PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19590902-8	2009	Significant decrease in the incidence of CRB was observed when prophylactic TPA/tobra ABL was used in the high-risk group (P = 0.0201).	Tetradecanoylphorbol Acetate	76-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89	
3477472-0	1987	The bcr-c-abl tyrosine kinase activity is extinguished by TPA in K562 leukemia cells.	Tetradecanoylphorbol Acetate	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13	
3477472-3	1987	In the present work the activity of the c-abl and c-src oncogene-encoded tyrosine kinase was investigated during phorbol diester (TPA) induced differentiation of the K562 CML cells.	Tetradecanoylphorbol Acetate	130-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45	
3477472-4	1987	The high tyrosine kinase activity of p210bcr-c-abl is strongly reduced during the initial 24 h of TPA treatment.	Tetradecanoylphorbol Acetate	98-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-50	
25041880-7	2014	At 3 months, 58 patients (64.4% TPA) obtained a BCR-ABL transcripts level <10%.	Tetradecanoylphorbol Acetate	32-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55	
19590902-11	2009	However, both the overall and infection-free survival of the catheters in the high-risk group significantly improved while the patients were receiving TPA/tobra ABL prophylaxis, becoming similar to the outcomes of the catheters in the average-risk group and exhibiting statistically non-significant differences (P = 0.5571 and P = 0.9711, respectively).	Tetradecanoylphorbol Acetate	151-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164	
8398898-1	1993	The kinase activity of the BCR-ABL gene product is known to be down-regulated in K562 cells treated with low concentrations of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA).	Tetradecanoylphorbol Acetate	145-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34	
14555991-5	2003	In K562 cells, Phorbol 12-myristate 13-acetate activates Erk1/2 and consequently increases Bim-EL phosphorylation and degradation by the proteasome, resulting in cell survival, while the Bcr-Abl inhibitor imatinib abrogates Bim-EL phosphorylation and degradation and induces caspase activation and apoptosis.	Tetradecanoylphorbol Acetate	15-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194	
10739005-8	2000	In the case of the monocytic maturation of HL-60 cells treated with phorbol esters (PMA), the abl and bcr homologous genes were repositioned closer to each other and closer to the nuclear centre.	Tetradecanoylphorbol Acetate	84-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97	
8398898-1	1993	The kinase activity of the BCR-ABL gene product is known to be down-regulated in K562 cells treated with low concentrations of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA).	Tetradecanoylphorbol Acetate	183-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34	
8398898-5	1993	Our results indicate that BCR-ABL/BCR complexes disappeared at precisely the same time after TPA treatment as the loss of autophosphorylation activity exhibited by total p210 BCR-ABL, which occurred 16-19 h after TPA treatment.	Tetradecanoylphorbol Acetate	93-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33	
8398898-5	1993	Our results indicate that BCR-ABL/BCR complexes disappeared at precisely the same time after TPA treatment as the loss of autophosphorylation activity exhibited by total p210 BCR-ABL, which occurred 16-19 h after TPA treatment.	Tetradecanoylphorbol Acetate	213-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33	
8398898-5	1993	Our results indicate that BCR-ABL/BCR complexes disappeared at precisely the same time after TPA treatment as the loss of autophosphorylation activity exhibited by total p210 BCR-ABL, which occurred 16-19 h after TPA treatment.	Tetradecanoylphorbol Acetate	213-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182	
8398898-6	1993	The loss of kinase activity preceded the loss of p210 BCR by more than 24 h. A degraded form of p210 BCR-ABL (about 175 kilodaltons) accounted for the residual autophosphorylation activity seen during the later phases of kinase inactivation following TPA treatment, and this form was preferentially sequestered within BCR-ABL/BCR complexes.	Tetradecanoylphorbol Acetate	251-254	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108	
8398898-8	1993	We conclude that 15 nM TPA treatment of K562 cells initiates effects that simultaneously interfere with the phosphorylation of p160 BCR in BCR-ABL complexes and inactivates the autophosphorylation activity of the full length BCR-ABL protein.	Tetradecanoylphorbol Acetate	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146	
8398898-8	1993	We conclude that 15 nM TPA treatment of K562 cells initiates effects that simultaneously interfere with the phosphorylation of p160 BCR in BCR-ABL complexes and inactivates the autophosphorylation activity of the full length BCR-ABL protein.	Tetradecanoylphorbol Acetate	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232