PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25245533-3	2014	In this study, we showed that PMA induces an interaction between IL-32alpha, PKCepsilon, and BCL6, forming a trimer.	Tetradecanoylphorbol Acetate	30-33	BCL6 transcription repressor	Homo sapiens	93-97	
28589317-0	2017	Bcl6 gene-silencing facilitates PMA-induced megakaryocyte differentiation in K562 cells.	Tetradecanoylphorbol Acetate	32-35	BCL6 transcription repressor	Homo sapiens	0-4	
25245533-7	2014	Further, the pan-PKC inhibitor and PKCepsilon inhibitor disrupted PMA-induced interaction between IL-32alpha and BCL6.	Tetradecanoylphorbol Acetate	66-69	BCL6 transcription repressor	Homo sapiens	113-117	
25245533-9	2014	PMA induces post-translational modification of BCL6 by conjugation to SUMO-2, while IL-32alpha inhibits.	Tetradecanoylphorbol Acetate	0-3	BCL6 transcription repressor	Homo sapiens	47-51	
25245533-10	2014	PKCepsilon inhibition eliminated PMA-induced SUMOylation of BCL6.	Tetradecanoylphorbol Acetate	33-36	BCL6 transcription repressor	Homo sapiens	60-64	
19337254-3	2009	Treatment with TPA resulted in BCL6 degradation and cyclin D2 upregulation.	Tetradecanoylphorbol Acetate	15-18	BCL6 transcription repressor	Homo sapiens	31-35	
19379553-4	2009	Meanwhile, PCR, cloning and direct DNA sequencing were used to identify mutations in the 5" regulatory region of bcl-6 in K562 cells before and after induction with TPA.	Tetradecanoylphorbol Acetate	165-168	BCL6 transcription repressor	Homo sapiens	113-118	
9188861-6	1997	BCL-6 phosphorylation significantly increased in Ramos cells following stimulation with 12-o-tetradecanoylphorbol-13-acetate (TPA) or BCL-6- and erk1-transfected COS-7 cells stimulated with epidermal growth factor (EGF), and the increase of phosphorylation was inhibited by MEK1 inhibitor, PD98059.	Tetradecanoylphorbol Acetate	88-124	BCL6 transcription repressor	Homo sapiens	0-5	
9188861-6	1997	BCL-6 phosphorylation significantly increased in Ramos cells following stimulation with 12-o-tetradecanoylphorbol-13-acetate (TPA) or BCL-6- and erk1-transfected COS-7 cells stimulated with epidermal growth factor (EGF), and the increase of phosphorylation was inhibited by MEK1 inhibitor, PD98059.	Tetradecanoylphorbol Acetate	126-129	BCL6 transcription repressor	Homo sapiens	0-5	
9180294-3	1997	Although the expression of BCL-6 transcripts was very low or undetectable in untreated HL-60 or U-937 cells, treatment of these cells with TPA to induce monocytic differentiation resulted in an apparent increase of BCL-6 mRNA, suggesting that BCL-6 gene expression is not limited to B cells and it is closely associated with monocytic lineage differentiation.	Tetradecanoylphorbol Acetate	139-142	BCL6 transcription repressor	Homo sapiens	27-32	
9180294-3	1997	Although the expression of BCL-6 transcripts was very low or undetectable in untreated HL-60 or U-937 cells, treatment of these cells with TPA to induce monocytic differentiation resulted in an apparent increase of BCL-6 mRNA, suggesting that BCL-6 gene expression is not limited to B cells and it is closely associated with monocytic lineage differentiation.	Tetradecanoylphorbol Acetate	139-142	BCL6 transcription repressor	Homo sapiens	215-220	
9180294-3	1997	Although the expression of BCL-6 transcripts was very low or undetectable in untreated HL-60 or U-937 cells, treatment of these cells with TPA to induce monocytic differentiation resulted in an apparent increase of BCL-6 mRNA, suggesting that BCL-6 gene expression is not limited to B cells and it is closely associated with monocytic lineage differentiation.	Tetradecanoylphorbol Acetate	139-142	BCL6 transcription repressor	Homo sapiens	215-220	
9180294-4	1997	The BCL-6 transcripts in TPA-treated U-937 cells were superinduced by the treatment with cycloheximide (CHX) and the half-life of the BCL-6 mRNA was apparently prolonged when TPA-treated U-937 cells were exposed to CHX in the presence of actinomycin D (ACD).	Tetradecanoylphorbol Acetate	25-28	BCL6 transcription repressor	Homo sapiens	4-9	
9180294-4	1997	The BCL-6 transcripts in TPA-treated U-937 cells were superinduced by the treatment with cycloheximide (CHX) and the half-life of the BCL-6 mRNA was apparently prolonged when TPA-treated U-937 cells were exposed to CHX in the presence of actinomycin D (ACD).	Tetradecanoylphorbol Acetate	25-28	BCL6 transcription repressor	Homo sapiens	134-139	
9180294-4	1997	The BCL-6 transcripts in TPA-treated U-937 cells were superinduced by the treatment with cycloheximide (CHX) and the half-life of the BCL-6 mRNA was apparently prolonged when TPA-treated U-937 cells were exposed to CHX in the presence of actinomycin D (ACD).	Tetradecanoylphorbol Acetate	175-178	BCL6 transcription repressor	Homo sapiens	4-9	
9180294-4	1997	The BCL-6 transcripts in TPA-treated U-937 cells were superinduced by the treatment with cycloheximide (CHX) and the half-life of the BCL-6 mRNA was apparently prolonged when TPA-treated U-937 cells were exposed to CHX in the presence of actinomycin D (ACD).	Tetradecanoylphorbol Acetate	175-178	BCL6 transcription repressor	Homo sapiens	134-139	
9180294-5	1997	Furthermore, the nuclear run-on assay revealed that the BCL-6 transcription signals were enhanced by TPA treatment.	Tetradecanoylphorbol Acetate	101-104	BCL6 transcription repressor	Homo sapiens	56-61	
9180294-6	1997	These results suggest that the increase of BCL-6 mRNA in U-937 cells stimulated with TPA to induce monocytic lineage differentiation is mediated by both transcriptional and post-transcriptional regulation.	Tetradecanoylphorbol Acetate	85-88	BCL6 transcription repressor	Homo sapiens	43-48