PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15286717-7	2004	U251MG cells expressed IL-8 receptors CXCR-1 and -2, and Matrigel invasion assay revealed that CsA attenuated A23187/PMA-dependent stimulation of invasive potential, probably by inhibiting IL-8 production.	Tetradecanoylphorbol Acetate	117-120	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	95-98	
6334715-8	1984	CSA also blocked lymphokine release from a phorbol myristate acetate-stimulated thymoma cell line, EL-4.	Tetradecanoylphorbol Acetate	43-68	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	0-3	
8093097-0	1994	Evidence that inhibition of phorbol ester-induced superoxide anion formation by cyclosporin A in phagocytes is not mediated by direct inhibition of protein kinase C. Cyclosporin A (CsA) has been reported to inhibit phorbol myristate acetate (PMA)-induced superoxide anion (O2-) formation in human neutrophils and murine macrophages.	Tetradecanoylphorbol Acetate	215-240	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	181-184	
10518804-3	1999	In these primary human cells, CsA significantly inhibited PMA/ionomycin-mediated and ionomycin-mediated activation of the MAPK kinase MKK6, as well as its downstream kinases SAPK2a (p38alpha) and MAPKAP-K2.	Tetradecanoylphorbol Acetate	58-61	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	30-33	
10518804-4	1999	PMA/ionomycin treatment also mediated activation of SAPK1 (JNKs) which was inhibited by CsA.	Tetradecanoylphorbol Acetate	0-3	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	88-91	
12176893-5	2002	When PBMCs were stimulated with phorbol myristate acetate/ionomycin or with anti-CD3/anti-CD28, the accumulation of LTalpha both at mRNA and protein levels was markedly inhibited by CsA.	Tetradecanoylphorbol Acetate	32-57	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	182-185	
8093097-1	1994	We found that CsA inhibited O2- formation in HL-60 cells induced by PMA (30 nM) and phorbol dibutyrate (200 nM) with a half-maximal effect at 1 and 0.75 microM, respectively.	Tetradecanoylphorbol Acetate	68-71	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	14-17	
8093097-0	1994	Evidence that inhibition of phorbol ester-induced superoxide anion formation by cyclosporin A in phagocytes is not mediated by direct inhibition of protein kinase C. Cyclosporin A (CsA) has been reported to inhibit phorbol myristate acetate (PMA)-induced superoxide anion (O2-) formation in human neutrophils and murine macrophages.	Tetradecanoylphorbol Acetate	242-245	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	181-184	
2048200-6	1991	Depletion of protein kinase C (PKC) activity from cells by pretreatment of Daudi cells with phorbol.12-myristate 13-acetate (PMA) abolished the G0/G1 arrest induced by both CsA and IFN-alpha.	Tetradecanoylphorbol Acetate	125-128	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	173-176	
8249125-6	1993	However, at therapeutic concentrations (0.1-5 micrograms/ml) vWF release by cells stimulated with thrombin, histamine, PMA, and the calcium ionophore A23187 was enhanced by both CsA and cremophor in a concentration-dependent manner.	Tetradecanoylphorbol Acetate	119-122	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	178-181