PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34339458-4	2021	We demonstrate that depletion of either YAP or TAZ inhibits the ability of phorbol ester (TPA) treatment, cellular differentiation or the EBV BRLF1 immediate-early (IE) protein to induce lytic EBV reactivation in oral keratinocytes, and show that over-expression of constitutively active forms of YAP and TAZ reactivate lytic EBV infection in conjunction with TEAD family members.	Tetradecanoylphorbol Acetate	90-93	Yes1 associated transcriptional regulator	Homo sapiens	40-43	
28322318-0	2017	12-O-Tetradecanoylphorbol-13-acetate (TPA) is anti-tumorigenic in liver cancer cells via inhibiting YAP through AMOT.	Tetradecanoylphorbol Acetate	0-36	Yes1 associated transcriptional regulator	Homo sapiens	100-103	
28322318-0	2017	12-O-Tetradecanoylphorbol-13-acetate (TPA) is anti-tumorigenic in liver cancer cells via inhibiting YAP through AMOT.	Tetradecanoylphorbol Acetate	38-41	Yes1 associated transcriptional regulator	Homo sapiens	100-103	
28322318-2	2017	However, we found that TPA inhibits transformative phenotypes in liver cancer cells via the translocation of YAP from the nucleus, where it functions as a transcriptional co-factor, to the cytoplasm.	Tetradecanoylphorbol Acetate	23-26	Yes1 associated transcriptional regulator	Homo sapiens	109-112	
28322318-4	2017	The inhibitory effects of TPA on YAP were AMOT dependent.	Tetradecanoylphorbol Acetate	26-29	Yes1 associated transcriptional regulator	Homo sapiens	33-36	
28322318-6	2017	Importantly, the depletion of YAP and AMOT blocked the TPA-reduced transformative phenotypes.	Tetradecanoylphorbol Acetate	55-58	Yes1 associated transcriptional regulator	Homo sapiens	30-33	
28322318-7	2017	In sum, TPA has been established as an anti-tumorigenic drug in liver cancer cells via YAP and AMOT.	Tetradecanoylphorbol Acetate	8-11	Yes1 associated transcriptional regulator	Homo sapiens	87-90