PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23599430-3	2013	Considering that MES is a form of physiological stress, we hypothesized that it can activate the tumor suppressor p53, which is a key modulator of the cell cycle and apoptosis in response to cell stresses.	2-(N-morpholino)ethanesulfonic acid	17-20	tumor protein p53	Homo sapiens	114-117	
24345738-7	2014	Interestingly, we identified a previously undetected point mutation of p53 (p.Arg249Ser) in IST-MES 2, and showed that RITA is also able to reactivate this p53 mutant protein and its apoptotic function.	2-(N-morpholino)ethanesulfonic acid	96-99	tumor protein p53	Homo sapiens	71-74	
23599430-6	2013	MES-induced p53 phosphorylation was inhibited by pretreatment with a p38 MAPK inhibitor and transfection of dominant-negative mutants of p38, MKK3b, and MKK6b, implying the involvement of the p38 MAPK signaling pathway.	2-(N-morpholino)ethanesulfonic acid	0-3	tumor protein p53	Homo sapiens	12-15	
23599430-7	2013	Furthermore, MES treatment enhanced p53 transcriptional function and increased the expression of p53 target genes p21, BAX, PUMA, NOXA, and IRF9.	2-(N-morpholino)ethanesulfonic acid	13-16	tumor protein p53	Homo sapiens	36-39	
23599430-7	2013	Furthermore, MES treatment enhanced p53 transcriptional function and increased the expression of p53 target genes p21, BAX, PUMA, NOXA, and IRF9.	2-(N-morpholino)ethanesulfonic acid	13-16	tumor protein p53	Homo sapiens	97-100	
23599430-10	2013	These findings identify some molecular targets of electrical stimulation and incorporate the p38-p53 signaling pathway among the transduction pathways that MES affects.	2-(N-morpholino)ethanesulfonic acid	156-159	tumor protein p53	Homo sapiens	97-100