PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16520894-5	2006	In addition, pioglitazone caused a down-regulation of the X chromosome-linked inhibitor of apoptosis (XIAP), Bcl-2, and cyclooxygenase-2 (COX-2) under conditions leading to PPARgamma down-regulation.	Pioglitazone	13-25	BCL2 apoptosis regulator	Homo sapiens	109-114	
17267584-6	2007	Pioglitazone (100 microM) induced apoptosis in human VSMC from diabetic and nondiabetic patients (NDP), analyzed by DNA fragmentation and by degradation of Bcl-2, in high-glucose-containing medium (15 and 25 mM).	Pioglitazone	0-12	BCL2 apoptosis regulator	Homo sapiens	156-161	
16731829-8	2006	Pioglitazone suppressed high glucose-induced phosphorylation of p44/42 mitogen-activated protein kinase and reduced Bcl-2 and p27(Kip1) protein levels.	Pioglitazone	0-12	BCL2 apoptosis regulator	Homo sapiens	116-121	
16520894-6	2006	These results suggest that pioglitazone may have therapeutic relevance or significance in the treatment of human CRC, and the down-regulation of XIAP, Bcl-2, and COX-2 may contribute to pioglitazone-induced apoptosis in these and other RB-deficient cell lines and tumors.	Pioglitazone	186-198	BCL2 apoptosis regulator	Homo sapiens	151-156	
15094967-6	2004	Pretreatment of cells with the PPAR-gamma ligand pioglitazone blocked TNF-alpha-mediated apoptosis, caspase-3 activation, expression of Bcl-2, and lipid peroxidation (P <.01 vs TNF-alpha alone).	Pioglitazone	49-61	BCL2 apoptosis regulator	Homo sapiens	136-141	
15094967-8	2004	The PPAR-gamma ligand pioglitazone modulates lipid peroxidation, alters Bcl-2 expression and caspase-3 activation, and finally reduces apoptosis.	Pioglitazone	22-34	BCL2 apoptosis regulator	Homo sapiens	72-77	
34466155-0	2021	Pioglitazone mediates apoptosis in Caki cells via downregulating c-FLIP(L) expression and reducing Bcl-2 protein stability.	Pioglitazone	0-12	BCL2 apoptosis regulator	Homo sapiens	99-104	
14686729-11	2003	Furthermore, treatment of fresh glioblastoma tissue from patients with PGZ, either alone or in combination with ATRA, induced a significant level of tumor cell apoptosis together with a downregulation of bcl-2 protein level as compared with untreated control brain tissue.	Pioglitazone	71-74	BCL2 apoptosis regulator	Homo sapiens	204-209	
14686729-9	2003	In addition, apoptosis occurred in both cell lines treated with either PGZ or ATRA, which was associated with a downregulation of bcl-2 and an upregulation of bax proteins.	Pioglitazone	71-74	BCL2 apoptosis regulator	Homo sapiens	130-135	
34466155-7	2021	The protein expression levels of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein (c-FLIP)(L) and Bcl-2, which were determined by western blotting, decreased after pioglitazone treatment in Caki cells.	Pioglitazone	188-200	BCL2 apoptosis regulator	Homo sapiens	122-127	
34466155-10	2021	Of note, it was found by western blot analysis that Bcl-2 protein expression was downregulated by the decreased protein stability of Bcl-2 in pioglitazone-treated Caki cells.	Pioglitazone	142-154	BCL2 apoptosis regulator	Homo sapiens	52-57	
34466155-10	2021	Of note, it was found by western blot analysis that Bcl-2 protein expression was downregulated by the decreased protein stability of Bcl-2 in pioglitazone-treated Caki cells.	Pioglitazone	142-154	BCL2 apoptosis regulator	Homo sapiens	133-138	
34466155-11	2021	In conclusion, these findings indicated that pioglitazone-induced apoptosis is regulated through caspase-mediated degradation of FLIP(L) and reduction of Bcl-2 protein stability, suggesting that pioglitazone is a feasible apoptotic agent that could be used in the treatment of human RC.	Pioglitazone	45-57	BCL2 apoptosis regulator	Homo sapiens	154-159	
34466155-11	2021	In conclusion, these findings indicated that pioglitazone-induced apoptosis is regulated through caspase-mediated degradation of FLIP(L) and reduction of Bcl-2 protein stability, suggesting that pioglitazone is a feasible apoptotic agent that could be used in the treatment of human RC.	Pioglitazone	195-207	BCL2 apoptosis regulator	Homo sapiens	154-159	
32881246-8	2020	Pioglitazone also reduced the activation of caspase-3 and caspase-9, lowered the ratio of Bax/Bcl-2, attenuated kidney pathological damage and dysfunction, down-regulated the expression of Acetyl-p53, PUMA-alpha and Bax and abated cell apoptosis after cisplatin treatment.	Pioglitazone	0-12	BCL2 apoptosis regulator	Homo sapiens	94-99	
32881246-6	2020	Pioglitazone treatment significantly increased cell viability, promoted SIRT1-p53 interaction, upregulated Bcl-2 expression, activated SIRT1 and elevated mitochondrial ATP synthesis after cisplatin treatment.	Pioglitazone	0-12	BCL2 apoptosis regulator	Homo sapiens	107-112