PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21537846-10	2011	The TBMS I-induced growth inhibition of L-02 cells was accompanied by the collapse of mitochondrial membrane potential, release of cyt-c from the mitochondria to the cytosol, activation of caspase-9 and -3, decrease of anti-apoptotic protein Bcl-2 levels and increase of the pro-apoptotic protein Bax levels, all indicative of apoptosis through the mitochondrial pathway.	tubeimoside I	4-10	BCL2 apoptosis regulator	Homo sapiens	242-247	
33664465-6	2021	TBM treatment alleviated oxidative stress by decreasing NOX2 and Ac-SOD2/SOD2 and decreased apoptosis by inhibiting cleaved caspse3 and Bax/Bcl-2.	tubeimoside I	0-3	BCL2 apoptosis regulator	Homo sapiens	140-145	
21628880-7	2011	TBMS I induced cell shrinkage, nuclear condensation and fragmentation, cell cycle arrest at the G2/M phase, mitochondrial membrane disruption, release of cytochrome c from the mitochondria, activation of caspase 3 and 9, and shifting Bax/Bcl-2 ratio from being anti-apoptotic to pro-apoptotic, all indicative of initiation and progression of apoptosis involving mitochondrial dysfunction.	tubeimoside I	0-6	BCL2 apoptosis regulator	Homo sapiens	238-243	
21461558-0	2011	Tubeimoside-1 inhibits proliferation and induces apoptosis by increasing the Bax to Bcl-2 ratio and decreasing COX-2 expression in lung cancer A549 cells.	tubeimoside I	0-13	BCL2 apoptosis regulator	Homo sapiens	84-89	
32627020-12	2020	In addition, TBMS1 triggered apoptosis via the PI3K/Akt-mediated Bcl-2 signaling pathway.	tubeimoside I	13-18	BCL2 apoptosis regulator	Homo sapiens	65-70	
30389907-6	2018	Mechanism studies showed that TBM increased autophagosome by two pathways: First, TBM could initiate autophagy by activating AMPK that would lead to stabilization of the Beclin1-Vps34 complex via dissociating Bcl-2 from Beclin1; Second, TBM could impair lysosomal cathepsin activity and block autophagic flux, leading to accumulation of impaired autophagolysosomes.	tubeimoside I	30-33	BCL2 apoptosis regulator	Homo sapiens	209-214	
30315250-7	2019	In three human breast cancer cell lines, we demonstrated that Akt-mTOR-eEF-2K pathway was involved in TBMS1-induced activation of autophagy, while Akt-mediated downregulations of Mcl-1, Bcl-xl, and Bcl-2 led to the activation of apoptosis of the breast cancer cells.	tubeimoside I	102-107	BCL2 apoptosis regulator	Homo sapiens	198-203	
21971569-7	2012	A decrease in Bcl-2/Bax ratio with increased expression of caspase-3, and intracellular Ca2+ provide compelling evidence that TBMS1-induced apoptosis is mediated by the mitochondrial pathway.	tubeimoside I	126-131	BCL2 apoptosis regulator	Homo sapiens	14-19	
30022842-12	2018	Furthermore, Western blot demonstrated that TBMS1 downregulated apoptosis-associated proteins such as PARP, p-ERK1/2, Bcl-2, caspase-3, caspase-7 and caspase-8 and upregulated cleaved PARP, cleaved caspase-3 and cleaved caspase-9.	tubeimoside I	44-49	BCL2 apoptosis regulator	Homo sapiens	118-123	
23425861-8	2013	Western blot analysis also showed that TBMS1 induced apoptosis by regulation of the Bcl-2 gene family in BGC823 cells.	tubeimoside I	39-44	BCL2 apoptosis regulator	Homo sapiens	84-89	
27292614-9	2016	In DU145 cells, TBMS1 induced mitochondrial apoptosis, evidenced by ROS generation, mitochondrial dysfunction, endoplasmic reticulum stress, modulated Bcl-2 family protein and cleaved caspase-3, and activated ASK-1 and its downstream targets p38 and JNK.	tubeimoside I	16-21	BCL2 apoptosis regulator	Homo sapiens	151-156