorbol Acetate	174-177	epidermal growth factor	Homo sapiens	195-198	
3278921-5	1988	Down regulation of PKC activity by treatment with TPA for 48-h blocks the stimulation of S6 kinase by TPA but leaves the activation by EGF, IGF-I and insulin unaffected.	Tetradecanoylphorbol Acetate	50-53	epidermal growth factor	Homo sapiens	135-138	
3259577-13	1988	12-O-Tetradecanoylphorbol-13-acetate (TPA), an exogenous activator of Ca2+/phospholipid-dependent protein kinase (protein kinase C), causes a dramatic, but transient, inhibition of the EGF-stimulated formation of inositol phosphates.	Tetradecanoylphorbol Acetate	0-36	epidermal growth factor	Homo sapiens	185-188	
3259577-13	1988	12-O-Tetradecanoylphorbol-13-acetate (TPA), an exogenous activator of Ca2+/phospholipid-dependent protein kinase (protein kinase C), causes a dramatic, but transient, inhibition of the EGF-stimulated formation of inositol phosphates.	Tetradecanoylphorbol Acetate	38-41	epidermal growth factor	Homo sapiens	185-188	
3136317-6	1988	The addition of TPA to NIH 3T3 cells expressing a wild-type human EGF receptor blocked the mitogenic capacity of EGF.	Tetradecanoylphorbol Acetate	16-19	epidermal growth factor	Homo sapiens	113-116	
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	epidermal growth factor	Homo sapiens	182-185	
3499220-4	1987	The action of EGF was antagonized by 12-O-tetradecanoylphorbol-13-acetate, which did not inhibit dexamethasone binding significantly, and by concanavalin A.	Tetradecanoylphorbol Acetate	37-73	epidermal growth factor	Homo sapiens	14-17	
3499220-7	1987	The effect of EGF on dexamethasone-inhibited cell growth also was antagonized by 12-O-tetradecanoylphorbol-13-acetate.	Tetradecanoylphorbol Acetate	81-117	epidermal growth factor	Homo sapiens	14-17	
3494448-2	1987	In cultured porcine thyroid cells, EGF and TPA stimulate PGE2 and 6-keto PGF1 alpha production; the maximum PG levels were obtained after 3-4 h incubation with EGF or TPA; the addition of as little as 10(-11) M EGF or 5 X 10(-11) M TPA resulted in increases in PGE2 and 6-keto PGF1 alpha, and the maximum levels were obtained with 10(-8)-10(-7) M EGF or TPA.	Tetradecanoylphorbol Acetate	43-46	epidermal growth factor	Homo sapiens	160-163	
3498001-1	1987	12-O-Tetradecanoylphorbol 13-acetate (TPA) is a potent tumour promoter and shows several biological activities of epidermal growth factor (EGF).	Tetradecanoylphorbol Acetate	0-36	epidermal growth factor	Homo sapiens	114-137	
3498001-1	1987	12-O-Tetradecanoylphorbol 13-acetate (TPA) is a potent tumour promoter and shows several biological activities of epidermal growth factor (EGF).	Tetradecanoylphorbol Acetate	38-41	epidermal growth factor	Homo sapiens	114-137	
3494731-3	1987	Here, we demonstrate that the tumor promotor, 12-O-tetradecanoylphorbol-13-acetate (TPA), like EGF, also stimulates receptor synthesis in the human breast carcinoma cell line, MDA468 cells.	Tetradecanoylphorbol Acetate	46-82	epidermal growth factor	Homo sapiens	95-98	
3494731-7	1987	Although TPA treatment resulted in an immediate loss of high affinity EGF-binding sites, the long-term effect was an increase in both the low and high affinity binding sites.	Tetradecanoylphorbol Acetate	9-12	epidermal growth factor	Homo sapiens	70-73	
3494731-10	1987	Nevertheless, the TPA-pretreated cells were still growth-inhibited by EGF.	Tetradecanoylphorbol Acetate	18-21	epidermal growth factor	Homo sapiens	70-73	
3494448-2	1987	In cultured porcine thyroid cells, EGF and TPA stimulate PGE2 and 6-keto PGF1 alpha production; the maximum PG levels were obtained after 3-4 h incubation with EGF or TPA; the addition of as little as 10(-11) M EGF or 5 X 10(-11) M TPA resulted in increases in PGE2 and 6-keto PGF1 alpha, and the maximum levels were obtained with 10(-8)-10(-7) M EGF or TPA.	Tetradecanoylphorbol Acetate	43-46	epidermal growth factor	Homo sapiens	160-163	
3494448-2	1987	In cultured porcine thyroid cells, EGF and TPA stimulate PGE2 and 6-keto PGF1 alpha production; the maximum PG levels were obtained after 3-4 h incubation with EGF or TPA; the addition of as little as 10(-11) M EGF or 5 X 10(-11) M TPA resulted in increases in PGE2 and 6-keto PGF1 alpha, and the maximum levels were obtained with 10(-8)-10(-7) M EGF or TPA.	Tetradecanoylphorbol Acetate	43-46	epidermal growth factor	Homo sapiens	160-163	
3494448-2	1987	In cultured porcine thyroid cells, EGF and TPA stimulate PGE2 and 6-keto PGF1 alpha production; the maximum PG levels were obtained after 3-4 h incubation with EGF or TPA; the addition of as little as 10(-11) M EGF or 5 X 10(-11) M TPA resulted in increases in PGE2 and 6-keto PGF1 alpha, and the maximum levels were obtained with 10(-8)-10(-7) M EGF or TPA.	Tetradecanoylphorbol Acetate	167-170	epidermal growth factor	Homo sapiens	35-38	
3494448-2	1987	In cultured porcine thyroid cells, EGF and TPA stimulate PGE2 and 6-keto PGF1 alpha production; the maximum PG levels were obtained after 3-4 h incubation with EGF or TPA; the addition of as little as 10(-11) M EGF or 5 X 10(-11) M TPA resulted in increases in PGE2 and 6-keto PGF1 alpha, and the maximum levels were obtained with 10(-8)-10(-7) M EGF or TPA.	Tetradecanoylphorbol Acetate	167-170	epidermal growth factor	Homo sapiens	35-38	
3494448-2	1987	In cultured porcine thyroid cells, EGF and TPA stimulate PGE2 and 6-keto PGF1 alpha production; the maximum PG levels were obtained after 3-4 h incubation with EGF or TPA; the addition of as little as 10(-11) M EGF or 5 X 10(-11) M TPA resulted in increases in PGE2 and 6-keto PGF1 alpha, and the maximum levels were obtained with 10(-8)-10(-7) M EGF or TPA.	Tetradecanoylphorbol Acetate	167-170	epidermal growth factor	Homo sapiens	35-38	
2866188-7	1985	The tumor promoter, 4 beta-phorbol 12-myristate 13-acetate, appears to mimic the action of EGF in inducing EGF-R accumulation in coated pits at the cell surface and receptor internalization.	Tetradecanoylphorbol Acetate	22-58	epidermal growth factor	Homo sapiens	107-112	
3015918-5	1986	This is inhibited when TPA-treated cells are exposed to EGF.	Tetradecanoylphorbol Acetate	23-26	epidermal growth factor	Homo sapiens	56-59	
3015918-10	1986	Indeed, we find that 12-O-tetradecanoylphorbol-13-acetate, added 10 min after EGF, further increases threonine 654 phosphorylation and induces the loss of tyrosine phosphate from A431 cell EGF receptors.	Tetradecanoylphorbol Acetate	21-57	epidermal growth factor	Homo sapiens	78-81	
3015918-10	1986	Indeed, we find that 12-O-tetradecanoylphorbol-13-acetate, added 10 min after EGF, further increases threonine 654 phosphorylation and induces the loss of tyrosine phosphate from A431 cell EGF receptors.	Tetradecanoylphorbol Acetate	21-57	epidermal growth factor	Homo sapiens	189-192	
3958045-2	1986	In urokinase-producing human carcinoma cells (A1251), a 20-40-fold increase in urokinase mRNA level is obtained after treatment with 10 nM phorbol myristate acetate (PMA), a smaller effect (two- to fourfold) with 2 ng/ml platelet-derived growth factor (PDGF) and no effect with epidermal growth factor (EGF) (up to 50 nM).	Tetradecanoylphorbol Acetate	139-164	epidermal growth factor	Homo sapiens	278-301	
3958045-2	1986	In urokinase-producing human carcinoma cells (A1251), a 20-40-fold increase in urokinase mRNA level is obtained after treatment with 10 nM phorbol myristate acetate (PMA), a smaller effect (two- to fourfold) with 2 ng/ml platelet-derived growth factor (PDGF) and no effect with epidermal growth factor (EGF) (up to 50 nM).	Tetradecanoylphorbol Acetate	139-164	epidermal growth factor	Homo sapiens	303-306	
3958045-2	1986	In urokinase-producing human carcinoma cells (A1251), a 20-40-fold increase in urokinase mRNA level is obtained after treatment with 10 nM phorbol myristate acetate (PMA), a smaller effect (two- to fourfold) with 2 ng/ml platelet-derived growth factor (PDGF) and no effect with epidermal growth factor (EGF) (up to 50 nM).	Tetradecanoylphorbol Acetate	166-169	epidermal growth factor	Homo sapiens	278-301	
3958045-2	1986	In urokinase-producing human carcinoma cells (A1251), a 20-40-fold increase in urokinase mRNA level is obtained after treatment with 10 nM phorbol myristate acetate (PMA), a smaller effect (two- to fourfold) with 2 ng/ml platelet-derived growth factor (PDGF) and no effect with epidermal growth factor (EGF) (up to 50 nM).	Tetradecanoylphorbol Acetate	166-169	epidermal growth factor	Homo sapiens	303-306	
2433285-6	1987	The EGF-dependent increases in both inositol triphosphate production and phosphatidylinositol 4-monophosphate levels were inhibited by pretreatment of the cells with 12-O-tetradecanoylphorbol-13-acetate.	Tetradecanoylphorbol Acetate	166-202	epidermal growth factor	Homo sapiens	4-7	
3484478-5	1986	The tumor promoter 12-O-tetradecanoylphorbol 13-acetate completely inhibits the EGF- and serum-induced increases in [Ca2+]i without affecting basal [Ca2+]i levels.	Tetradecanoylphorbol Acetate	19-55	epidermal growth factor	Homo sapiens	80-83	
2982592-9	1985	TPA interacted with EGF by reducing the affinity of membrane receptors for [125I]iodo-EGF.	Tetradecanoylphorbol Acetate	0-3	epidermal growth factor	Homo sapiens	20-23	
2982592-9	1985	TPA interacted with EGF by reducing the affinity of membrane receptors for [125I]iodo-EGF.	Tetradecanoylphorbol Acetate	0-3	epidermal growth factor	Homo sapiens	86-89	
2982592-10	1985	Although the alteration in EGF-receptor interaction induced by TPA may play a role in mediating TPA"s biological effects, the additive effects of TPA and EGF on iodine metabolism suggest that TPA does not act solely through the EGF receptor-effector system.	Tetradecanoylphorbol Acetate	63-66	epidermal growth factor	Homo sapiens	27-30	
2982592-10	1985	Although the alteration in EGF-receptor interaction induced by TPA may play a role in mediating TPA"s biological effects, the additive effects of TPA and EGF on iodine metabolism suggest that TPA does not act solely through the EGF receptor-effector system.	Tetradecanoylphorbol Acetate	96-99	epidermal growth factor	Homo sapiens	27-30	
2982592-10	1985	Although the alteration in EGF-receptor interaction induced by TPA may play a role in mediating TPA"s biological effects, the additive effects of TPA and EGF on iodine metabolism suggest that TPA does not act solely through the EGF receptor-effector system.	Tetradecanoylphorbol Acetate	96-99	epidermal growth factor	Homo sapiens	27-30	
2982592-10	1985	Although the alteration in EGF-receptor interaction induced by TPA may play a role in mediating TPA"s biological effects, the additive effects of TPA and EGF on iodine metabolism suggest that TPA does not act solely through the EGF receptor-effector system.	Tetradecanoylphorbol Acetate	96-99	epidermal growth factor	Homo sapiens	27-30	
6321474-3	1984	Phosphoamino acid analysis of radiolabeled EGF receptors isolated from these cells revealed several differences: the relative abundance of phosphotyrosine in EGF receptors was increased in cells treated with EGF, but decreased in cells treated with TPA; the overall relative abundance of phosphothreonine in EGF receptors was decreased in cells treated with EGF, but remained constant within the limits of experimental detection in cells treated with TPA.	Tetradecanoylphorbol Acetate	249-252	epidermal growth factor	Homo sapiens	158-161	
6208480-4	1984	The receptor was phosphorylated on serine and threonine residues in normally growing and quiescent cells, and treatment with EGF or the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in a two- to threefold increase in receptor-bound phosphate.	Tetradecanoylphorbol Acetate	151-187	epidermal growth factor	Homo sapiens	125-128	
6208480-7	1984	Prior treatment with TPA inhibited the EGF-dependent appearance of phosphotyrosine in the receptor.	Tetradecanoylphorbol Acetate	21-24	epidermal growth factor	Homo sapiens	39-42	
2984222-2	1985	We have investigated the effects of the tumor promoter phorbol myristate acetate [PMA] on EGF/eTGF receptors in intact A431 cells.	Tetradecanoylphorbol Acetate	55-80	epidermal growth factor	Homo sapiens	90-93	
2984222-2	1985	We have investigated the effects of the tumor promoter phorbol myristate acetate [PMA] on EGF/eTGF receptors in intact A431 cells.	Tetradecanoylphorbol Acetate	82-85	epidermal growth factor	Homo sapiens	90-93	
2984222-3	1985	Treatment with PMA at 37 degrees C induces a complete loss of high-affinity (Kd = 35-50 pM) binding sites for eTGF and EGF on the cell surface of A431 cells.	Tetradecanoylphorbol Acetate	15-18	epidermal growth factor	Homo sapiens	110-122	
6208480-10	1984	Treatment of cells with TPA before addition of EGF inhibited all three of these EGF-dependent responses.	Tetradecanoylphorbol Acetate	24-27	epidermal growth factor	Homo sapiens	80-83	
6321474-3	1984	Phosphoamino acid analysis of radiolabeled EGF receptors isolated from these cells revealed several differences: the relative abundance of phosphotyrosine in EGF receptors was increased in cells treated with EGF, but decreased in cells treated with TPA; the overall relative abundance of phosphothreonine in EGF receptors was decreased in cells treated with EGF, but remained constant within the limits of experimental detection in cells treated with TPA.	Tetradecanoylphorbol Acetate	249-252	epidermal growth factor	Homo sapiens	158-161	
6321474-3	1984	Phosphoamino acid analysis of radiolabeled EGF receptors isolated from these cells revealed several differences: the relative abundance of phosphotyrosine in EGF receptors was increased in cells treated with EGF, but decreased in cells treated with TPA; the overall relative abundance of phosphothreonine in EGF receptors was decreased in cells treated with EGF, but remained constant within the limits of experimental detection in cells treated with TPA.	Tetradecanoylphorbol Acetate	249-252	epidermal growth factor	Homo sapiens	158-161	
6321474-3	1984	Phosphoamino acid analysis of radiolabeled EGF receptors isolated from these cells revealed several differences: the relative abundance of phosphotyrosine in EGF receptors was increased in cells treated with EGF, but decreased in cells treated with TPA; the overall relative abundance of phosphothreonine in EGF receptors was decreased in cells treated with EGF, but remained constant within the limits of experimental detection in cells treated with TPA.	Tetradecanoylphorbol Acetate	249-252	epidermal growth factor	Homo sapiens	158-161	
6321474-3	1984	Phosphoamino acid analysis of radiolabeled EGF receptors isolated from these cells revealed several differences: the relative abundance of phosphotyrosine in EGF receptors was increased in cells treated with EGF, but decreased in cells treated with TPA; the overall relative abundance of phosphothreonine in EGF receptors was decreased in cells treated with EGF, but remained constant within the limits of experimental detection in cells treated with TPA.	Tetradecanoylphorbol Acetate	451-454	epidermal growth factor	Homo sapiens	158-161	
6321474-3	1984	Phosphoamino acid analysis of radiolabeled EGF receptors isolated from these cells revealed several differences: the relative abundance of phosphotyrosine in EGF receptors was increased in cells treated with EGF, but decreased in cells treated with TPA; the overall relative abundance of phosphothreonine in EGF receptors was decreased in cells treated with EGF, but remained constant within the limits of experimental detection in cells treated with TPA.	Tetradecanoylphorbol Acetate	451-454	epidermal growth factor	Homo sapiens	158-161	
6321474-3	1984	Phosphoamino acid analysis of radiolabeled EGF receptors isolated from these cells revealed several differences: the relative abundance of phosphotyrosine in EGF receptors was increased in cells treated with EGF, but decreased in cells treated with TPA; the overall relative abundance of phosphothreonine in EGF receptors was decreased in cells treated with EGF, but remained constant within the limits of experimental detection in cells treated with TPA.	Tetradecanoylphorbol Acetate	451-454	epidermal growth factor	Homo sapiens	158-161	
6321474-3	1984	Phosphoamino acid analysis of radiolabeled EGF receptors isolated from these cells revealed several differences: the relative abundance of phosphotyrosine in EGF receptors was increased in cells treated with EGF, but decreased in cells treated with TPA; the overall relative abundance of phosphothreonine in EGF receptors was decreased in cells treated with EGF, but remained constant within the limits of experimental detection in cells treated with TPA.	Tetradecanoylphorbol Acetate	451-454	epidermal growth factor	Homo sapiens	158-161	
6321474-4	1984	Two-dimensional mapping of the radiolabeled phosphopeptides produced from EGF receptors isolated by immunoprecipitation and treated with trypsin revealed 9 independent labeled regions, 2 of which contained phosphothreonine and were present only in EGF- or TPA-treated cells.	Tetradecanoylphorbol Acetate	256-259	epidermal growth factor	Homo sapiens	74-77	
6321474-5	1984	These two phosphopeptide regions were more highly labeled in cells treated with TPA than with EGF.	Tetradecanoylphorbol Acetate	80-83	epidermal growth factor	Homo sapiens	94-97	
6323154-5	1983	Among a variety of phorbol esters tested, tetradecanoyl phorbol acetate, a potent tumor promotor, was shown to be the most effective compound in inhibiting 125I-labeled EGF binding to its receptors.	Tetradecanoylphorbol Acetate	42-71	epidermal growth factor	Homo sapiens	169-172	
6311852-0	1983	Effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the growth inhibitory and increased phosphatidylinositol (PI) responses induced by epidermal growth factor (EGF) in A431 cells.	Tetradecanoylphorbol Acetate	10-46	epidermal growth factor	Homo sapiens	139-162	
6311852-0	1983	Effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the growth inhibitory and increased phosphatidylinositol (PI) responses induced by epidermal growth factor (EGF) in A431 cells.	Tetradecanoylphorbol Acetate	10-46	epidermal growth factor	Homo sapiens	164-167	
6311852-0	1983	Effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the growth inhibitory and increased phosphatidylinositol (PI) responses induced by epidermal growth factor (EGF) in A431 cells.	Tetradecanoylphorbol Acetate	48-51	epidermal growth factor	Homo sapiens	139-162	
6311852-0	1983	Effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the growth inhibitory and increased phosphatidylinositol (PI) responses induced by epidermal growth factor (EGF) in A431 cells.	Tetradecanoylphorbol Acetate	48-51	epidermal growth factor	Homo sapiens	164-167	
6330113-1	1984	4 beta-Phorbol 12 beta-myristate 13 alpha-acetate (PMA) markedly inhibited the binding of low concentrations (less than 10(-9 m) of 125I-epidermal growth factor (EGF) to A431 human epidermoid carcinoma cells.	Tetradecanoylphorbol Acetate	51-54	epidermal growth factor	Homo sapiens	132-160	
6330113-1	1984	4 beta-Phorbol 12 beta-myristate 13 alpha-acetate (PMA) markedly inhibited the binding of low concentrations (less than 10(-9 m) of 125I-epidermal growth factor (EGF) to A431 human epidermoid carcinoma cells.	Tetradecanoylphorbol Acetate	51-54	epidermal growth factor	Homo sapiens	162-165	
6330113-4	1984	In order to examine this action of PMA on the EGF receptor, the receptor phosphorylation state was evaluated in A431 cells that had been incubated with [32P]phosphate for 3 h prior to the addition of PMA.	Tetradecanoylphorbol Acetate	35-38	epidermal growth factor	Homo sapiens	46-49