PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9263993-13	1997	In contrast, cytokines in combination with pyrrolidine dithiocarbamate, which blocks endogenous superoxide dismutase, allowed p53 and Bax accumulation as well as DNA fragmentation.	pyrrolidine dithiocarbamic acid	43-70	BCL2 associated X, apoptosis regulator	Homo sapiens	134-137	
15102481-10	2004	CONCLUSION: These findings suggest that PDTC-induced apoptosis is related with Bax, and that G1 arrest is possibly related with p21.	pyrrolidine dithiocarbamic acid	40-44	BCL2 associated X, apoptosis regulator	Homo sapiens	79-82	
10777712-7	2000	The antioxidant and GSH precursor N-acetyl-l-cysteine favored Bcl-2 at the expense of Bax/p53, whereas pyrrolidine dithiocarbamate induced Bax against Bcl-2, with mild effect on p53.	pyrrolidine dithiocarbamic acid	103-130	BCL2 associated X, apoptosis regulator	Homo sapiens	139-142	
10794522-8	1999	Bax and gadd45 gene induction could be efficiently blocked by pretreating the cells with the antioxidant compound pyrrolidine dithiocarbamate, suggesting that oxidative stress was involved in these responses.	pyrrolidine dithiocarbamic acid	114-141	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3	
29545865-7	2018	Investigation of molecular mechanism revealed that the pretreatment with liquiritin and pyrrolidinedithiocarbamic acid (PDTC) obviously blocked the expression of NF-kappaB p65 in nuclear protein increased by oxybuprocaine and the expression levels of total proteins, caspase-3 and Bax.Moreover, tumor necrosis factor-alpha (TNF-alpha) blocked the inhibitory effect of liquiritin on the expression of NF-kappaB p65 in nuclear protein and total proteins, caspase-3 and Bax, thus obstructing the protective effect of liquiritin on corneal epithelial cells.	pyrrolidine dithiocarbamic acid	88-118	BCL2 associated X, apoptosis regulator	Homo sapiens	281-284	
29545865-7	2018	Investigation of molecular mechanism revealed that the pretreatment with liquiritin and pyrrolidinedithiocarbamic acid (PDTC) obviously blocked the expression of NF-kappaB p65 in nuclear protein increased by oxybuprocaine and the expression levels of total proteins, caspase-3 and Bax.Moreover, tumor necrosis factor-alpha (TNF-alpha) blocked the inhibitory effect of liquiritin on the expression of NF-kappaB p65 in nuclear protein and total proteins, caspase-3 and Bax, thus obstructing the protective effect of liquiritin on corneal epithelial cells.	pyrrolidine dithiocarbamic acid	88-118	BCL2 associated X, apoptosis regulator	Homo sapiens	467-470	
29545865-7	2018	Investigation of molecular mechanism revealed that the pretreatment with liquiritin and pyrrolidinedithiocarbamic acid (PDTC) obviously blocked the expression of NF-kappaB p65 in nuclear protein increased by oxybuprocaine and the expression levels of total proteins, caspase-3 and Bax.Moreover, tumor necrosis factor-alpha (TNF-alpha) blocked the inhibitory effect of liquiritin on the expression of NF-kappaB p65 in nuclear protein and total proteins, caspase-3 and Bax, thus obstructing the protective effect of liquiritin on corneal epithelial cells.	pyrrolidine dithiocarbamic acid	120-124	BCL2 associated X, apoptosis regulator	Homo sapiens	281-284	
29545865-7	2018	Investigation of molecular mechanism revealed that the pretreatment with liquiritin and pyrrolidinedithiocarbamic acid (PDTC) obviously blocked the expression of NF-kappaB p65 in nuclear protein increased by oxybuprocaine and the expression levels of total proteins, caspase-3 and Bax.Moreover, tumor necrosis factor-alpha (TNF-alpha) blocked the inhibitory effect of liquiritin on the expression of NF-kappaB p65 in nuclear protein and total proteins, caspase-3 and Bax, thus obstructing the protective effect of liquiritin on corneal epithelial cells.	pyrrolidine dithiocarbamic acid	120-124	BCL2 associated X, apoptosis regulator	Homo sapiens	467-470