PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20732338-11	2011	Hormone treatment sustained the growth of the lesions induced by MNU by increasing expression of Areg, Bcl-2, Ccnd-1 and Vegf genes, while decreasing expression of Bad, Bax, Casp 3, 8, 9 and p53 genes.	Methylnitrosourea	65-68	BCL2, apoptosis regulator	Rattus norvegicus	103-108	
28786001-8	2017	Two days after first MNU administration, some genes associated with apoptosis were altered in the mammary tissue from the TCDD group (Bax and Caspase 3 down- and Bcl-2 upregulated) but were also partially reestablished by maternal Res.	Methylnitrosourea	21-24	BCL2, apoptosis regulator	Rattus norvegicus	162-167	
10930042-6	2000	In the apoptosis cascade, upregulation of Bax, downregulation of Bcl-2, and increased CPP32 protease (caspase-3) activity were seen 12 hours after MNU dosing.	Methylnitrosourea	147-150	BCL2, apoptosis regulator	Rattus norvegicus	65-70	
18788994-3	2008	After NS or MNU treatment for different times, the apoptotic index of the photoreceptor cell was detected by TUNEL labeling, whereas the mRNA expressions and the protein levels of antiapoptotic Bcl-2 and proapoptotic Bax were determined by reverse transcriptase polymerase chain reaction and Western blotting, respectively.	Methylnitrosourea	12-15	BCL2, apoptosis regulator	Rattus norvegicus	194-199	
18788994-8	2008	As compared with the MNU-treated group, MaFGF significantly upregulated the expression of Bcl-2 mRNA and protein and downregulated the expression of Bax mRNA and protein (P = <0.001).	Methylnitrosourea	21-24	BCL2, apoptosis regulator	Rattus norvegicus	90-95	
16047940-7	2005	Extensive investigation in the rats revealed that MNU-induced photoreceptor cell loss was due to apoptosis with a decrease of Bcl-2 protein, increase of Bax protein, and activation of caspase families.	Methylnitrosourea	50-53	BCL2, apoptosis regulator	Rattus norvegicus	126-131	
10930042-7	2000	Therefore, the pathogenesis of MNU-induced cataract was associated with DNA adduct formation in the lens epithelial cell nuclei leading to apoptosis by upregulation of Bax protein, downmodulation of Bcl-2 protein, and activation of caspase-3.	Methylnitrosourea	31-34	BCL2, apoptosis regulator	Rattus norvegicus	199-204	
10576206-5	1999	Therefore MNU-induced photoreceptor cell death was attributed to DNA adduct formation restricted to photoreceptor cell nuclei leading to photoreceptor cell apoptosis by up-regulation of Bax protein, down-modulation of Bcl-2 protein, and activation of caspases 3, 6, and 8.	Methylnitrosourea	10-13	BCL2, apoptosis regulator	Rattus norvegicus	218-223	
34325589-10	2021	Strong expression of BCL-2, IL-6, COX 2, beta-catenin and iNOS in (NMU + BaP)-administered rats were observed.	Methylnitrosourea	67-70	BCL2, apoptosis regulator	Rattus norvegicus	21-26	
32184629-0	2020	Omega-3PUFA Attenuates MNU-Induced Colorectal Cancer in Rats by Blocking PI3K/AKT/Bcl-2 Signaling.	Methylnitrosourea	23-26	BCL2, apoptosis regulator	Rattus norvegicus	82-87	
32184629-12	2020	Conclusion: Omega-3PUFA can attenuate MNU-induced colorectal cancer in rats by blocking PI3K/AKT/Bcl-2 signaling, which suggests that Omega-3PUFA may be a potent agent for CRC treatment.	Methylnitrosourea	38-41	BCL2, apoptosis regulator	Rattus norvegicus	97-102