PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10037682-3	1999	Long term, but not acute, treatment of cultured cerebellar granule cells with LiCl induces a concentration-dependent decrease in mRNA and protein levels of proapoptotic p53 and Bax; conversely, mRNA and protein levels of cytoprotective Bcl-2 are remarkably increased.	Lithium Chloride	78-82	BCL2 associated X, apoptosis regulator	Homo sapiens	177-180	
10037682-6	1999	Pretreatment with LiCl for 7 days prevents glutamate-induced increase in p53 and Bax expression and maintains Bcl-2 in an elevated state.	Lithium Chloride	18-22	BCL2 associated X, apoptosis regulator	Homo sapiens	81-84	
25206585-5	2013	The level of active Caspase-3 and the ratio of Bax/Bcl-2 in hippocampal neurons treated with TLR4 antibody or the GSK-3beta inhibitor, LiCl, creased before intervention with lipopolysaccharide, but increased after treatment with the AKT hibitor, LY294002.	Lithium Chloride	135-139	BCL2 associated X, apoptosis regulator	Homo sapiens	47-50	
34883226-3	2022	Through cell culture, virus infection, and RT-qPCR, we found that LiCl could down-regulate the apoptosis-related genes Caspase-3 and Bax, up-regulate Bcl-2, and down-regulate the inflammatory-related genes (NF-kappaB, NLRP3, TNF-alpha, and IL-1beta) via inhibiting virus replication.	Lithium Chloride	66-70	BCL2 associated X, apoptosis regulator	Homo sapiens	133-136	
29773200-0	2018	Lithium chloride attenuates mitomycin C induced necrotic cell death in MDA-MB-231 breast cancer cells via HMGB1 and Bax signaling.	Lithium Chloride	0-16	BCL2 associated X, apoptosis regulator	Homo sapiens	116-119	
29773200-8	2018	LiCl combined with mitomycin C significantly down-regulated HMGB1, MMP9 and Bcl-2 gene expression but significantly increased the level of Bax protein.	Lithium Chloride	0-4	BCL2 associated X, apoptosis regulator	Homo sapiens	139-142	
23054864-7	2012	The results showed breast cancer cells respond in a diverse manner to LiCl, i.e., at lower concentrations (1, 5, and 10 mM), LiCl induces cell survival by inhibiting apoptosis through regulation of GSK-3beta, caspase-2, Bax, and cleaved caspase-7 and by activating anti-apoptotic proteins (Akt, beta-catenin, Bcl-2, and cyclin D1).	Lithium Chloride	125-129	BCL2 associated X, apoptosis regulator	Homo sapiens	220-223	
11520785-8	2001	Furthermore, lithium chloride, but not caspase inhibition, prevented the appearance of the conformational form of Bax associated with apoptosis induction.	Lithium Chloride	13-29	BCL2 associated X, apoptosis regulator	Homo sapiens	114-117