PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15666830-5	2004	TPA but not AII increased the level of the transcription factor JunB in nuclear extracts and the increase was partially abolished by the MEK1 inhibitor PD98059.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	64-68	
15666830-7	2004	Taken together these results suggest that TPA inhibits the AII-dependent activation of CYP11B2 via the p44/42 MAPK signaling pathway leading to an increase of the level of nuclear JunB.	Tetradecanoylphorbol Acetate	42-45	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	180-184	
15627897-4	2004	Here we analyzed the role of AP-1 on the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced human hepatocellular transformation.	Tetradecanoylphorbol Acetate	41-77	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	29-33	
15329596-0	2004	Sevoflurane inhibits phorbol-myristate-acetate-induced activator protein-1 activation in human T lymphocytes in vitro: potential role of the p38-stress kinase pathway.	Tetradecanoylphorbol Acetate	21-46	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	55-74	
15329596-6	2004	Phorbol-myristate-acetate-dependent effects of sevoflurane on the phosphorylation of the mitogen-activated protein kinases were studied using Western blots, the trans-activating potency of AP-1 was determined using reporter gene assays, and the cytokine release was measured using enzyme-linked immunosorbent assays.	Tetradecanoylphorbol Acetate	0-25	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	189-193	
15627897-4	2004	Here we analyzed the role of AP-1 on the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced human hepatocellular transformation.	Tetradecanoylphorbol Acetate	79-82	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	29-33	
15627897-5	2004	TPA promoted the formation of anchorage-independent colonies, induced the AP-1 activity, and enhanced the DNA-binding ability of AP-1 in human hepatocytes.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	74-78	
15627897-5	2004	TPA promoted the formation of anchorage-independent colonies, induced the AP-1 activity, and enhanced the DNA-binding ability of AP-1 in human hepatocytes.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	129-133	
15627897-6	2004	The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway.	Tetradecanoylphorbol Acetate	94-97	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	186-190	
15627897-6	2004	The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway.	Tetradecanoylphorbol Acetate	106-109	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	118-122	
15627897-6	2004	The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway.	Tetradecanoylphorbol Acetate	106-109	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	186-190	
15627897-6	2004	The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway.	Tetradecanoylphorbol Acetate	106-109	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	118-122	
15627897-6	2004	The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway.	Tetradecanoylphorbol Acetate	106-109	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	186-190	
15627897-7	2004	Moreover, retinoic acid and PD98059, which inhibited the AP-1 activity, abolished the TPA-induced transformation.	Tetradecanoylphorbol Acetate	86-89	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	57-61	
15627897-8	2004	Our findings indicated that AP-1 and ERKs activations were required for TPA-induced human hepatocellular transformation.	Tetradecanoylphorbol Acetate	72-75	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	28-32	
14627504-8	2003	The activation of AP-1 induced by PMA was also extensively inhibited by resveratrol at 0.1, 1, and 10 micromol/L.	Tetradecanoylphorbol Acetate	34-37	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	18-22	
15037572-9	2004	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased nuclear AP1 factor level and binding to the hINV gene AP1-1 response element.	Tetradecanoylphorbol Acetate	15-51	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	171-174	
15037572-9	2004	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased nuclear AP1 factor level and binding to the hINV gene AP1-1 response element.	Tetradecanoylphorbol Acetate	15-51	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	217-222	
15037572-9	2004	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased nuclear AP1 factor level and binding to the hINV gene AP1-1 response element.	Tetradecanoylphorbol Acetate	53-56	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	171-174	
15037572-9	2004	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased nuclear AP1 factor level and binding to the hINV gene AP1-1 response element.	Tetradecanoylphorbol Acetate	53-56	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	217-222	
14673171-4	2004	We report here that ATF-3, JunB, and BRG-1 (the ATPase subunit of the 2-MDa human chromatin remodeling machine SWI/SNF) are recruited to the 3" boundary of nuc-1 following phorbol myristate acetate stimulation in Jurkat T cells.	Tetradecanoylphorbol Acetate	172-197	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-31	
12592382-4	2003	On the other hand, expressions of proto-oncogene c-jun, junB and c-fos were induced by TPA and Saikosaponin a during 30 min to 6 h of treatment.	Tetradecanoylphorbol Acetate	87-90	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	56-60	
12297018-5	2002	Likewise, the TPA-induced DNA binding of the activator protein-1 (AP-1) was inhibited by curcumin pretreatment.	Tetradecanoylphorbol Acetate	14-17	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	45-64	
12123542-3	2002	RESULTS: Transient transfection of RARbeta expression vector into MKN-45 cells resulted in the RARbeta concentration dependent repression of AP-1 activity induced by 12-o-tetradecanoylphorbol-13-acetate (TPA), regardless of the presence of ATRA.	Tetradecanoylphorbol Acetate	166-202	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	141-145	
12123542-3	2002	RESULTS: Transient transfection of RARbeta expression vector into MKN-45 cells resulted in the RARbeta concentration dependent repression of AP-1 activity induced by 12-o-tetradecanoylphorbol-13-acetate (TPA), regardless of the presence of ATRA.	Tetradecanoylphorbol Acetate	204-207	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	141-145	
12009305-7	2002	For AP-1 binding activity induced by TPA, the repressive effect of ATRA was only observed in BGC-823 and RARalpha and RARbeta stably transfected MKN-45 cells, but not in intact MKN-45 cells.	Tetradecanoylphorbol Acetate	37-40	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	4-8	
12297018-5	2002	Likewise, the TPA-induced DNA binding of the activator protein-1 (AP-1) was inhibited by curcumin pretreatment.	Tetradecanoylphorbol Acetate	14-17	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-70	
11714372-8	2001	After stimulation by PMA, a dose-dependent inhibition of AP-1 was observed with the six phenolic acids in the 20 nM-20 microM concentration range: gallic acid > caffeic > protocatechic, paracoumaric, sinapic acids > ferulic acid.	Tetradecanoylphorbol Acetate	21-24	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	57-61	
11861377-6	2002	We also demonstrated that nobiletin suppressed the 12-O-tetradecanoylphorbol 13-acetate-induced binding activity of activator protein-1.	Tetradecanoylphorbol Acetate	51-87	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	116-135	
12162432-4	2002	TPA and EGF, acting through the MAP kinase pathway, activate AP-1 and subsequently NF-kappaB proteins and downstream transcription processes that are involved in the transformation response in transformation-sensitive (P+) JB6 cells.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	61-65	
11948401-9	2002	The transcriptional activities of full-length JunB and full-length Fra-1, but not the transactivation domain fusions, were increased by TPA treatment and suppressed by RA.	Tetradecanoylphorbol Acetate	136-139	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	46-50	
11751871-3	2002	Further analysis demonstrated that serum or 12-O-tetradecanoylphorbol-13-acetate activation of several immediate early genes including fos, fosB, junB, and egr1 was inhibited by Wnt signaling.	Tetradecanoylphorbol Acetate	44-80	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	146-150	
11605784-4	2001	NF-kappaB and AP-1 DNA-binding abilities were significantly increased both at baseline and after stimulation by phorbol 12-myristate 13-acetate (TPA) in PBMC from MCNS patients compared with controls, but declined to normal levels after treatment with dexamethasone (DEX).	Tetradecanoylphorbol Acetate	145-148	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-18	
11216470-8	2000	Likewise, both compounds inhibited NF-kappaB and AP-1 activation in cultured human promyelocytic leukemia (HL-60) cells stimulated with TPA.	Tetradecanoylphorbol Acetate	136-139	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	49-53	
11532088-5	2001	The effect of LMW heparin on the binding of nuclear proteins to a regulatory activator protein-1 (AP-1) site, which mediates the high glucose and PMA responsiveness of the TGF-beta 1 promoter, was studied by electrophoretic mobility shift assays.	Tetradecanoylphorbol Acetate	146-149	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-96	
11532088-5	2001	The effect of LMW heparin on the binding of nuclear proteins to a regulatory activator protein-1 (AP-1) site, which mediates the high glucose and PMA responsiveness of the TGF-beta 1 promoter, was studied by electrophoretic mobility shift assays.	Tetradecanoylphorbol Acetate	146-149	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	98-102	
11448162-0	2001	12-O-tetradecanoylphorbol-13-acetate induces Epstein-Barr virus reactivation via NF-kappaB and AP-1 as regulated by protein kinase C and mitogen-activated protein kinase.	Tetradecanoylphorbol Acetate	0-36	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	95-99	
11448162-6	2001	Electrophoretic mobility shift assays demonstrated that transcription factors NF-kappaB and AP-1 were also activated by TPA in a time-dependent manner.	Tetradecanoylphorbol Acetate	120-123	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	92-96	
11448162-10	2001	These results show that TPA induces EBV reactivation via NF-kappaB and AP-1 and that PKC is an important mediator in regulating gene expression leading to EBV reactivation after TPA treatment of GT38 cells.	Tetradecanoylphorbol Acetate	24-27	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	71-75	
10807873-8	2000	Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele.	Tetradecanoylphorbol Acetate	0-31	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-77	
10807873-8	2000	Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele.	Tetradecanoylphorbol Acetate	0-31	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	104-108	
10807873-8	2000	Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele.	Tetradecanoylphorbol Acetate	33-36	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-77	
10807873-8	2000	Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele.	Tetradecanoylphorbol Acetate	33-36	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	104-108	
11605784-4	2001	NF-kappaB and AP-1 DNA-binding abilities were significantly increased both at baseline and after stimulation by phorbol 12-myristate 13-acetate (TPA) in PBMC from MCNS patients compared with controls, but declined to normal levels after treatment with dexamethasone (DEX).	Tetradecanoylphorbol Acetate	112-143	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-18	
11145168-1	2000	Interaction between a tumor promoter, 12-O-tetradecanoylphorbol 13-acetate (TPA), and ligands of nuclear receptors has been interpreted as the result of crosstalk between the nuclear receptors and oncogenic transcription factor AP-1.	Tetradecanoylphorbol Acetate	38-74	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	228-232	
11145168-1	2000	Interaction between a tumor promoter, 12-O-tetradecanoylphorbol 13-acetate (TPA), and ligands of nuclear receptors has been interpreted as the result of crosstalk between the nuclear receptors and oncogenic transcription factor AP-1.	Tetradecanoylphorbol Acetate	76-79	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	228-232	
11121152-6	2000	Atopic dermatitis keratinocyte nuclear lysates had higher constitutive levels of c-Jun, and phorbol myristate acetate promoted an earlier and stronger expression of c-Jun, JunB, and of the phosphorylated forms of c-Fos.	Tetradecanoylphorbol Acetate	92-117	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	172-176	
9837861-9	1998	The results showed that TPA induced endogenous MnSOD expression and inhibited both AP-1 and NF-kappaB.	Tetradecanoylphorbol Acetate	24-27	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	83-87	
10514454-10	1999	Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway.	Tetradecanoylphorbol Acetate	25-28	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	86-90	
10514454-10	1999	Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway.	Tetradecanoylphorbol Acetate	70-73	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	86-90	
10514454-10	1999	Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway.	Tetradecanoylphorbol Acetate	70-73	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	86-90	
10329043-7	1999	RESULTS: The CCA reporter line exhibited a radiation dose-responsive induction of AP-1 activity that was decreased by 5 microM 9cRA and increased by 50 ng/ml TPA.	Tetradecanoylphorbol Acetate	158-161	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	82-86	
10329043-8	1999	Simultaneous treatment with TPA and 9cRA prevented 9cRA repression of AP-1 and resulted in AP-1 activity above basal level.	Tetradecanoylphorbol Acetate	28-31	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-74	
10329043-8	1999	Simultaneous treatment with TPA and 9cRA prevented 9cRA repression of AP-1 and resulted in AP-1 activity above basal level.	Tetradecanoylphorbol Acetate	28-31	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	91-95	
10329043-11	1999	CONCLUSION: Although TPA prevented AP-1 repression by 9cRA, it did not prevent radiosensitization in CCA cultures, therefore the mechanism of radiosensitization of CCA by 9cRA is independent of AP-1 repression.	Tetradecanoylphorbol Acetate	21-24	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	35-39	
10514454-9	1999	However, it inhibited TPA-induced AP-1 activity in ZR75-1 cells and the constitutive AP-1 activity in H460 and H292 cells.	Tetradecanoylphorbol Acetate	22-25	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	34-38	
9419345-2	1998	Tumor promoters, such as 12-O-tetradecanoylphorbol 13-acetate (TPA) or epidermal growth factor (EGF), induce high levels of activator protein 1 (AP-1) activity and large, tumorigenic, anchorage-independent colonies in soft agar at a high frequency in JB6 P+ cells, but not in JB6 P- cells.	Tetradecanoylphorbol Acetate	25-61	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	124-143	
9668098-8	1998	Further mutational analysis revealed that full TPA induction required interplay between several regulatory elements with homology to Ets, AP-1, and CAATT/enhancer binding protein C/EBP sites.	Tetradecanoylphorbol Acetate	47-50	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	138-142	
9668098-9	1998	In addition, deletion or mutation of a 10-base pair region juxtaposed to the AP-1 site dramatically increased TPA induced FGF-BP gene expression.	Tetradecanoylphorbol Acetate	110-113	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-81	
9668098-11	1998	Gel shift analysis showed specific and TPA-inducible protein binding to the Ets, AP-1, and C/EBP sites.	Tetradecanoylphorbol Acetate	39-42	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	81-85	
9523597-8	1998	These effects are compatible with (but likely not exclusively due to) an effect on the DNA binding of the 12-O-tetradecanoylphorbol 13-acetate response element to the AP-1 family of transcription factors.	Tetradecanoylphorbol Acetate	106-142	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	167-171	
9419345-2	1998	Tumor promoters, such as 12-O-tetradecanoylphorbol 13-acetate (TPA) or epidermal growth factor (EGF), induce high levels of activator protein 1 (AP-1) activity and large, tumorigenic, anchorage-independent colonies in soft agar at a high frequency in JB6 P+ cells, but not in JB6 P- cells.	Tetradecanoylphorbol Acetate	25-61	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	145-149	
9419345-2	1998	Tumor promoters, such as 12-O-tetradecanoylphorbol 13-acetate (TPA) or epidermal growth factor (EGF), induce high levels of activator protein 1 (AP-1) activity and large, tumorigenic, anchorage-independent colonies in soft agar at a high frequency in JB6 P+ cells, but not in JB6 P- cells.	Tetradecanoylphorbol Acetate	63-66	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	124-143	
9467952-4	1998	Whereas insulin stimulates prolonged induction of c-jun, but not of junB mRNA, resulting in c-jun expression during the entire G1 period, the growth inhibitor TPA induces junB much longer than c-jun.	Tetradecanoylphorbol Acetate	159-162	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	171-175	
9467952-5	1998	Inhibition of the Erk2 pathway by PD98059, specific for the upstream MAP kinase kinase (MEK1), abolishes TPA-stimulated junB but not insulin-induced c-jun.	Tetradecanoylphorbol Acetate	105-108	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	120-124	
9434740-10	1997	In vitro DNA binding studies confirmed strong AP-1 activation under conditions where NF kappa B is blocked but the MnSOD transcript is strongly induced (e.g., PMA treatment in the presence of PDTC).	Tetradecanoylphorbol Acetate	159-162	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	46-50	
9388222-5	1997	However, AP1 induction by 4beta-phorbol 12-myristate 13-acetate, which up-regulates Ras activity in a protein kinase C-dependent, TCR/tyrosine kinase-independent manner, was not affected by Cbl overexpression.	Tetradecanoylphorbol Acetate	26-63	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	9-12	
9176246-9	1997	The GR antagonist RU-486 inhibited the repressive effect of Dex on TNF-alpha-induced NF-kappa B activity by 81% but only counteracted the repressive effect of Dex on TPA-induced AP-1 activity by 43%.	Tetradecanoylphorbol Acetate	166-169	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	178-182	
9356353-1	1997	Activating protein-1 (AP-1) binding TPA responsive elements (TRE) are located downstream of the transcription initiation site in the U5 region of the HIV-1 long terminal repeat (LTR).	Tetradecanoylphorbol Acetate	36-39	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	22-26	
9377579-0	1997	Re-expression of elafin in 21MT2 breast carcinomas by phorbol 12-myristate 13-acetate is mediated by the Ap1 site in the elafin promoter.	Tetradecanoylphorbol Acetate	54-85	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	105-108	
9377579-4	1997	By deletion analysis and mutagenesis, we have identified the Ap1 site in the promoter as the cis element mediating transcriptional activation of elafin in 70N normal breast cells and its induction by phorbol 12-myristate 13-acetate (PMA) in 21MT2 breast tumors.	Tetradecanoylphorbol Acetate	200-231	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	61-64	
9377579-4	1997	By deletion analysis and mutagenesis, we have identified the Ap1 site in the promoter as the cis element mediating transcriptional activation of elafin in 70N normal breast cells and its induction by phorbol 12-myristate 13-acetate (PMA) in 21MT2 breast tumors.	Tetradecanoylphorbol Acetate	233-236	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	61-64	
9419345-2	1998	Tumor promoters, such as 12-O-tetradecanoylphorbol 13-acetate (TPA) or epidermal growth factor (EGF), induce high levels of activator protein 1 (AP-1) activity and large, tumorigenic, anchorage-independent colonies in soft agar at a high frequency in JB6 P+ cells, but not in JB6 P- cells.	Tetradecanoylphorbol Acetate	63-66	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	145-149	
9419345-5	1998	TPA and EGF induce transactivation of AP-1 activity in P+ cells but not in P- cells.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	38-42	
9419345-7	1998	Stable transfection of wild-type MAPK (Erk2) into P- cells restored its response to TPA and EGF for both AP-1 activation and cell transformation.	Tetradecanoylphorbol Acetate	84-87	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	105-109	
8955111-3	1996	A series of deletion and mutation analyses of the enhancer sequences defined the 45-base pair core region (DR-1 core) containing two short elements with similarity to AP-1 (12-O-tetradecanoylphorbol-13-acetate response element; TRE) and CREB/ATF (cyclic AMP response element; CRE) binding sites, both of which were necessary for full enhancer activity.	Tetradecanoylphorbol Acetate	173-209	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	167-171	
9108029-8	1997	This process seems to be essential for AP-1 activation by redox modification because co-overexpression of TRX and Ref-1 in COS-7 cells potentiated AP-1 activity only after TRX was transported into the nucleus by phorbol 12-myristate 13 acetate treatment.	Tetradecanoylphorbol Acetate	212-243	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	39-43	
9138284-3	1997	The Activator Protein-1 (AP-1) site at approximately -70 bp upstream of the transcriptional start site has long been thought to play a dominant role in the transcriptional activation of the MMP promoters, particularly in response to stimulation with phorbol myristate acetate (PMA).	Tetradecanoylphorbol Acetate	250-275	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	4-23	
9138284-3	1997	The Activator Protein-1 (AP-1) site at approximately -70 bp upstream of the transcriptional start site has long been thought to play a dominant role in the transcriptional activation of the MMP promoters, particularly in response to stimulation with phorbol myristate acetate (PMA).	Tetradecanoylphorbol Acetate	250-275	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	25-29	
9138284-3	1997	The Activator Protein-1 (AP-1) site at approximately -70 bp upstream of the transcriptional start site has long been thought to play a dominant role in the transcriptional activation of the MMP promoters, particularly in response to stimulation with phorbol myristate acetate (PMA).	Tetradecanoylphorbol Acetate	277-280	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	4-23	
9138284-3	1997	The Activator Protein-1 (AP-1) site at approximately -70 bp upstream of the transcriptional start site has long been thought to play a dominant role in the transcriptional activation of the MMP promoters, particularly in response to stimulation with phorbol myristate acetate (PMA).	Tetradecanoylphorbol Acetate	277-280	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	25-29	
8631129-10	1996	TCDD did not increase mRNA of c-fos, c-jun, junB or junD (in contrast to TPA which markedly increased the expression of c-fos and junB), nor did TCDD increase AP-1 activity.	Tetradecanoylphorbol Acetate	73-76	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	130-134	
8649827-5	1996	In cultured ovarian cancer cells, c-jun and jun-B expression is inducible by serum and TPA and is therefore not constitutive.	Tetradecanoylphorbol Acetate	87-90	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	44-49	
7982981-0	1994	In vitro study of functional involvement of Sp1, NF-kappa B/Rel, and AP1 in phorbol 12-myristate 13-acetate-mediated HIV-1 long terminal repeat activation.	Tetradecanoylphorbol Acetate	76-107	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	69-72	
11725057-7	1995	Both the AP-1/AP-2/SP-1 dyad protein binding region and, to a lesser extent, the YY1 tandem-repeat cluster conferred responsiveness to TPA when placed upstream of a heterologous promoter in transient expression assays.	Tetradecanoylphorbol Acetate	135-138	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	9-13	
7898939-1	1995	The product of the junB gene is a member of the AP-1 family of transcription factors that activate transcription by binding to TPA-responsive elements (TREs) within the promoters of target genes.	Tetradecanoylphorbol Acetate	127-130	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	19-23	
7864072-3	1995	TNF-alpha, IL-1 beta and phorbol myristate acetate (PMA) treatment increased AP-1 and NF kappa B DNA binding by up to 200% but decreased CREB binding (38%) over a 60-min time course.	Tetradecanoylphorbol Acetate	25-50	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-81	
7864072-3	1995	TNF-alpha, IL-1 beta and phorbol myristate acetate (PMA) treatment increased AP-1 and NF kappa B DNA binding by up to 200% but decreased CREB binding (38%) over a 60-min time course.	Tetradecanoylphorbol Acetate	52-55	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-81	
8114743-5	1994	We demonstrate that tetradecanoyl phorbol acetate treatment results in a marked and prolonged increase in AP-1 binding activity on these elements, which can be accounted for almost entirely by c-jun and junB.	Tetradecanoylphorbol Acetate	20-49	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	106-110	
8171009-4	1994	Within this sequence there is a 12-O-tetradecanoylphorbol 13-acetate (TPA)-responsive element (TRE) which is essential for T1 promoter induction in response to the forced expression of the transcription factor AP-1 in NIH 3T3 fibroblasts and F9 teratocarcinoma cells.	Tetradecanoylphorbol Acetate	32-68	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	210-214	
8171009-4	1994	Within this sequence there is a 12-O-tetradecanoylphorbol 13-acetate (TPA)-responsive element (TRE) which is essential for T1 promoter induction in response to the forced expression of the transcription factor AP-1 in NIH 3T3 fibroblasts and F9 teratocarcinoma cells.	Tetradecanoylphorbol Acetate	70-73	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	210-214	
8001557-4	1994	Hydrogen peroxide prevented phorbol-myristate-acetate-stimulated AP-1 binding to DNA but stimulated it if protein kinase C was down-regulated or inhibited.	Tetradecanoylphorbol Acetate	28-53	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	65-69	
8114743-5	1994	We demonstrate that tetradecanoyl phorbol acetate treatment results in a marked and prolonged increase in AP-1 binding activity on these elements, which can be accounted for almost entirely by c-jun and junB.	Tetradecanoylphorbol Acetate	20-49	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	203-207	
8396805-10	1993	The response to the phorbol ester TPA also required a cooperation of M33 and AP1.	Tetradecanoylphorbol Acetate	34-37	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-80	
8404639-4	1993	In K562 cells, this selective junB mRNA induction was synergistically augmented by treatment with 12-O-tetradecanoyl phorbol-13-acetate but not affected by forskolin.	Tetradecanoylphorbol Acetate	98-135	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-34	
8180129-6	1994	AP-1 binding activity was enhanced by 12-O-tetradecanoylphorbol-13-acetate (TPA) and in a temporally dependent manner, with conversion of a high to low mobility band shift occurring after a 12-h exposure to TPA.	Tetradecanoylphorbol Acetate	38-74	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-4	
8180129-6	1994	AP-1 binding activity was enhanced by 12-O-tetradecanoylphorbol-13-acetate (TPA) and in a temporally dependent manner, with conversion of a high to low mobility band shift occurring after a 12-h exposure to TPA.	Tetradecanoylphorbol Acetate	76-79	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-4	
8180129-6	1994	AP-1 binding activity was enhanced by 12-O-tetradecanoylphorbol-13-acetate (TPA) and in a temporally dependent manner, with conversion of a high to low mobility band shift occurring after a 12-h exposure to TPA.	Tetradecanoylphorbol Acetate	207-210	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-4	
8180129-7	1994	After a 72-h exposure, AP-1 binding activity was maximally increased by 1 nM TPA and remained elevated to a similar degree even after treatment with 600 nM TPA.	Tetradecanoylphorbol Acetate	77-80	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	23-27	
8180129-7	1994	After a 72-h exposure, AP-1 binding activity was maximally increased by 1 nM TPA and remained elevated to a similar degree even after treatment with 600 nM TPA.	Tetradecanoylphorbol Acetate	156-159	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	23-27	
8180129-8	1994	Enhanced AP-1 binding activity was dependent upon continuous exposure to TPA and was not secondary to differentiation.	Tetradecanoylphorbol Acetate	73-76	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	9-13	
8180129-9	1994	A 72-h treatment with one nM TPA maximally increased expression of c-jun, krox-24, and jun-B mRNA transcripts.	Tetradecanoylphorbol Acetate	29-32	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	87-92	
1445798-4	1992	junB and fosB were rapidly induced following stimulation with TPA.	Tetradecanoylphorbol Acetate	62-65	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-4	
8389757-8	1993	Other studies further demonstrate that the jun-B and fra-1 genes are induced by TPA in both HL-60/vinc and HL-60/vinc/R cells, whereas c-fos expression is attenuated in the HL-60/vinc line.	Tetradecanoylphorbol Acetate	80-83	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	43-48	
1634545-0	1992	Interaction of AP-1-, AP-2-, and Sp1-like proteins with two distinct sites in the upstream regulatory region of the plasminogen activator inhibitor-1 gene mediates the phorbol 12-myristate 13-acetate response.	Tetradecanoylphorbol Acetate	168-199	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	15-19	
7860222-2	1993	The promoter and adjacent regulatory sequences of the 92-kD type IV collagenase have been identified previously and three cis-acting elements homologous to the binding sites for AP-1, NF-KB and SP-1 proteins contributed to induction of the promoter activity by 12-O-tetradecanoylphorbol 13-acetate (TPA) and tumor necrosis factor (TNF-alpha) in HT1080 cells.	Tetradecanoylphorbol Acetate	261-297	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	178-182	
7860222-2	1993	The promoter and adjacent regulatory sequences of the 92-kD type IV collagenase have been identified previously and three cis-acting elements homologous to the binding sites for AP-1, NF-KB and SP-1 proteins contributed to induction of the promoter activity by 12-O-tetradecanoylphorbol 13-acetate (TPA) and tumor necrosis factor (TNF-alpha) in HT1080 cells.	Tetradecanoylphorbol Acetate	299-302	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	178-182	
1445798-6	1992	The expression of fos and jun during T-cell activation was accompanied by increased specific binding of JunB, FosB, and fos-related antigen containing complexes to the TPA responsive element.	Tetradecanoylphorbol Acetate	168-171	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	104-108	
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	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	13-18	
1653238-11	1991	Two putative 12-O-tetradecanoyl-phorbol-13-acetate (TPA) response elements, that might serve as binding sites for the transcription factor AP-1 and a consensus sequence of a transforming growth factor beta 1 (TGF-beta 1) inhibitory element were found in the promoter region.	Tetradecanoylphorbol Acetate	13-50	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	139-143	
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	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	138-142	
1655978-8	1991	TPA induced c-fos and junB mRNAs transiently and preceding NGF mRNA induction but c-jun mRNA remained undetectable.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	22-26	
1653238-11	1991	Two putative 12-O-tetradecanoyl-phorbol-13-acetate (TPA) response elements, that might serve as binding sites for the transcription factor AP-1 and a consensus sequence of a transforming growth factor beta 1 (TGF-beta 1) inhibitory element were found in the promoter region.	Tetradecanoylphorbol Acetate	52-55	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	139-143	
1901643-3	1991	This fragment contains a sequence with a high degree of similarity to the binding site for the transcription factor activator protein-1 (AP-1) and indeed, the AP-1 sequence of this fragment is necessary but not sufficient for the maximal response to phorbol 12-myristate 13-acetate (phorbol) or interleukin-1.	Tetradecanoylphorbol Acetate	250-281	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	116-135	
1900155-6	1991	The role of Jun-containing TRE binding proteins in promoting B cell cycle progression remains uncertain inasmuch as Jun-B has been associated with transcriptional inhibition of the TPA response element, rather than activation as produced by c-Jun.	Tetradecanoylphorbol Acetate	181-184	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	116-121	
1711045-8	1991	The promoter region also contains several potential binding sites for the transcription factors AP-1 and AP-2; consistent with the presence of these sites, Northern blot analysis demonstrated that the level of VEGF transcripts is elevated in cultured vascular smooth muscle cells after treatment with the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate.	Tetradecanoylphorbol Acetate	319-356	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	96-100	
1901643-3	1991	This fragment contains a sequence with a high degree of similarity to the binding site for the transcription factor activator protein-1 (AP-1) and indeed, the AP-1 sequence of this fragment is necessary but not sufficient for the maximal response to phorbol 12-myristate 13-acetate (phorbol) or interleukin-1.	Tetradecanoylphorbol Acetate	250-281	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	137-141	
1901643-3	1991	This fragment contains a sequence with a high degree of similarity to the binding site for the transcription factor activator protein-1 (AP-1) and indeed, the AP-1 sequence of this fragment is necessary but not sufficient for the maximal response to phorbol 12-myristate 13-acetate (phorbol) or interleukin-1.	Tetradecanoylphorbol Acetate	250-281	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	159-163	
34114342-5	2021	The NF-kB /AP-1 transcription factors mediated effects of LPS and TPA on 20alpha-HSD gene transcription.	Tetradecanoylphorbol Acetate	66-69	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	11-15	
2007095-3	1991	The present studies have examined the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of jun-B gene expression during induction of monocytic differentiation.	Tetradecanoylphorbol Acetate	49-85	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-118	
2007095-3	1991	The present studies have examined the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of jun-B gene expression during induction of monocytic differentiation.	Tetradecanoylphorbol Acetate	87-90	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-118	
2007095-5	1991	In contrast, treatment with TPA was associated with rapid increases in jun-B mRNA levels that were maximal at 3 h and remained elevated at 48 h. The induction of jun-B expression by TPA in these cells preceded that of the c-jun and c-fos genes.	Tetradecanoylphorbol Acetate	28-31	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	71-76	
2007095-5	1991	In contrast, treatment with TPA was associated with rapid increases in jun-B mRNA levels that were maximal at 3 h and remained elevated at 48 h. The induction of jun-B expression by TPA in these cells preceded that of the c-jun and c-fos genes.	Tetradecanoylphorbol Acetate	182-185	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	71-76	
2007095-9	1991	In contrast, inhibition of protein synthesis was associated with superinduction of TPA-induced jun-B mRNA levels and an increase in stability of this transcript.	Tetradecanoylphorbol Acetate	83-86	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	95-100	
2513128-1	1989	c-Jun, Jun-B, and Jun-D proteins bind to the TPA response element (TRE) either as homodimers or as Jun-Fos heterodimers.	Tetradecanoylphorbol Acetate	45-48	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	7-12	
34093777-6	2021	The results demonstrated that triptolide decreased the expression of MMP-9 through inhibition of the TPA-induced phosphorylation of extracellular signal-regulated kinase (ERK) and the downregulation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) activity.	Tetradecanoylphorbol Acetate	101-104	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	240-259	
2513129-2	1989	jun-B is less potent that c-jun in transforming and immortalizing primary rat embryo cells in cooperation with activated ras (effects enhanced by c-fos and TPA); unlike c-jun, jun-B does not transform Rat-1A cells alone.	Tetradecanoylphorbol Acetate	156-159	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5	
3034432-3	1987	Footprinting analysis indicated that these TPA-responsive elements (TREs) are recognized by a common cellular protein: the previously described transcription factor AP-1.	Tetradecanoylphorbol Acetate	43-46	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	165-169	
27035791-12	2016	Our findings revealed that the anti-invasive effects of Rev-AuNPs in response to TPA-stimulation were mediated by the suppression of MMP-9, COX-2, NF-kappaB, AP-1, PI3K/Akt and ERK and/or the activation of HO-1 signaling cascades.	Tetradecanoylphorbol Acetate	81-84	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	158-162	
33760219-0	2021	Bruton"s agammaglobulinemia tyrosine kinase (Btk) regulates TPA-induced breast cancer cell invasion via PLCgamma2/PKCbeta/NF-kappaB/AP-1-dependent matrix metalloproteinase-9 activation.	Tetradecanoylphorbol Acetate	60-63	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	132-136	
30466990-0	2018	Orientin inhibits invasion by suppressing MMP-9 and IL-8 expression via the PKCalpha/ ERK/AP-1/STAT3-mediated signaling pathways in TPA-treated MCF-7 breast cancer cells.	Tetradecanoylphorbol Acetate	132-135	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-94	
30466990-7	2018	TPA-induced membrane translocation of protein kinase C alpha (PKCalpha), phosphorylation of extracellular signal regulated kinase (ERK), and nuclear translocations of activator protein-1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) were downregulated by orientin.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	167-186	
30466990-7	2018	TPA-induced membrane translocation of protein kinase C alpha (PKCalpha), phosphorylation of extracellular signal regulated kinase (ERK), and nuclear translocations of activator protein-1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) were downregulated by orientin.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	188-192	
29371085-6	2018	MMPP inhibited PMA-induced membrane translocation of PKCdelta, phosphorylation of JNK, and nuclear translocation of AP-1, resulting in downregulation of cyclooxygenase-2 and chemokine ligand 5 production.	Tetradecanoylphorbol Acetate	15-18	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	116-120	
29371085-7	2018	These findings indicate that MMPP inhibits inflammatory responses in THP-1 cells by mitigating PMA-induced activation of PKCdelta and JNK and nuclear translocation of AP-1.	Tetradecanoylphorbol Acetate	95-98	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	167-171	
28927117-0	2017	Salvia miltiorrhiza extract inhibits TPA-induced MMP-9 expression and invasion through the MAPK/AP-1 signaling pathway in human breast cancer MCF-7 cells.	Tetradecanoylphorbol Acetate	37-40	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	96-100	
28927117-10	2017	SME suppressed TPA-induced MMP-9 expression and MCF-7 cell invasion by blocking the transcriptional activation of AP-1.	Tetradecanoylphorbol Acetate	15-18	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	114-118	
27538486-7	2017	In non-Hodgkin B-cell lines, small interfering RNA-mediated PDLIM2 knockdown results in superactivation of TFs NF-kappaB and AP-1 following phorbol 12-myristate 13-acetate (PMA) stimulation.	Tetradecanoylphorbol Acetate	140-171	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	125-129	
30133131-6	2018	TPA-induced membrane translocation of PKCalpha, phosphorylation of JNK, and the nuclear translocations of AP-1 and NF-kappaB were downregulated by mLU8C-PU in MCF-7 cells.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	106-110	
30133131-8	2018	These results indicate that mLU8C-PU inhibits migratory and invasive responses in MCF-7 breast cancer cells by suppressing MMP-9 and IL-8 expression through mitigating TPA-induced PKCalpha, JNK activation, and the nuclear translocation of AP-1 and NF-kappaB.	Tetradecanoylphorbol Acetate	168-171	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	239-243	
29371085-0	2018	(E)-2-Methoxy-4-(3-(4-methoxyphenyl) prop-1-en-1-yl) phenol attenuates PMA-induced inflammatory responses in human monocytic cells through PKCdelta/JNK/AP-1 pathways.	Tetradecanoylphorbol Acetate	71-74	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	152-156	
27035791-7	2016	Furthermore, Rev-AuNP treatment remarkably downregulated TPA-induced nuclear translocation and transcriptional activation of nuclear transcription factor-kappaB (NF-kappaB) and activator protein-1 (AP-1).	Tetradecanoylphorbol Acetate	57-60	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	177-196	
27035791-7	2016	Furthermore, Rev-AuNP treatment remarkably downregulated TPA-induced nuclear translocation and transcriptional activation of nuclear transcription factor-kappaB (NF-kappaB) and activator protein-1 (AP-1).	Tetradecanoylphorbol Acetate	57-60	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	198-202	
25051397-6	2014	The expression levels of AP-1 transcription factors were increased in HepG2 cells following induction by phorbol 12-myristate 13-acetate, but ginsenoside Rh2 suppressed this induced AP-1 expression.	Tetradecanoylphorbol Acetate	105-136	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	25-29	
23615401-9	2013	Furthermore, TPA-induced extracellular signal-regulated kinase (ERK) 1/2 and Akt phosphorylation and the DNA binding activity of activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) were attenuated by pretreatment with AP and HO-1 end products.	Tetradecanoylphorbol Acetate	13-16	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	129-148	
24317440-10	2014	Furthermore, in MNK-74 and SC-M1 cells treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) and 5 or 10 microM of ATPR significantly suppressed the activity of the AP-1 reporter as compared to treatment with ATRA (P<0.05).	Tetradecanoylphorbol Acetate	52-88	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	167-171	
24317440-10	2014	Furthermore, in MNK-74 and SC-M1 cells treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) and 5 or 10 microM of ATPR significantly suppressed the activity of the AP-1 reporter as compared to treatment with ATRA (P<0.05).	Tetradecanoylphorbol Acetate	90-93	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	167-171	
23615401-9	2013	Furthermore, TPA-induced extracellular signal-regulated kinase (ERK) 1/2 and Akt phosphorylation and the DNA binding activity of activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) were attenuated by pretreatment with AP and HO-1 end products.	Tetradecanoylphorbol Acetate	13-16	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	150-154	
23615401-10	2013	In conclusion, these results suggest that AP inhibits TPA-induced cell migration and invasion by reducing MMP-9 activation, which is mediated mainly by inhibition of the ERK1/2 and phosphatidylinositol 3-kinase/Akt signaling pathways and subsequent AP-1 and NF-kappaB transactivation.	Tetradecanoylphorbol Acetate	54-57	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	249-253	
21381080-2	2011	The stomach isoform of Cldn18, Cldn18a2 is regulated via a PKC/MAPK/AP-1-dependent pathway in PKC activator 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated gastric cancer cells.	Tetradecanoylphorbol Acetate	108-144	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-72	
23288142-8	2013	EMSA showed that DHA, LA, PD98059, and wortmannin decreased TPA-induced NF-kappaB and AP-1 DNA-binding activity.	Tetradecanoylphorbol Acetate	60-63	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	86-90	
23615261-6	2013	TPA substantially increased NF-kappaB and AP-1 DNA binding activity.	Tetradecanoylphorbol Acetate	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	42-46	
23242121-3	2013	Cis-guggulsterone inhibited TPA-induced MMP expression             by blocking IkappaB kinase (IKK)/NF-kappaB signaling, whereas trans-guggulsterone blocked             mitogen-activated protein kinase (MAPK)/AP-1 signaling.	Tetradecanoylphorbol Acetate	28-31	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	209-213	
23151889-5	2013	Surfactin attenuated TPA-induced nuclear             translocation and activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1             (AP-1).	Tetradecanoylphorbol Acetate	21-24	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	123-142	
23151889-5	2013	Surfactin attenuated TPA-induced nuclear             translocation and activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1             (AP-1).	Tetradecanoylphorbol Acetate	21-24	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	156-160	
21381080-2	2011	The stomach isoform of Cldn18, Cldn18a2 is regulated via a PKC/MAPK/AP-1-dependent pathway in PKC activator 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated gastric cancer cells.	Tetradecanoylphorbol Acetate	146-149	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-72	
21246637-0	2011	Evodiamine inhibits 12-O-tetradecanoylphorbol-13-acetate-induced activator protein 1 transactivation and cell transformation in human hepatocytes.	Tetradecanoylphorbol Acetate	20-56	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	65-84	
21246637-5	2011	The Chang/AP-1 cells were treated with E. rutaecarpa and its bioactive constituents, and challenged with the AP-1 stimulator 12-O-tetradecanoylphorbol-13- acetate (TPA).	Tetradecanoylphorbol Acetate	125-162	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	109-113	
21246637-6	2011	The present study showed that the methanol extract of E. rutaecarpa decreased the TPA-induced AP-1 transactivation in Chang/AP-1 cells, with an EC50 value of 24.72 mug/mL.	Tetradecanoylphorbol Acetate	82-85	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	94-98	
21246637-6	2011	The present study showed that the methanol extract of E. rutaecarpa decreased the TPA-induced AP-1 transactivation in Chang/AP-1 cells, with an EC50 value of 24.72 mug/mL.	Tetradecanoylphorbol Acetate	82-85	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	124-128	
21246637-7	2011	EVO inhibited the TPA-induced AP-1 transactivation and colony formation, with EC50 values of 82 muM and 8.2 muM, respectively.	Tetradecanoylphorbol Acetate	18-21	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-34	
21246637-9	2011	These results suggested that EVO treatment suppressed the TPA-induced AP-1 activity via the ERKs pathway.	Tetradecanoylphorbol Acetate	58-61	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-74	
21262201-5	2011	DHAvD also suppressed activation of mitogen-activated protein kinase (MAPK), and MAPK-mediated nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) activations in TPA-treated MCF-7 cells.	Tetradecanoylphorbol Acetate	176-179	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	134-153	
21262201-5	2011	DHAvD also suppressed activation of mitogen-activated protein kinase (MAPK), and MAPK-mediated nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) activations in TPA-treated MCF-7 cells.	Tetradecanoylphorbol Acetate	176-179	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	155-159	
21262201-6	2011	The results indicate that DHAvD-mediated inhibition of TPA-induced MMP-9 expression and cell invasion involves the suppression of the MAPK/NF-kappaB and MAPK/AP-1 pathways in MCF-7 cells.	Tetradecanoylphorbol Acetate	55-58	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	158-162	
20959602-8	2011	Reciprocally, AP-1 TFs were up-regulated by RUNX1 after 12-O-tetradecanoylphorbol-13-acetate induction and recruited to RUNX1-occupied sites lacking AP-1 motifs.	Tetradecanoylphorbol Acetate	56-92	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-18	
21129776-5	2011	Finally, in line with the known TPA pathway, we found that nuclear proteins could bind a sequence corresponding to a unique AP1 site on promoter 2 selectively in the activated cell fraction.	Tetradecanoylphorbol Acetate	32-35	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	124-127	
20669087-10	2011	Likewise, the constitutive nuclear NF- kappaB (p65) activity as well as phorbol 12-myristate 13-acetate (PMA)- and sodium N-butyrate (SnB)-induced AP-1 binding activity in Raji cells were significantly reduced following treatment with maslinic acid.	Tetradecanoylphorbol Acetate	72-103	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	147-151	
20669087-10	2011	Likewise, the constitutive nuclear NF- kappaB (p65) activity as well as phorbol 12-myristate 13-acetate (PMA)- and sodium N-butyrate (SnB)-induced AP-1 binding activity in Raji cells were significantly reduced following treatment with maslinic acid.	Tetradecanoylphorbol Acetate	105-108	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	147-151	
20082219-5	2010	In addition, melittin suppressed the PMA-induced phosphorylations of ERK and JNK mitogen-activated protein kinases, upstream factors involved in Ap-1 and NF-kappaB.	Tetradecanoylphorbol Acetate	37-40	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	145-149	
20138977-7	2010	Hesperidin suppressed TPA-stimulated NF-kappaB translocation into the nucleus through IkappaB inhibitory signaling pathways and also inhibited TPA-induced AP-1 activity by the inhibitory phosphorylation of p38 kinase and c-Jun N-terminal kinase (JNK) signaling pathways.	Tetradecanoylphorbol Acetate	143-146	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	155-159	
20550117-7	2010	The EEGC also showed an inhibitory effect on the PMA-induced phosphorylation of extracellular signal-regulated kinase (ERK1/2) and protein kinase B (Akt) in cytosol, as well as the activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) levels in the nucleus of HepG2 cells.	Tetradecanoylphorbol Acetate	49-52	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	181-200	
20550117-7	2010	The EEGC also showed an inhibitory effect on the PMA-induced phosphorylation of extracellular signal-regulated kinase (ERK1/2) and protein kinase B (Akt) in cytosol, as well as the activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) levels in the nucleus of HepG2 cells.	Tetradecanoylphorbol Acetate	49-52	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	202-206	
19447859-6	2009	Transient transfection experiments also showed that pterostilbene strongly inhibited TPA-stimulated nuclear factor kappa B (NF-kappaB) and activator protein-1 (AP-1)-dependent transcriptional activity in HepG(2) cells.	Tetradecanoylphorbol Acetate	85-88	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	139-158	
20053986-2	2010	To bind to its target AP-1/12-O-tetradecanoylphorbol-13-acetate-responsive element or cAMP-responsive element DNA sequences in gene promoters and exert its transcriptional part, c-Fos must heterodimerize with other bZip proteins, its best studied partners being the Jun proteins (c-Jun, JunB, and JunD).	Tetradecanoylphorbol Acetate	27-63	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	287-291	
19420016-5	2009	Using specific inhibitors, we confirmed that PMA-induced cell invasion and MMP-9 expression is primarily regulated by nuclear factor-kappa B (NF-kappaB) activation via phosphatidylinositol 3-kinase (PI3K)/Akt and activator protein-1 (AP-1) activation via extracellular signal-regulated kinase (ERK)1/2.	Tetradecanoylphorbol Acetate	45-48	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	213-232	
19420016-5	2009	Using specific inhibitors, we confirmed that PMA-induced cell invasion and MMP-9 expression is primarily regulated by nuclear factor-kappa B (NF-kappaB) activation via phosphatidylinositol 3-kinase (PI3K)/Akt and activator protein-1 (AP-1) activation via extracellular signal-regulated kinase (ERK)1/2.	Tetradecanoylphorbol Acetate	45-48	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	234-238	
19420016-6	2009	KPS-A decreased PMA-induced transcriptional activation of NF-kappaB and AP-1 and inhibited PMA-induced phosphorylation of ERK1/2 and Akt.	Tetradecanoylphorbol Acetate	16-19	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	72-76	
19420016-9	2009	These results suggest that KPS-A inhibits PMA-induced invasion by reducing MMP-9 activation, mainly via the PI3K/Akt/NF-kappaB and PKCdelta/ERK/AP-1 pathways in MCF-7 cells and blocks tumor growth and MMP-9-mediated invasiveness in mice with breast carcinoma.	Tetradecanoylphorbol Acetate	42-45	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	144-148	
19447859-7	2009	Moreover, pterostilbene can suppress TPA-induced activation of extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase, c-Jun N-terminal kinases 1/2 and phosphatidylinositol 3-kinase/Akt and protein kinase C that are upstream of NF-kappaB and AP-1.	Tetradecanoylphorbol Acetate	37-40	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	267-271	
19447859-6	2009	Transient transfection experiments also showed that pterostilbene strongly inhibited TPA-stimulated nuclear factor kappa B (NF-kappaB) and activator protein-1 (AP-1)-dependent transcriptional activity in HepG(2) cells.	Tetradecanoylphorbol Acetate	85-88	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	160-164	
17114644-0	2007	Ascofuranone suppresses PMA-mediated matrix metalloproteinase-9 gene activation through the Ras/Raf/MEK/ERK- and Ap1-dependent mechanisms.	Tetradecanoylphorbol Acetate	24-27	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-116	
18992303-4	2009	Promoter activities of IL-2, nuclear factor of activated T cells (NFAT), and activator protein-1 (AP-1), after 6 h stimulation with PMA and ionomycin, gradually decreased in high glucose cultures to approximately 20% of those in normal glucose at 12 weeks.	Tetradecanoylphorbol Acetate	132-135	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-96	
18992303-4	2009	Promoter activities of IL-2, nuclear factor of activated T cells (NFAT), and activator protein-1 (AP-1), after 6 h stimulation with PMA and ionomycin, gradually decreased in high glucose cultures to approximately 20% of those in normal glucose at 12 weeks.	Tetradecanoylphorbol Acetate	132-135	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	98-102	
18245498-4	2008	The activation of activator protein-1 and nuclear factor-kappaB induced by TPA was dose dependently inhibited by RWE or quercetin treatment.	Tetradecanoylphorbol Acetate	75-78	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	18-37	
17114644-6	2007	In addition, ascofuranone suppressed PMA-induced phosphorylation of Ras, Raf, MEK and extracellular signal-regulated kinase (ERK), upstream factors involved in AP-1activation, whereas the phosphorylation of p38 and JNK/mitogen-activated protein kinase was not affected by ascofuranone, suggesting that the primary target of ascofuranone for suppression of the AP-1 induction is present in upstream of ERK signaling pathway.	Tetradecanoylphorbol Acetate	37-40	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	160-164	
17114644-6	2007	In addition, ascofuranone suppressed PMA-induced phosphorylation of Ras, Raf, MEK and extracellular signal-regulated kinase (ERK), upstream factors involved in AP-1activation, whereas the phosphorylation of p38 and JNK/mitogen-activated protein kinase was not affected by ascofuranone, suggesting that the primary target of ascofuranone for suppression of the AP-1 induction is present in upstream of ERK signaling pathway.	Tetradecanoylphorbol Acetate	37-40	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	360-364	
17207890-10	2007	An AP-1 and a NF-kappaB recognition sites were necessary for full induction of IL-8 promoter activity by TNF-alpha and TPA.	Tetradecanoylphorbol Acetate	119-122	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	3-7	
17207890-12	2007	Immunoblotting experiments showed that TPA was more potent than TNF-alpha to induce in a PKCalpha/beta dependent manner the p44/p42 mitogen-activated protein kinases (MAPK) signaling cascade which controls AP-1 activity.	Tetradecanoylphorbol Acetate	39-42	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	206-210	
17394101-4	2007	Deerberry fruit extracts also blocked TPA- or UVB-induced phosphorylation of ERKs and MEK 1/2, two upstream regulators of AP-1 and inhibited proliferation of human leukemia HL-60 cancer cells and human lung epithelial cancer A549 cells and induced apoptosis of HL-60 cells.	Tetradecanoylphorbol Acetate	38-41	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	122-126	
17394101-5	2007	These results suggest that the inhibition of TPA- or UVB-induced AP-1 and NF-kappaB activity, inhibition of HL-60 cells and cancer A549 cells proliferation and induction of apoptotic in human leukemia HL-60 cancer cells may be mediated through the ERKs and MEK 1/2 signal pathway.	Tetradecanoylphorbol Acetate	45-48	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	65-69	
15878157-8	2005	Phorbol ester 12-O-teradecanoyl-phorbol-13-acetate (TPA) activated AP-1 in B82L and B82M721 cells, but not B82 cells.	Tetradecanoylphorbol Acetate	52-55	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	67-71	
17438848-6	2007	The percentage of cells of active AP-1, IL-5 protein in supernatants of allergic rhinitis T lymphocytes stimulated with PMA and curcumin were significantly lower than those of allergic rhinitis T lymphocytes stimulated with PMA (P < 0.01); but significantly higher than those of allergic rhinitis T lymphocytes stimulated without PMA and those of deflection of nasal septum T lymphocytes stimulated.	Tetradecanoylphorbol Acetate	120-123	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	34-38	
16267831-11	2006	Similarly, AP-1 binding activity showed a transient variation in both cell lines after TPA treatment but with different kinetics.	Tetradecanoylphorbol Acetate	87-90	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	11-15	
15878157-11	2005	Ethanol selectively inhibited TPA-induced phosphorylation of ERK and PKCdelta, and modestly suppressed TPA-stimulated AP-1 activation in B82L and B82M721 cells.	Tetradecanoylphorbol Acetate	103-106	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	118-122	
15797241-1	2005	The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) induces activator protein-1 (AP-1) transcription factors, early response genes involved in a diverse set of transcriptional regulatory processes, and protein kinase C (PKC) activity.	Tetradecanoylphorbol Acetate	27-63	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	78-97	
15797241-1	2005	The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) induces activator protein-1 (AP-1) transcription factors, early response genes involved in a diverse set of transcriptional regulatory processes, and protein kinase C (PKC) activity.	Tetradecanoylphorbol Acetate	27-63	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	99-103	
15797241-1	2005	The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) induces activator protein-1 (AP-1) transcription factors, early response genes involved in a diverse set of transcriptional regulatory processes, and protein kinase C (PKC) activity.	Tetradecanoylphorbol Acetate	65-68	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	78-97	
15797241-1	2005	The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) induces activator protein-1 (AP-1) transcription factors, early response genes involved in a diverse set of transcriptional regulatory processes, and protein kinase C (PKC) activity.	Tetradecanoylphorbol Acetate	65-68	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	99-103	
15790882-10	2005	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element.	Tetradecanoylphorbol Acetate	15-51	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	163-166	
15790882-10	2005	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element.	Tetradecanoylphorbol Acetate	15-51	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	185-189	
15790882-10	2005	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element.	Tetradecanoylphorbol Acetate	15-51	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	216-219	
15790882-10	2005	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element.	Tetradecanoylphorbol Acetate	53-56	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	163-166	
15790882-10	2005	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element.	Tetradecanoylphorbol Acetate	53-56	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	185-189	
15790882-10	2005	Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element.	Tetradecanoylphorbol Acetate	53-56	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	216-219	
15465640-5	2004	Results in this experiment showed that SNL glycoprotein inhibits 12-O-Tetra decanoylphorbol-13-acetate (TPA; 100 nM)-induced DNA-binding activities of NF-kappaB and AP-1, and enhances NO production in MCF-7 cells.	Tetradecanoylphorbol Acetate	104-107	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	165-169