PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
28409209-8	2017	THI rescues inhibitory H2O2-effect on 661W cell viability and impairs H2O2-induced apoptosis by increasing Bcl-2/Bax ratio.	2-acetyl-4(5)-tetrahydroxybutylimidazole	0-3	BCL2-associated X protein	Mus musculus	113-116
28456683-11	2017	The study also demonstrated that PA inhibited the DSS-induced cell death signaling by modulating the apoptosis related Bax and Bcl-2 proteins and down-regulating the necroptosis related RIP3 and MLKL proteins.	patchouli alcohol	33-35	BCL2-associated X protein	Mus musculus	119-122
28456683-11	2017	The study also demonstrated that PA inhibited the DSS-induced cell death signaling by modulating the apoptosis related Bax and Bcl-2 proteins and down-regulating the necroptosis related RIP3 and MLKL proteins.	Dextran Sulfate	50-53	BCL2-associated X protein	Mus musculus	119-122
28543910-8	2017	Wheatgrass-derived polysaccharide also attenuated hepatic cell death by modulating caspase-3 and apoptosis associated mitochondrial proteins, such as, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (Bax).	wheatgrass-derived polysaccharide	0-33	BCL2-associated X protein	Mus musculus	181-199
28543910-8	2017	Wheatgrass-derived polysaccharide also attenuated hepatic cell death by modulating caspase-3 and apoptosis associated mitochondrial proteins, such as, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (Bax).	wheatgrass-derived polysaccharide	0-33	BCL2-associated X protein	Mus musculus	201-204
28674496-10	2017	API-induced apoptosis was sustained by the increase of Bax/Bcl-2 ratio, increase of p53 expression, activation of both caspase 9 and caspase 8, cleavage of PARP-1, and increase of the percentage of cells in subG1 phase.	Apigenin	0-3	BCL2-associated X protein	Mus musculus	55-58
28376402-6	2017	Western blot analysis further revealed that metapristone treatment elicited a decline of Akt and ERK phosphorylation and Bcl-2, and facilitated expression of total P53 and Bax in A375 cells.	metapristone	44-56	BCL2-associated X protein	Mus musculus	172-175
28289752-5	2017	In addition, as a consequence of upstream inhibition of the inflammatory pathway following treatment with moringin + alpha-CD, the modulation of the oxidative stress (results focused on the expression of iNOS and nitrotyrosine) and apoptotic pathway (Bax and Bcl-2) was demonstrated.	moringin	106-114	BCL2-associated X protein	Mus musculus	251-254
28289752-5	2017	In addition, as a consequence of upstream inhibition of the inflammatory pathway following treatment with moringin + alpha-CD, the modulation of the oxidative stress (results focused on the expression of iNOS and nitrotyrosine) and apoptotic pathway (Bax and Bcl-2) was demonstrated.	alpha-cyclodextrin	117-125	BCL2-associated X protein	Mus musculus	251-254
28086065-11	2017	In addition, rapamycin suppressed cell apoptosis, and decreased Bax/Bcl-2 ratio and cleaved caspase-3 expression.	Sirolimus	13-22	BCL2-associated X protein	Mus musculus	64-67
28481901-5	2017	Analysis of the mechanisms of these events indicated that beta-lapachone regulated the expression of Bcl-2, Bcl-xL, and Bax, resulting in the activation of caspase-3, -8, -9, and poly-ADP-ribose polymerase (PARP).	beta-lapachone	58-72	BCL2-associated X protein	Mus musculus	120-123
28216619-8	2017	15d-PGJ2 pretreatment upregulated the Bcl-2/Bax ratio, thus reducing the number of apoptotic cells in the livers.	15-deoxy-delta(12,14)-prostaglandin J2	0-8	BCL2-associated X protein	Mus musculus	44-47
28553235-12	2017	The anti-apoptotic Blc2/Bax ratio was significantly increased in ALC cells treated with fluoride/4PBA compared to fluoride treatment alone.	Fluorides	88-96	BCL2-associated X protein	Mus musculus	24-27
28553235-12	2017	The anti-apoptotic Blc2/Bax ratio was significantly increased in ALC cells treated with fluoride/4PBA compared to fluoride treatment alone.	Fluorides	114-122	BCL2-associated X protein	Mus musculus	24-27
28481246-8	2017	Moreover, CMP in combination with 5-FU alleviated severe liver injury induced by 5-FU via reducing the levels of ROS, IL-1beta, and IL-6, decreasing expression of p-IkappaB-alpha, NF-kappaB, p-NF-kappaB, pp38 and Bax, and elevating levels of Nrf2, GCL, HO-1 and Bcl-2.	Fluorouracil	34-38	BCL2-associated X protein	Mus musculus	213-216
28369206-10	2017	Anti-apoptotic protein Bcl-2 was up-regulated and apoptosis-promoting protein Bax was down-regulated in Gnaq-SY5Y cells after treatment with H2O2.	Hydrogen Peroxide	141-145	BCL2-associated X protein	Mus musculus	78-81
28492347-9	2017	Moreover, the inhibition of Vglycin-induced cell proliferation in colon cancer cells was accompanied by alteration of the expression levels of the apoptosis-related proteins Bax, Bcl-2 and Mcl-1, and an increase of caspase-3 activity.	vglycin	28-35	BCL2-associated X protein	Mus musculus	174-177
28224201-10	2017	Mice treated with DEX exhibited less apoptotic tubular cells in response to cisplatin insult, which was associated with decreased Bax and reduced activation of p53 and caspase-3.	Dexmedetomidine	18-21	BCL2-associated X protein	Mus musculus	130-133
28188924-4	2017	Further investigation indicated that Daph significantly suppressed cytochrome c release and NLRP3 inflammasome activation and modulated apoptosis-related protein Bcl-2, Bax, and caspase-3 expression.	daphnetin	37-41	BCL2-associated X protein	Mus musculus	169-172
28224201-10	2017	Mice treated with DEX exhibited less apoptotic tubular cells in response to cisplatin insult, which was associated with decreased Bax and reduced activation of p53 and caspase-3.	Cisplatin	76-85	BCL2-associated X protein	Mus musculus	130-133
28368517-13	2017	In addition, 2-DG administration suppresses sepsis-increased expression of apoptotic inducers Bak and Bax as well as JNK phosphorylation in the myocardium.	Deoxyglucose	13-17	BCL2-associated X protein	Mus musculus	102-105
28282576-6	2017	Pretreatment with Pae also inhibited hepatocyte apoptosis by reducing the expression of caspases 3, 8, 9, and Bax, and increasing Bcl-2.	paeonol	18-21	BCL2-associated X protein	Mus musculus	110-113
27599972-10	2017	Moreover, PBA significantly prevented APAP-induced Bax translocation to the mitochondria, and the expression of heme oxygenase-1 mRNA and 4-hydroxynonenal.	Acetaminophen	38-42	BCL2-associated X protein	Mus musculus	51-54
29029408-7	2017	Western blotting showed that levels of activated Bax and cleaved caspase 3 were decreased, while Bcl-2 and pro-caspase 3 were increased in NMDA-treated mRGCs and murine retinal tissues, which corroborated the decreased apoptosis.	N-Methylaspartate	139-143	BCL2-associated X protein	Mus musculus	49-52
28070015-8	2017	RSL, a known agonist of deacetylase SIRT1, supported AEC2 survival by stimulating SIRT1 expression, promoting p53 destabilisation and decreasing Bax expression and by maintaining expression levels of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha), activated p-Akt and p-Mdm2 and inactivated Phospho-Phosphatase and tensin homolog (p-PTEN).	Resveratrol	0-3	BCL2-associated X protein	Mus musculus	145-148
28487766-5	2017	Malathion reduced cell viability mainly by apoptosis through mitochondrial dysfunction in N2a cells, as judged by an increase in the level of the pro-apoptotic protein Bax and decrease in the levels of the anti-apoptotic proteins p-Akt and Bcl2, resulting in cytochrome c release and caspase-dependent DNA fragmentation and condensation.	Malathion	0-9	BCL2-associated X protein	Mus musculus	168-171
28384256-7	2017	Probucol treatment reduced the number of cells positive for 8-hydroxyl-2"-deoxyguanosine or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and suppressed NF-kappaB activation, Bax expression, and caspase-9 activation in lung tissues from hyperoxia-exposed mice.	Probucol	0-8	BCL2-associated X protein	Mus musculus	198-201
28469767-7	2017	Melatonin treatment also could reduce malondialdehyde (MDA) level, MDA5, Gp91phox, Caspase3 and Bax expression, and increase total antioxidant activity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and Bcl-2 expression by up-regulating SIRT1 signaling.	Melatonin	0-9	BCL2-associated X protein	Mus musculus	96-99
28129627-0	2017	Camel whey protein improves oxidative stress and histopathological alterations in lymphoid organs through Bcl-XL/Bax expression in a streptozotocin-induced type 1 diabetic mouse model.	Streptozocin	133-147	BCL2-associated X protein	Mus musculus	113-116
28369137-13	2017	The atorvastatin infusion significantly reduced ER stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE-/- mice, compared with mice treated by Ang II alone.	Atorvastatin	4-16	BCL2-associated X protein	Mus musculus	145-148
28173746-11	2017	The associated results also demonstrated that Dex treatment ameliorated the LPS-induced neuronal apoptosis, probably by upregulating the Bcl-2 expression and downregulating the Bax expression.	Dexmedetomidine	46-49	BCL2-associated X protein	Mus musculus	177-180
28110215-6	2017	Moreover, NAS suppressed glutamate-induced apoptosis by suppressing expression of AIF, Bax, calpain, cytochrome c and cleaved caspase-3, whereas it enhanced expression of Bcl-2.	N-acetylserotonin	10-13	BCL2-associated X protein	Mus musculus	87-90
28110215-6	2017	Moreover, NAS suppressed glutamate-induced apoptosis by suppressing expression of AIF, Bax, calpain, cytochrome c and cleaved caspase-3, whereas it enhanced expression of Bcl-2.	Glutamic Acid	25-34	BCL2-associated X protein	Mus musculus	87-90
28115273-9	2017	Paraquat triggered O2- production, lipid peroxidation and apoptosis as evidenced by increased DHE staining, 4-HNE, caspase-3 activity, Bax and reduced Bcl-2 levels in association with unchanged ER stress.	Paraquat	0-8	BCL2-associated X protein	Mus musculus	135-138
28219760-8	2017	In addition, PFOA administration inhibited activities of superoxide dismutase and catalase, and increased generation of hydrogen peroxide and malondialdehyde, and down-regulated level of Bcl-2 and up-regulated p53 and BAX proteins.	perfluorooctanoic acid	13-17	BCL2-associated X protein	Mus musculus	218-221
28322323-6	2017	In eye tissue, administration of shikonin also attenuated DM/hypoxia-induced pre-apoptotic protein BAX expression as well as the production of inflammatory proteins cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS).	shikonin	33-41	BCL2-associated X protein	Mus musculus	99-102
28241801-9	2017	Further, we found CoCl2 treatment could up-regulate the expression of PP2A, BAX, cleaved caspase three and cause the phosphorylation of nNOS-Ser1412, but it down-regulated the expression of Bcl-2 and the phosphorylation of CAMKIIalpha and nNOS-Ser847.	cobaltous chloride	18-23	BCL2-associated X protein	Mus musculus	76-79
28344789-8	2017	Rosiglitazone significantly decreased p-NF-kB p65 phosphorylation and TGFbeta protein expression at 24 and 72 hours post-irradiation and significantly decreased gene expression of Collagen1, Mmp13, Tnfalpha and Bax at 24 hours and p53 at 72 hours post-irradiation.	Rosiglitazone	0-13	BCL2-associated X protein	Mus musculus	211-214
27401946-5	2017	However, capsaicin pre-treatment significantly suppressed the spermatogenic cell death, oxidative stress (levels of MDA, PHGPx immunoreactivity, and Hsp72, PHGPx, and MnSOD mRNA) and apoptosis (levels of TUNEL-positive cells, and Bcl-xL and Bax mRNA) in testes by HS.	Capsaicin	9-18	BCL2-associated X protein	Mus musculus	241-244
28190476-10	2017	The MPTP-induced changes of Bcl-2, Bax and caspase 3 protein expressions in the striatum could be reversed by icariin pretreatment.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	4-8	BCL2-associated X protein	Mus musculus	35-38
28190476-10	2017	The MPTP-induced changes of Bcl-2, Bax and caspase 3 protein expressions in the striatum could be reversed by icariin pretreatment.	icariin	110-117	BCL2-associated X protein	Mus musculus	35-38
29371918-8	2017	TC improved Bcl2/Bax ratio, decreased apoptosis, CYP2E1 protein expression and liver fibrosis levels, however, EV offered no such protection.	Tacrolimus	0-2	BCL2-associated X protein	Mus musculus	17-20
27982695-8	2017	In addition, Western blot and real-time reverse transcription-polymerase chain reaction indicated that 17-DMAG inhibited the H/R-induced upregulation of Bax/Bcl-2 ratio and cleaved caspase-3 expression.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	103-110	BCL2-associated X protein	Mus musculus	153-156
26948951-10	2017	Radiation-induced gastrointestinal DNA strand breaks, lipid peroxidation, and expression of proapoptotic-p53, Bax, and antiapoptotic-Bcl-xL proteins were reversed in melatonin pretreated mice.	Melatonin	166-175	BCL2-associated X protein	Mus musculus	110-113
26990902-5	2017	Triptolide increased protein levels of Fas, Fas-L, Bax, cytochrome c, caspase-9, Endo G, Apaf-1, PARP, caspase-3 but reduced levels of AIF, ATF6alpha, ATF6beta, and GRP78 in WEHI-3 cells.	triptolide	0-10	BCL2-associated X protein	Mus musculus	51-54
27832398-7	2017	Additionally, berberine obviously decreased the cell apoptosis and enzymatic activity of caspase-3, which was further confirmed by the facts that berberine clearly lowered Bax/Bcl-2 ratio and expression of cleaved caspase-3 protein.	Berberine	14-23	BCL2-associated X protein	Mus musculus	172-175
27832398-7	2017	Additionally, berberine obviously decreased the cell apoptosis and enzymatic activity of caspase-3, which was further confirmed by the facts that berberine clearly lowered Bax/Bcl-2 ratio and expression of cleaved caspase-3 protein.	Berberine	146-155	BCL2-associated X protein	Mus musculus	172-175
26698318-4	2017	Our results show that iMACs work through at least two mechanisms: 1) by blocking relocation of the cytoplasmic Bax protein to mitochondria and 2) by disassembling Bax and Bak oligomers in the mitochondrial outer membrane.	imidazoleacetic acid	22-27	BCL2-associated X protein	Mus musculus	111-114
26698318-4	2017	Our results show that iMACs work through at least two mechanisms: 1) by blocking relocation of the cytoplasmic Bax protein to mitochondria and 2) by disassembling Bax and Bak oligomers in the mitochondrial outer membrane.	imidazoleacetic acid	22-27	BCL2-associated X protein	Mus musculus	163-166
26698318-5	2017	iMACs exert comparable effects on channel conductance of Bax or Bak and similarly affect cytochrome c release from Bax or Bak-containing mitochondria.	imidazoleacetic acid	0-5	BCL2-associated X protein	Mus musculus	57-60
26698318-5	2017	iMACs exert comparable effects on channel conductance of Bax or Bak and similarly affect cytochrome c release from Bax or Bak-containing mitochondria.	imidazoleacetic acid	0-5	BCL2-associated X protein	Mus musculus	115-118
27987732-5	2017	Molecular biology analysis showed that graphene nanoplatelets injected intravenously lead to overexpression of BAX gene in both kidney and liver tissues (P>=0.01).	Graphite	39-47	BCL2-associated X protein	Mus musculus	111-114
27889855-8	2017	Moreover, EGCG also decreased the expression of pro-apoptotic proteins (Bax, caspase-3), reduced the activity of the anti-inflammatory agent NF-kappaB and inhibited the oxidative stress by decreasing the levels of ROS and MDA and increasing the expression of MnSOD.	epigallocatechin gallate	10-14	BCL2-associated X protein	Mus musculus	72-75
27465753-12	2017	Systemic administration of EGF to septic alcohol-fed mice also decreased intestinal apoptosis with an improvement in the Bax/Bcl-2 ratio.	Alcohols	41-48	BCL2-associated X protein	Mus musculus	121-124
27590616-13	2017	PD98059 treatment of 32 C ischemia-reperfusion mice significantly decreased the renal HIF-1 level (P < .05) and increased the BUN, s-Cr, renal Bax, and caspase-3 expression levels; the tissue injury score; and the proportions of TUNEL- and 8-OHdG-positive cells.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	0-7	BCL2-associated X protein	Mus musculus	146-149
28112220-5	2017	Furthermore, TUNEL assays revealed that chrysophanol attenuated MNU-induced photoreceptor cell apoptosis and inhibited the expression of the apoptosis-associated proteins PARP, Bax, and caspase-3.	chrysophanic acid	40-52	BCL2-associated X protein	Mus musculus	177-180
27998766-6	2017	Western blot showed that DON significantly increased the expression levels of apoptosis-related protein including Caspase-9, Caspase-3, poly (ADP-ribose) polymerase (PARP) and the ratio of Bax/Bcl-2.	deoxynivalenol	25-28	BCL2-associated X protein	Mus musculus	189-192
27939357-6	2017	Additionally, significant recovery of the number of apoptotic cells and the ratio of apoptosis proteins (Bcl-2/Bax) were detected in the SP+ICO treated group than the SP+Vehicle treated group.	Scopolamine	137-139	BCL2-associated X protein	Mus musculus	111-114
27939357-6	2017	Additionally, significant recovery of the number of apoptotic cells and the ratio of apoptosis proteins (Bcl-2/Bax) were detected in the SP+ICO treated group than the SP+Vehicle treated group.	alpha-iso-cubebenol	140-143	BCL2-associated X protein	Mus musculus	111-114
27940053-6	2017	Moreover, paeonol inhibited epirubicin-induced apoptosis by suppressing the activation of caspase-9 and caspase-3, the Bax/Bcl-2 imbalance and cytochrome c release.	paeonol	10-17	BCL2-associated X protein	Mus musculus	119-122
27940053-6	2017	Moreover, paeonol inhibited epirubicin-induced apoptosis by suppressing the activation of caspase-9 and caspase-3, the Bax/Bcl-2 imbalance and cytochrome c release.	Epirubicin	28-38	BCL2-associated X protein	Mus musculus	119-122
27894919-5	2017	Moreover, Res rescued MPP+- induced a decline on the level of p-AKT, p-GSK-3betaand the ratio of Bcl-2/Bax, and an elevation on the expression of Bax and caspase-3, 9.	mangion-purified polysaccharide (Candida albicans)	22-26	BCL2-associated X protein	Mus musculus	103-106
27894919-5	2017	Moreover, Res rescued MPP+- induced a decline on the level of p-AKT, p-GSK-3betaand the ratio of Bcl-2/Bax, and an elevation on the expression of Bax and caspase-3, 9.	mangion-purified polysaccharide (Candida albicans)	22-26	BCL2-associated X protein	Mus musculus	146-149
28052764-6	2017	In addition, Tat-HSP22 markedly inhibited H2O2-induced mitochondrial membrane potential, cytochrome c release, cleaved caspase-3, and Bax expression levels, while Bcl-2 expression levels were increased in HT-22 cells.	Hydrogen Peroxide	42-46	BCL2-associated X protein	Mus musculus	134-137
27539478-0	2017	Sesamol Induces Apoptosis by Altering Expression of Bcl-2 and Bax Proteins and Modifies Skin Tumor Development in Balb/c Mice.	sesamol	0-7	BCL2-associated X protein	Mus musculus	62-65
27539478-8	2017	Further, downregulation of bcl-2 and stimulation of bax protein expression on treatment with both free and encapsulated sesamol was responsible for the induction of apoptosis in tumor cells.	sesamol	120-127	BCL2-associated X protein	Mus musculus	52-55
27539478-10	2017	CONCLUSION: Both free and encapsulated sesamol demonstrated the inhibition of tumor progression by inducing skin cell apoptosis via bcl-2/bax mediated pathway.	sesamol	39-46	BCL2-associated X protein	Mus musculus	138-141
27995363-9	2017	Treatment with AZP-531 rescued the myocardium from cell death at early reperfusion by stimulating protein synthesis, inhibiting Bax/caspase 3-induced apoptosis as well as ROS accumulation and oxidative stress-induced necrosis.	cyclic des-acyl ghrelin (6-13)	15-22	BCL2-associated X protein	Mus musculus	128-131
28240526-4	2017	Result: In the heart and lung, nicotine caused significant decrease in P53, Bax and Caspase-3 mRNAexpression levels compared to the control group.	Nicotine	31-39	BCL2-associated X protein	Mus musculus	76-79
27209023-7	2017	In addition, baicalin enhanced the Bcl-2/Bax ratio associated with apoptosis in the kidney.	baicalin	13-21	BCL2-associated X protein	Mus musculus	41-44
27903423-6	2017	Using PCR Array, we found that trans-chalcone and LicoA trigger apoptosis mediated by the intrinsic pathway as demonstrated by the inhibition of Bcl-2 and induction of Bax.	Chalcone	31-45	BCL2-associated X protein	Mus musculus	168-171
27903423-6	2017	Using PCR Array, we found that trans-chalcone and LicoA trigger apoptosis mediated by the intrinsic pathway as demonstrated by the inhibition of Bcl-2 and induction of Bax.	licoa	50-55	BCL2-associated X protein	Mus musculus	168-171
28867726-10	2017	With respect to gastric mucosal apoptosis, acetate suppressed caspase-3 activity and BAX expression in favor of cell survival.	Acetates	43-50	BCL2-associated X protein	Mus musculus	85-88
28393075-7	2017	Immunohistochemistry revealed that maternal exposure of BPA increased Bax and decreased Bcl-2 at the protein levels in testicular and ovary tissues in the offspring mice.	bisphenol A	56-59	BCL2-associated X protein	Mus musculus	70-73
28480221-6	2017	PQ exposure induced upregulation of the proapoptotic gene Bax and downregulation of the antiapoptotic gene Bcl-2, leading to marked cell apoptosis in the lung tissues.	Paraquat	0-2	BCL2-associated X protein	Mus musculus	58-61
27769789-9	2017	Furthermore, resveratrol up-regulated the protein expression of p-JNK and Bcl-2, down-regulated the expression of Bax and the number of Fluoro-Jade C (FJC) positive neurons.	Resveratrol	13-24	BCL2-associated X protein	Mus musculus	114-117
28214881-13	2017	But Atv mitigated the reduction of Bcl-2/Bax level in heart of cold-treated mice.	Atorvastatin	4-7	BCL2-associated X protein	Mus musculus	41-44
29035884-10	2017	Pretreatment with quercetin also inhibited osteoblast apoptosis, significantly restored the down-regulated expression of Bcl-2 and Bcl-XL and decreased the upregulated expression of caspase-3, Bax, and cytochrome c in MC3T3-E1 cells induced by LPS.	Quercetin	18-27	BCL2-associated X protein	Mus musculus	193-196
29132134-12	2017	The expression of pro-apoptotic molecules including Fas and Bax was increased in the intestinal epithelia in CCI4-treated mice compared with that in control.	cci4	109-113	BCL2-associated X protein	Mus musculus	60-63
28270853-5	2017	Moreover, harmine dose-dependently induced apoptosis of TPC-1 cells through regulating the ratio of Bcl-2/Bax.	Harmine	10-17	BCL2-associated X protein	Mus musculus	106-109
28880739-8	2017	Methionine-deprived diet reduced expression of Col3a1, Cdh5, Fabp3, Bax, and Hbegf and increased expression of Sell, Ccl5, Itga2, Birc3, Msr1, Bcl2a1a, Il1r2, and Selp.	Methionine	0-10	BCL2-associated X protein	Mus musculus	68-71
26764232-10	2017	Silencing of Kv1.5 with siRNA reduced palmitate-induced endothelial apoptosis, intracellular ROS generation, mitochondrial ROS generation and membrane potential (Deltapsim) alteration and cleaved caspase-3 protein expression; while increased cell viability and ratio of Bcl-2/Bax.	Palmitates	38-47	BCL2-associated X protein	Mus musculus	276-279
27738712-6	2017	Our data showed that OEA treatment alleviated cell apoptosis in a mouse model of ischemic stroke, accompanied by suppression of Bax, as well as upregulation of antiapoptotic protein Bcl-2 level.	oleoylethanolamide	21-24	BCL2-associated X protein	Mus musculus	128-131
28191274-10	2017	In addition, western blot analysis revealed that carvacrol modulates the protein expression of Bcl-2, Bax, caspase-3, and p-ERK, without influence of p-JNK and p-p38.	carvacrol	49-58	BCL2-associated X protein	Mus musculus	102-105
28373901-11	2017	Rapamycin also attenuated Bax and increased Bcl-2/Bax ratio.	Sirolimus	0-9	BCL2-associated X protein	Mus musculus	26-29
28373901-11	2017	Rapamycin also attenuated Bax and increased Bcl-2/Bax ratio.	Sirolimus	0-9	BCL2-associated X protein	Mus musculus	50-53
28626497-6	2017	Western blot analysis revealed that FMF pretreatment significantly abrogated APAP-mediated phosphorylation of MAPKs, activation of proapoptotic protein caspase-3/9 and Bax, and restored expression of antiapoptotic protein Bcl2.	Acetaminophen	77-81	BCL2-associated X protein	Mus musculus	168-171
29201275-11	2017	Furthermore, Res and/or MK reversed PQ-induced apoptosis assessed by differential expression of p53, Bax, and Bcl-2.	Paraquat	36-38	BCL2-associated X protein	Mus musculus	101-104
27813540-8	2016	Moreover, mechanistic studies illustrated that ASP could upregulate the expression of PPARgamma and liver insulin signaling proteins, including IRS-2, PI3K, Akt, p-Akt and GLUT2, increase anti-apoptotic protein Bcl-2, decrease pro-apoptotic protein Bax expressions, and protect the mice against hepatic damage.	Aspartic Acid	47-50	BCL2-associated X protein	Mus musculus	249-252
27206668-10	2016	Similarly, proapoptotic protein bax and ROS production significantly decreased in cells after incubation with vinpocetine (p = 0.01) or VIP in the presence of Mn (p < 0.001).	vinpocetine	110-121	BCL2-associated X protein	Mus musculus	32-35
27856111-8	2016	Moreover, production of ROS subsequently activated p53, which in turn initiated release of mitochondrial cytochrome c via up-regulation of Bax and down-regulation of Bcl-2.	Reactive Oxygen Species	24-27	BCL2-associated X protein	Mus musculus	139-142
28081748-9	2016	Additionally, ROS inhibition caused a decrease in the Bcl-2/Bax ratio as well as promoting activation of apoptosis both in vitro and in vivo.	Reactive Oxygen Species	14-17	BCL2-associated X protein	Mus musculus	60-63
29949703-0	2016	Effect of quercetin on the expression of Bcl-2/Bax apoptotic proteins in endometrial cells of lipopolysaccharide-induced-abortion.	Quercetin	10-19	BCL2-associated X protein	Mus musculus	47-50
29949703-1	2016	OBJECTIVE: To explore the effect of quercetin on the expressions of Bcl-2/Bax apoptotic proteins inendometrial cells in mice with abortion induced by lipopolysaccharide.	Quercetin	36-45	BCL2-associated X protein	Mus musculus	74-77
29949703-11	2016	CONCLUSION: These results suggest that quercetin has protective effect by partially regulating the expressionof Bcl-2/Bax proteins, which in turn inhibits endometrial cell apoptosis and benefits the embryoimplantation.	Quercetin	39-48	BCL2-associated X protein	Mus musculus	118-121
26785383-4	2016	Data indicate that DDSD induced the generation of ROS, consequentially caused alteration in Bax/Bcl-2 ratio that disrupted the inner mitochondrial transmembrane potential (DeltaPsim) resulting in cytochrome c redistribution to the cytoplasm and activation of caspase-mediated apoptotic pathway.	N,O-Didecanoyl serinal dimethylacetal	19-23	BCL2-associated X protein	Mus musculus	92-95
26785383-4	2016	Data indicate that DDSD induced the generation of ROS, consequentially caused alteration in Bax/Bcl-2 ratio that disrupted the inner mitochondrial transmembrane potential (DeltaPsim) resulting in cytochrome c redistribution to the cytoplasm and activation of caspase-mediated apoptotic pathway.	ros	50-53	BCL2-associated X protein	Mus musculus	92-95
27748887-6	2016	Furthermore, the ratio of Bcl-2/Bax and the cleavage of caspase-3 and -9 were increased by gefitinib during oxaliplatin-induced apoptosis.	Gefitinib	91-100	BCL2-associated X protein	Mus musculus	32-35
27748887-6	2016	Furthermore, the ratio of Bcl-2/Bax and the cleavage of caspase-3 and -9 were increased by gefitinib during oxaliplatin-induced apoptosis.	Oxaliplatin	108-119	BCL2-associated X protein	Mus musculus	32-35
27843711-11	2016	Iron contributed to the permeabilizatio of mitochondria, leading to the release of cytochrome C (cyto C), which, in turn, induced mitochondrial apoptosis in osteoblasts via activation of Caspase-3, up-regulation of Bax, and down-regulation of Bcl-2.	Iron	0-4	BCL2-associated X protein	Mus musculus	215-218
27553677-6	2016	However, hematoxylin-eosin and bax-immunohistochemical stainings revealed that capmatinib (at a dose of 10, but not 5mg/kg) aggravated DEN-induced hepatocellular ballooning and apoptosis, respectively.	capmatinib	79-89	BCL2-associated X protein	Mus musculus	31-34
27562518-8	2016	Meanwhile, ginkgolide and bilobalide also attenuated the OGD/R-induced increases in TLR2, TLR4, MyD88, Bak, RIP3 levels and reversed cleaved caspase-3/caspase-3, Bax/Bcl-2 and cleaved PARP-1/PARP-1 ratio.	Ginkgolides	11-21	BCL2-associated X protein	Mus musculus	162-165
27562518-8	2016	Meanwhile, ginkgolide and bilobalide also attenuated the OGD/R-induced increases in TLR2, TLR4, MyD88, Bak, RIP3 levels and reversed cleaved caspase-3/caspase-3, Bax/Bcl-2 and cleaved PARP-1/PARP-1 ratio.	bilobalide	26-36	BCL2-associated X protein	Mus musculus	162-165
28836850-7	2016	Further, we found that EFV promoted increased lactate dehydrogenase (LDH) release, activation of p38 mitogen-activated protein kinase (MAPK), and increased Bax expression in cultured NSCs.	efavirenz	23-26	BCL2-associated X protein	Mus musculus	156-159
27625036-11	2016	Adelmidrol treatment produced a reduction of Bax and an intensification of Bcl-2 expression.	adelmidrol	0-10	BCL2-associated X protein	Mus musculus	45-48
27522965-9	2016	Anthocyanins also prevent overexpression of various apoptotic markers, i.e., Bax, cytosolic cytochrome C, cleaved caspase-3 and PARP-1.	Anthocyanins	0-12	BCL2-associated X protein	Mus musculus	77-80
27983966-11	2016	Moreover, increased cell apoptosis and pro-apoptotic protein Bax and caspase 3 were observed in ethanol treated mice, while the anti-apoptotic protein Bcl 2 was inhibited.	Ethanol	96-103	BCL2-associated X protein	Mus musculus	61-64
27582542-5	2016	Western blots showed 100muM propranolol significantly reduced the expression of Bcl-2 while increasing the expressions of Bax, cytochrome c, cleaved capase-9 and cleaved caspase-3, and down-regulated the levels of p-AKT, p-BRAF, p-MEK1/2 and p-ERK1/2 in melanoma cells, after a 24h incubation.	Propranolol	28-39	BCL2-associated X protein	Mus musculus	122-125
26683659-8	2016	Dexmedetomidine pretreatment effectively improved histological outcome and restored levels of caspase-3, the Bax/Bcl-2 ratio, NF-kappaB, and COX-2.	Dexmedetomidine	0-15	BCL2-associated X protein	Mus musculus	109-112
27250656-6	2016	In addition, the mitochondrial dysfunction shown through the decrease in the activities of mitochondrial enzymes and imbalance in the Bax/Bcl-2 expression in the livers and kidneys of bromobenzene-treated mice was effectively prevented by pre-administration of withaferin A.	bromobenzene	184-196	BCL2-associated X protein	Mus musculus	134-137
27250656-6	2016	In addition, the mitochondrial dysfunction shown through the decrease in the activities of mitochondrial enzymes and imbalance in the Bax/Bcl-2 expression in the livers and kidneys of bromobenzene-treated mice was effectively prevented by pre-administration of withaferin A.	withaferin A	261-273	BCL2-associated X protein	Mus musculus	134-137
27546300-3	2016	The hepatic histopathological and serum biochemical assessment revealed that ruxolitinib pre-treatments dose-dependently reduced TAA-induced liver injury, caspase 3 cleavage and increase in number of hepatocytes positive for the pro-apoptotic Bax, as well as inflammatory cells positive for F4/80 and myeloperoxidase activity in the liver.	ruxolitinib	77-88	BCL2-associated X protein	Mus musculus	243-246
27271513-5	2016	Treatment of RAW 264.7 cells with MSU crystals induced activation of Bax, caspase-3, caspase-9, and PARP1 at the early phase, in addition to enhancing IL-1beta expression, but these findings were attenuated at the late phase.	Uric Acid	34-37	BCL2-associated X protein	Mus musculus	69-72
27241100-8	2016	Inhibition of NF-kappaB activation with the specific NF-kappaB inhibitor, PDTC (pyrrolidine dithiocarbamate), reversed Bcl-xL down-regulation and Bax up-regulation, and led to a significant increase in LIGHT- and IFN-gamma-treated cell viability.	pyrrolidine dithiocarbamic acid	80-107	BCL2-associated X protein	Mus musculus	146-149
27234990-10	2016	Moreover, sevoflurane induced a significant increase of pro-apoptotic protein BIM and Bax but a reduction of anti-apoptotic proteins Bcl-2 in the hippocampus.	Sevoflurane	10-21	BCL2-associated X protein	Mus musculus	86-89
27706063-7	2016	Furthermore, pretreatment with koumine suppressed LPS-mediated p53 activation, loss of mitochondrial membrane potential, caspase-3 activation, decrease of Bcl-2 expression, and elevation of Bax and caspase-3 expressions, suggesting that koumine might act directly on RAW 264.7 cells to inhibit LPS-induced apoptosis.	koumine	31-38	BCL2-associated X protein	Mus musculus	190-193
27706063-7	2016	Furthermore, pretreatment with koumine suppressed LPS-mediated p53 activation, loss of mitochondrial membrane potential, caspase-3 activation, decrease of Bcl-2 expression, and elevation of Bax and caspase-3 expressions, suggesting that koumine might act directly on RAW 264.7 cells to inhibit LPS-induced apoptosis.	koumine	237-244	BCL2-associated X protein	Mus musculus	190-193
27619562-7	2016	Instead, inhibition of Drp1 mitochondrial translocation diminished MPTP-induced p53, BAX and PUMA mitochondrial translocation.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	67-71	BCL2-associated X protein	Mus musculus	85-88
27649238-10	2016	Furthermore, ginsenoside Rg5 supplementation inhibited activation of apoptotic pathways through increasing Bcl-2 and decreasing Bax expression levels.	Ginsenosides	13-24	BCL2-associated X protein	Mus musculus	128-131
27698928-5	2016	After CTPG treatment, the expressions of BAX and BCL-2 were up-regulated and down-regulated, respectively.	ctpg	6-10	BCL2-associated X protein	Mus musculus	41-44
27660471-6	2016	CBL-G2 dendrimer conjugate was able to checkmate antiapoptotic Bcl-2 expression and Bcl-2/Bax ratio in a large scale compared with the control group and CBL alone (P<0.005).	Chlorambucil	0-3	BCL2-associated X protein	Mus musculus	90-93
27346131-12	2016	Apoptosis was induced mostly when treatments were done with ascorbate, causing PARP and Bax cleavage, and increased Bax/Bcl-xL ratio.	Ascorbic Acid	60-69	BCL2-associated X protein	Mus musculus	88-91
26438401-9	2016	We found that KCa3.1 blockade attenuated cytochrome c release and the increase in the intrinsic apoptotic mediators Bax, Bak, and caspase-9 after cisplatin treatment.	Cisplatin	146-155	BCL2-associated X protein	Mus musculus	116-119
27292166-8	2016	Our results showed that busulfan-treated platelets displayed increased mitochondrial membrane depolarization, decreased expression of Bcl-2, increased expression of Bax and caspase 3 activation in dose-dependent manner, which were inhibited by QVD-Oph.	Busulfan	24-32	BCL2-associated X protein	Mus musculus	165-168
27261070-11	2016	DHPG also increased the expression of Bcl2A1, an antiapoptotic oncogene and simultaneously reduced the expression of Bax, a pro-apoptotic marker.	3,4-dihydroxyphenylglycol	0-4	BCL2-associated X protein	Mus musculus	117-120
27317935-5	2016	However, in DA-p53KO mice treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that the induction of Bax and p53 up-regulated modulator of apoptosis (PUMA) mRNA and protein levels by MPTP were diminished in both striatum and substantia nigra of these mice.	Dopamine	12-14	BCL2-associated X protein	Mus musculus	138-141
27317935-5	2016	However, in DA-p53KO mice treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that the induction of Bax and p53 up-regulated modulator of apoptosis (PUMA) mRNA and protein levels by MPTP were diminished in both striatum and substantia nigra of these mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	54-98	BCL2-associated X protein	Mus musculus	138-141
27317935-5	2016	However, in DA-p53KO mice treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that the induction of Bax and p53 up-regulated modulator of apoptosis (PUMA) mRNA and protein levels by MPTP were diminished in both striatum and substantia nigra of these mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	100-104	BCL2-associated X protein	Mus musculus	138-141
27317935-5	2016	However, in DA-p53KO mice treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that the induction of Bax and p53 up-regulated modulator of apoptosis (PUMA) mRNA and protein levels by MPTP were diminished in both striatum and substantia nigra of these mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	220-224	BCL2-associated X protein	Mus musculus	138-141
27317935-9	2016	Our results further support the role of programmed cell death mediated by p53 in this animal model of PD and identify Bax, BAD and PUMA genes as downstream targets of p53 in modulating DA neuronal death in the in vivo MPTP-induced PD model.	Dopamine	185-187	BCL2-associated X protein	Mus musculus	118-121
27317935-9	2016	Our results further support the role of programmed cell death mediated by p53 in this animal model of PD and identify Bax, BAD and PUMA genes as downstream targets of p53 in modulating DA neuronal death in the in vivo MPTP-induced PD model.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	218-222	BCL2-associated X protein	Mus musculus	118-121
27317935-10	2016	We deleted p53 gene in dopaminergic neurons in late developmental stages and found that DA specific p53 deletion is protective in acute MPTP animal model possibly through blocking MPTP-induced BAX and PUMA up-regulation.	Dopamine	88-90	BCL2-associated X protein	Mus musculus	193-196
27317935-10	2016	We deleted p53 gene in dopaminergic neurons in late developmental stages and found that DA specific p53 deletion is protective in acute MPTP animal model possibly through blocking MPTP-induced BAX and PUMA up-regulation.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	136-140	BCL2-associated X protein	Mus musculus	193-196
27317935-10	2016	We deleted p53 gene in dopaminergic neurons in late developmental stages and found that DA specific p53 deletion is protective in acute MPTP animal model possibly through blocking MPTP-induced BAX and PUMA up-regulation.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	180-184	BCL2-associated X protein	Mus musculus	193-196
27449757-8	2016	We demonstrate that OXA attenuates PA-induced hypothalamic cell death via reduced caspase-3/7 apoptosis, stabilization of Bcl-2 gene expression, and reduced Bax/Bcl-2 gene expression ratio.	Palmitic Acid	35-37	BCL2-associated X protein	Mus musculus	157-160
27180190-0	2016	Protective Effect of Aliskiren in Experimental Ischemic Stroke: Up-Regulated p-PI3K, p-AKT, Bcl-2 Expression, Attenuated Bax Expression.	aliskiren	21-30	BCL2-associated X protein	Mus musculus	121-124
27580845-6	2016	Treatment with CsA and FK506 also inhibited PAN-induced podocytes apoptosis, which was associated with the induction of Bcl-xL and inhibition of Bax, cleaved caspase 3, and cleaved PARP expression.	Cyclosporine	15-18	BCL2-associated X protein	Mus musculus	145-148
27580845-6	2016	Treatment with CsA and FK506 also inhibited PAN-induced podocytes apoptosis, which was associated with the induction of Bcl-xL and inhibition of Bax, cleaved caspase 3, and cleaved PARP expression.	Tacrolimus	23-28	BCL2-associated X protein	Mus musculus	145-148
27605908-6	2016	Our results showed that TTC treatment reduced the expression of autophagy markers (Becn1, Atg5, Lc3, and p62) and pro-apoptotic genes such as Bax and Casp3 in spinal cord.	6-thiotheophylline	24-27	BCL2-associated X protein	Mus musculus	142-145
27311853-7	2016	Moreover, this polyphenol suppressed p-STAT3 production as well as its downstream proteins response for apoptosis, such as Bcl-2 and Bax.	Polyphenols	15-25	BCL2-associated X protein	Mus musculus	133-136
27286704-5	2016	Immunoblotting and real-time quantitative polymerase chain reaction (RT-qPCR) revealed that ZEA treatment increased the ratio of Bax/Bcl-2.	Zearalenone	92-95	BCL2-associated X protein	Mus musculus	129-132
27470358-8	2016	Additionally, apoptosis was induced by hyperoside via Bcl-2/Bax-regulated Caspase3 activation, suggesting that hyperoside might inhibit lung cancer progression through apoptotic induction.	hyperoside	39-49	BCL2-associated X protein	Mus musculus	60-63
27470358-8	2016	Additionally, apoptosis was induced by hyperoside via Bcl-2/Bax-regulated Caspase3 activation, suggesting that hyperoside might inhibit lung cancer progression through apoptotic induction.	hyperoside	111-121	BCL2-associated X protein	Mus musculus	60-63
27470360-10	2016	And carnosic acid nanoparticles also suppressed the ischemia/reperfusion-induced up-regulation in the pro-apoptotic protein and mRNA levels of Bax, Cyto-c, Apaf-1 and Caspase-9/3 while increased ischemia/reperfusion-induced decrease of anti-apoptotic factor of Bcl-2.	salvin	4-17	BCL2-associated X protein	Mus musculus	143-146
26976669-4	2016	with twice injections at 1 h and 12 h after transient middle cerebral artery occlusion (tMCAO) respectively alleviated neurological deficits and neuronal apoptosis in a mouse ischemic stroke model, accompanied by inhibiting interleukin-1beta (IL-1beta), Bax and p53 expression and upregulating anti-apoptotic protein Bcl-2 level.	tmcao	88-93	BCL2-associated X protein	Mus musculus	254-257
27208085-7	2016	Treatment with BaP elevated the expression of BAX protein at 6 h and activated downstream caspases-9 and -3 at 24 h in a concentration-dependent manner in germ cells of fetal ovaries.	Benzo(a)pyrene	15-18	BCL2-associated X protein	Mus musculus	46-49
27208085-10	2016	Our findings show that BaP exposure increases caspase-dependent and BAX-associated germ cell apoptosis in the mouse fetal ovary, leading to germ cell depletion.	Benzo(a)pyrene	23-26	BCL2-associated X protein	Mus musculus	68-71
27504096-8	2016	OtoN may reduce PTZ-induced cleavage of poly ADP-ribose polymerase and upregulation of the Bax/Bcl-2 ratio and decrease the expression level of c-Fos.	Pentylenetetrazole	16-19	BCL2-associated X protein	Mus musculus	91-94
27151150-9	2016	Exposure of glutamate-treated cells to emodin induced an increase in the level of Bcl-2 expression, whereas the expression of Bax and active caspase-3 proteins was significantly reduced.	Glutamic Acid	12-21	BCL2-associated X protein	Mus musculus	126-129
27391020-7	2016	Dapagliflozin reduced renal expression of Bax, renal tubule injury and TUNEL-positive cells and increased renal expression of HIF1 in IR-injured mice.	dapagliflozin	0-13	BCL2-associated X protein	Mus musculus	42-45
27447538-6	2016	Meanwhile, the reduction of free radical formation and proinflammatory cytokines, as well as the increase of hypoxia-inducible factor-1alpha pathway proteins and Bcl2/Bax ratio, further indicated that DFO was effective for liver protection and hepatic adaptation.	Deferoxamine	201-204	BCL2-associated X protein	Mus musculus	167-170
27017962-7	2016	Meanwhile, the Bcl2/Bax ratio was decreased significantly by MPTP in the striatum and SN of MtFt knockout (MtFt-/-) mice compared with controls.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	61-65	BCL2-associated X protein	Mus musculus	20-23
27310206-5	2016	In relation to increased apoptosis, bax, cleaved caspase-9 and cleaved caspase-3 levels elevated significantly, indicating that PFOS induced germ cell apoptosis by activating the mitochondrial pathway.	perfluorooctane sulfonic acid	128-132	BCL2-associated X protein	Mus musculus	36-39
27215129-6	2016	Significant upregulation of Bcl-2 and downregulation of Bax and cleaved caspase-3 was observed in cells treated with cannabidiol-moringin combination.	Cannabidiol	117-128	BCL2-associated X protein	Mus musculus	56-59
27215129-6	2016	Significant upregulation of Bcl-2 and downregulation of Bax and cleaved caspase-3 was observed in cells treated with cannabidiol-moringin combination.	moringin	129-137	BCL2-associated X protein	Mus musculus	56-59
27756959-16	2016	Bax was up-regulated and anti-apoptotic protein Bcl-2 was down-regulated resulting in decrease of the Bcl-2/Bax ratio by MEAC treatment.	meac	121-125	BCL2-associated X protein	Mus musculus	0-3
27756959-16	2016	Bax was up-regulated and anti-apoptotic protein Bcl-2 was down-regulated resulting in decrease of the Bcl-2/Bax ratio by MEAC treatment.	meac	121-125	BCL2-associated X protein	Mus musculus	108-111
25730317-8	2016	In addition, lutein repressed the MPTP-induced neuronal damage/apoptosis by inhibiting the activation of pro-apoptotic markers (Bax, caspases-3, 8 and 9) and enhancing anti-apoptotic marker (Bcl-2) expressions.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	34-38	BCL2-associated X protein	Mus musculus	128-131
27320914-4	2016	Subsequent tBid recruitment to mitochondria, which is facilitated by its receptor MTCH2 at the outer mitochondrial membrane (OMM), is a critical step for commitment to apoptosis via the effector proteins Bax or Bak.	tBID	11-15	BCL2-associated X protein	Mus musculus	204-207
27137932-3	2016	In Pdx1 haploinsufficient mice, Bax ablation in beta-cells increased beta-cell mass, decreased the number of TUNEL positive cells and improved glucose tolerance after glucose challenge.	Glucose	143-150	BCL2-associated X protein	Mus musculus	32-35
27235712-10	2016	Berberine potentiated G0/G1 cell cycle arrest by inhibiting proliferation, cyclin dependent kinases and cyclins resulting in apoptosis through increased bax/bcl-2 ratio.	Berberine	0-9	BCL2-associated X protein	Mus musculus	153-156
27060504-5	2016	Our data showed that Cd exposure decreased the numbers of impregnated females and litter sizes, which was concomitant with sperm count reduction, histological changes in the cauda epididymal ducts and seminiferous epithelium, and testicular cell apoptosis as evaluated by terminal dUTP nick-end labeling (TUNEL) assay and immunoblotting with increased levels of cleaved caspase 3, PARP and Bax and a decreased level of Bcl-2.	Cadmium	21-23	BCL2-associated X protein	Mus musculus	390-393
27271364-3	2016	Climacostol caused a reduction of viability/proliferation of B16-F10 mouse melanoma cells, a rapidly occurring DNA damage, and induced the intrinsic apoptotic pathway characterised by the dissipation of the mitochondrial membrane potential, the translocation of Bax to the mitochondria, the release of Cytochrome c from the mitochondria, and the activation of Caspase 9-dependent cleavage of Caspase 3.	climacostol	0-11	BCL2-associated X protein	Mus musculus	262-265
26428408-9	2016	The number of TUNEL-positive cells was increased, and the BAX and caspase-3 expressions were upregulated in EL4 cells for group that received an effective dose of cisplatin).	Cisplatin	163-172	BCL2-associated X protein	Mus musculus	58-61
27514534-6	2016	Compared with DG groups, EPA and DHA further enhanced Bax expression.	Eicosapentaenoic Acid	25-28	BCL2-associated X protein	Mus musculus	54-57
27514534-6	2016	Compared with DG groups, EPA and DHA further enhanced Bax expression.	Docosahexaenoic Acids	33-36	BCL2-associated X protein	Mus musculus	54-57
26996132-9	2016	Additionally, the effects of DFO on increasing the Bcl-2/Bax ratio were further validated in vitro and in vivo.	Deferoxamine	29-32	BCL2-associated X protein	Mus musculus	57-60
26490536-4	2016	METHODS: Bax siRNA was transfected into a sinusoidal endothelial cell line (M1) to suppress apoptosis induced by an anti-Fas antibody and staurosporine.	Staurosporine	138-151	BCL2-associated X protein	Mus musculus	9-12
26450947-5	2016	Intriguingly, resveratrol attenuated the doxorubicin-induced elevations of apoptotic and catabolic markers measured as Bax, caspase 3 activity, apoptotic DNA fragmentation, MuRF-1, ubiquitinated proteins, and proteasomal activity in aged muscles, whereas these beneficial effects were abolished on inhibition of sirtuin 1 by sirtinol or EX527.	Resveratrol	14-25	BCL2-associated X protein	Mus musculus	119-122
28348416-8	2017	On the other hand, CBG was found to increase anti-oxidant defense of cells by modulating superoxide dismutase-1 (SOD-1) expression and thus inhibiting cell death (results focused on balance between Bax and Bcl-2).	cannabigerol	19-22	BCL2-associated X protein	Mus musculus	198-201
28187727-12	2017	Tumors from ATO combined with CT-treated mice showed decreased levels of phosphorylated-STAT3Tyr705 and the anti-apoptotic protein Bcl-2 but an increased level of pro-apoptotic protein Bax.	cryptotanshinone	30-32	BCL2-associated X protein	Mus musculus	185-188
26450947-5	2016	Intriguingly, resveratrol attenuated the doxorubicin-induced elevations of apoptotic and catabolic markers measured as Bax, caspase 3 activity, apoptotic DNA fragmentation, MuRF-1, ubiquitinated proteins, and proteasomal activity in aged muscles, whereas these beneficial effects were abolished on inhibition of sirtuin 1 by sirtinol or EX527.	Doxorubicin	41-52	BCL2-associated X protein	Mus musculus	119-122
27342530-12	2016	CD8+ T cell apoptosis in iron overload group was significantly higher than that in control groups (P<0.01); the expression of BCL-2 at mRNA level was lower than that in control group, but the expression of BAX at mRNA level was higher than that in control group (P<0.05).	Iron	25-29	BCL2-associated X protein	Mus musculus	209-212
27159560-5	2016	Our structure-function analyses revealed that the BH3 binding capacity of MCL-1 and its suppression of BAX are impaired by molecular engagement, a phenomenon recapitulated by C286W mutagenic mimicry in vitro and in mouse cells.	BH 3	50-53	BCL2-associated X protein	Mus musculus	103-106
27382379-4	2016	Significant suppression of acetylcholinesterase (AChE) activity and Bax/Bcl-2 expression was also observed in the DG treated TG mice (TG+DG group) when compared with those of the vehicle (VC) treated TG mice (TG+VC group).	Thioguanine	125-127	BCL2-associated X protein	Mus musculus	68-71
27382379-4	2016	Significant suppression of acetylcholinesterase (AChE) activity and Bax/Bcl-2 expression was also observed in the DG treated TG mice (TG+DG group) when compared with those of the vehicle (VC) treated TG mice (TG+VC group).	Thioguanine	134-136	BCL2-associated X protein	Mus musculus	68-71
27382379-4	2016	Significant suppression of acetylcholinesterase (AChE) activity and Bax/Bcl-2 expression was also observed in the DG treated TG mice (TG+DG group) when compared with those of the vehicle (VC) treated TG mice (TG+VC group).	Polyvinyl Chloride	188-190	BCL2-associated X protein	Mus musculus	68-71
27382379-4	2016	Significant suppression of acetylcholinesterase (AChE) activity and Bax/Bcl-2 expression was also observed in the DG treated TG mice (TG+DG group) when compared with those of the vehicle (VC) treated TG mice (TG+VC group).	Thioguanine	134-136	BCL2-associated X protein	Mus musculus	68-71
27382379-4	2016	Significant suppression of acetylcholinesterase (AChE) activity and Bax/Bcl-2 expression was also observed in the DG treated TG mice (TG+DG group) when compared with those of the vehicle (VC) treated TG mice (TG+VC group).	Thioguanine	134-136	BCL2-associated X protein	Mus musculus	68-71
27171144-7	2016	Furthermore, Sirt1 also deacetylated p53 and then increased the binding of p53 to Bax, resulting in increased cytosolic cytochrome C. The effect of PPARgamma inactivation by PFOS was validated using the PPARgamma antagonist GW9662, whereas the adverse effects of PFOS were prevented by PPARgamma overexpression and activators, rosiglitozone and L-carnitine, in RTCs.	perfluorooctane sulfonic acid	174-178	BCL2-associated X protein	Mus musculus	82-85
27262802-7	2016	In addition, SA pretreatment increased Bcl-2 expression and decreased the expression of Bax and cleaved caspase-3 in H2O2-induced RGC-5 cells.	syringic acid	13-15	BCL2-associated X protein	Mus musculus	88-91
27262802-7	2016	In addition, SA pretreatment increased Bcl-2 expression and decreased the expression of Bax and cleaved caspase-3 in H2O2-induced RGC-5 cells.	Hydrogen Peroxide	117-121	BCL2-associated X protein	Mus musculus	88-91
27274198-12	2016	CONCLUSION: The combination of blueberry juice and probiotics reduces apoptosis in AFLD by suppressing FOXO1, phosphorylated FOXO1, acetylated FOXO1, FasL, caspase-3, BAX, and Bcl-2 via the upregulation of SIRT1.	blueberry juice	31-46	BCL2-associated X protein	Mus musculus	167-170
26854718-8	2016	Further, inhibition of ROS with NAC not only rescued glioma cell necrosis but also suppressed JNK activation, mitigated Bax/Bcl-2 ratio, maintained mitochondrial membrane potential, and inhibited AIF translocation into nucleus.	ros	23-26	BCL2-associated X protein	Mus musculus	120-123
27029485-4	2016	Caffeic acid (CA) inhibits JAK-STAT3 signaling, thereby induces apoptotic cell death by upregulating Bax, Cytochrome-C, Caspase-9 and Caspase-3 expression in mouse skin.	caffeic acid	0-12	BCL2-associated X protein	Mus musculus	101-104
28891624-11	2016	The proliferation and differentiation of hematopoietic progenitor cells in bone marrow were promoted, the apoptosis of bone marrow cells was significantly up-regulated and the expression of cleaved caspase-3 and Bax was significantly reduced in SSD and catechin group.	Catechin	253-261	BCL2-associated X protein	Mus musculus	212-215
26854718-4	2016	We found that pristimerin inhibited the viabilities of glioma cells in vitro and the growth of xenograft gliomas in vivo, which was accompanied by upregulation of JNK and phosphor-JNK, nuclear accumulation of AIF, and elevation in the ratio of Bax/Bcl-2.	pristimerin	14-25	BCL2-associated X protein	Mus musculus	244-247
27124579-8	2016	Furthermore, DMBA treatment triggered the upregulation of pro-apoptotic (Bid, Apaf1, Bax), cell death (Tnfrsf10b, Ripk1) and cell cycle inhibitor (Cdkn1a, Cdkn2c) genes in the mammary glands.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	13-17	BCL2-associated X protein	Mus musculus	85-88
27108902-11	2016	Western blot analysis showed that the ratio of BAX to BCL2 protein level was increased in UUO model compared with that in sham mice, and the increment also was diminished by valsartan treatment (P < 0.05).	Valsartan	174-183	BCL2-associated X protein	Mus musculus	47-50
26968952-7	2016	Furthermore, CoQ0 treatment induced apoptosis through caspase-9/-3 activation, PARP degradation, Bcl-2/Bax dysregulation, and p53 expression.	ubiquinone-O	13-17	BCL2-associated X protein	Mus musculus	103-106
27175086-8	2016	In addition, expressions of Fas and Fas ligand could be detected in MA-10 cells with midazolam treatments, and Bax translocation and cytochrome c release were also involved in midazolam-induced MA-10 cell apoptosis.	Midazolam	176-185	BCL2-associated X protein	Mus musculus	111-114
27070587-8	2016	Also, expression of the Bcl-2, truncated Bid, Cu/Zn- superoxide dismutase (SOD), and Mn-SOD proteins were significantly increased by melatonin treatment, whereas levels of Bax and catalase were decreased.	Melatonin	133-142	BCL2-associated X protein	Mus musculus	172-175
27050422-9	2016	Moreover, pre-treatment with quercetin not only inhibited OA-induced apoptosis via the reduction of Bax, and up-regulation of cleaved caspase 3, but also via the inhibition of PI3K/Akt/GSK3beta, MAPKs and activation of NF-kappaB p65.	Quercetin	29-38	BCL2-associated X protein	Mus musculus	100-103
26881453-5	2016	Although naringenin induces apoptosis in cancer cells we found that it can protect against radiation-induced apoptosis in normal cells by modulating the expression of p53, Bax, and Bcl-2.	naringenin	9-19	BCL2-associated X protein	Mus musculus	172-175
26850368-4	2016	Treatment with cocaine resulted in significant decreases in expression of Bcl-2 and Bcl-xl in the kidney of non-TG mice, which resulted in significant increases in Bax and cleaved-caspase 3.	Cocaine	15-22	BCL2-associated X protein	Mus musculus	164-167
27009084-7	2016	NVP-Bez235 combined with lenalidomide remarkably increased apoptosis through intrinsic pathway by upregulating Bim, Bax and downregulating Bcl-xL.	dactolisib	4-10	BCL2-associated X protein	Mus musculus	116-119
27009084-7	2016	NVP-Bez235 combined with lenalidomide remarkably increased apoptosis through intrinsic pathway by upregulating Bim, Bax and downregulating Bcl-xL.	Lenalidomide	25-37	BCL2-associated X protein	Mus musculus	116-119
25895139-11	2016	At the same time, TMT-induced inhibition of phosphoinositol 3-kinase (PI3K)/Akt signaling was evident, thereby decreasing phospho-Bad, expression of Bcl-xL and Bcl-2, and the interaction between phospho-Bad and 14-3-3 protein, and increasing Bax expression and caspase-3 cleavage were observed.	trimethyltin	18-21	BCL2-associated X protein	Mus musculus	242-245
26921633-5	2016	However, only DFO decreased liver apoptosis through the reduced Bax/Bcl-2 ratio in wild type (WT) mice.	Deferoxamine	14-17	BCL2-associated X protein	Mus musculus	64-67
27031959-6	2016	We found that DHA-activated caspase-3 increased Bax/Bcl-2 ratio during LPS-induced osteoclastogenesis.	artenimol	14-17	BCL2-associated X protein	Mus musculus	48-51
26719366-6	2016	SS-31 attenuated renal cell apoptosis and expression of Bax and reversed the expression of Bcl-2 in diabetic mice kidneys.	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	0-5	BCL2-associated X protein	Mus musculus	56-59
26719366-8	2016	In vitro experiments using MMCs revealed that SS-31 inhibited HG-mediated ROS generation, apoptosis, expression of cleaved caspase-3, Bax/Bcl-2 ratio, and cytochrome c (cyt c) release from mitochondria.	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	46-51	BCL2-associated X protein	Mus musculus	134-137
27455660-7	2016	ZnO-NP induced the down-regulation of Bcl2 (an anti-apoptotic factor) and up-regulation of Bax (an apoptotic factor) through the stabilization of p53 protein.	zno-np	0-6	BCL2-associated X protein	Mus musculus	91-94
26709117-0	2016	Disturbance of Bcl-2, Bax, Caspase-3, Ki-67 and C-myc expression in acute and subchronic exposure to benzo(a)pyrene in cervix.	Benzo(a)pyrene	101-115	BCL2-associated X protein	Mus musculus	22-25
26709117-4	2016	Here we present the findings of exposure to BaP on the expression of Bcl-2, C-myc, Ki-67, Caspase-3 and Bax genes in mouse cervix.	Benzo(a)pyrene	44-47	BCL2-associated X protein	Mus musculus	104-107
26709117-7	2016	In sub chronic intraperitoneal and oral gavage administration of BaP (2.5, 5, 10mg/kg body weight), similar significant increase was observed for all the examined genes as compared to the control and vehicle groups, however the expression of Bax decreased in a dose dependent manner.	Benzo(a)pyrene	65-68	BCL2-associated X protein	Mus musculus	242-245
25976060-7	2016	Indeed, treatment of miR-124 agomir in MPTP-treated mice inhibited Bim expression, thus suppressing Bax translocation to mitochondria.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	39-43	BCL2-associated X protein	Mus musculus	100-103
26607398-8	2016	Mechanistically, melatonin enhanced SIRT1 signaling, which was accompanied with the increased expression of anti-apoptotic protein Bcl2, and decreased the expression of Ac-FoxO1, Ac-p53, Ac-NF-KappaB, and Bax.	Melatonin	17-26	BCL2-associated X protein	Mus musculus	205-208
26796245-9	2016	Furthermore, the effects of paeoniflorin decreased inflammation and caspase-3 activity, and inhibited cell death via increasing the Bcl-2/Bax ratio and p-Akt expression levels, and downregulating p-p38 MAPK expression in AD mice.	peoniflorin	28-40	BCL2-associated X protein	Mus musculus	138-141
27239851-0	2016	[Influence of chronic alcohol treatment on the expression of the Bdnf, Bax, Bcl-xL, and CASP3 genes in the mouse brain: Role of the C1473G polymorphism in the gene encoding tryptophan hydroxylase 2].	Alcohols	22-29	BCL2-associated X protein	Mus musculus	71-74
27239851-3	2016	The influence of chronic ethanol consumption on the expression of the Bdnf, Bax, Bcl-xL, and CASP3 genes was studied in the brain structures of B6-1473C (C/C) and B6-1473G (G/G) mice that had been obtained on the base of the C57BL/6 strain.	Ethanol	25-32	BCL2-associated X protein	Mus musculus	76-79
26918825-7	2016	In addition, Hex significantly reduced STZ-induced expression of cleaved Caspases-3, Caspases-9 and the ratio of pro-apoptotic protein Bax to anti-apoptotic protein Bcl-2 in MIN6 cells.	hexarelin	13-16	BCL2-associated X protein	Mus musculus	135-138
25561437-5	2016	SLB reversed the decreased level of procaspase-3 and balanced Bcl-2 and Bax expression upon H2O2 insult to inhibit cell apoptosis.	Hydrogen Peroxide	92-96	BCL2-associated X protein	Mus musculus	72-75
26918825-7	2016	In addition, Hex significantly reduced STZ-induced expression of cleaved Caspases-3, Caspases-9 and the ratio of pro-apoptotic protein Bax to anti-apoptotic protein Bcl-2 in MIN6 cells.	Streptozocin	39-42	BCL2-associated X protein	Mus musculus	135-138
26918825-10	2016	Hex also ameliorated STZ-induced expression of cleaved Caspase-9 and the Bax in beta-cells.	hexarelin	0-3	BCL2-associated X protein	Mus musculus	73-76
26918825-10	2016	Hex also ameliorated STZ-induced expression of cleaved Caspase-9 and the Bax in beta-cells.	Streptozocin	21-24	BCL2-associated X protein	Mus musculus	73-76
26875785-10	2016	Pravastatin induced islet dysfunction was associated with marked reductions of exocytosis-related SNARE proteins (SNAP25, Syntaxin 1A, VAMP2) and increased apoptosis markers (Bax/Bcl2 protein ratio, cleaved caspase-3 and lower NAD(P)H production rates) observed in pancreatic islets from treated mice.	Pravastatin	0-11	BCL2-associated X protein	Mus musculus	175-178
26679980-0	2016	Subchronic exposure of benzo(a)pyrene interferes with the expression of Bcl-2, Ki-67, C-myc and p53, Bax, Caspase-3 in sub-regions of cerebral cortex and hippocampus.	Benzo(a)pyrene	23-37	BCL2-associated X protein	Mus musculus	101-104
26716512-6	2016	Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38.	Fluorouracil	38-52	BCL2-associated X protein	Mus musculus	133-136
26716512-6	2016	Treatment of breast cancer cells with 5-fluorouracil (5-FU) increased the expression of pro-apoptotic and anti-proliferative factor, BAX and p21 protein through phosphorylation of p53 and p38.	Fluorouracil	54-58	BCL2-associated X protein	Mus musculus	133-136
26676762-12	2016	Additionally, 661W cells exposed to sodium formate for 24 h exhibited increased levels of p-JNK, Bax, cleaved caspase-3, cleaved caspase-9 and LC3II (the phosphatidylethanolamine-modified form of LC3), although the level of Bcl-2 was decreased.	formic acid	36-50	BCL2-associated X protein	Mus musculus	97-100
26676112-8	2016	Losartan also increased the B-cell lymphoma 2 (Bcl2)/Bcl-2-associated X protein (Bax) ratio and suppressed caspase-3 induction.	Losartan	0-8	BCL2-associated X protein	Mus musculus	53-79
26676112-8	2016	Losartan also increased the B-cell lymphoma 2 (Bcl2)/Bcl-2-associated X protein (Bax) ratio and suppressed caspase-3 induction.	Losartan	0-8	BCL2-associated X protein	Mus musculus	81-84
26676112-10	2016	The effects of losartan were partially mediated through increasing the Bcl-2/Bax ratio and subsequently suppressing the induction of the proapoptotic mediator caspase-3.	Losartan	15-23	BCL2-associated X protein	Mus musculus	77-80
26721359-7	2016	In addition to ROS scavenging activity in Dex-induced thymocyte, BA administration decreased lipid peroxidation, up-regulated antioxidant enzymes, restored mitochondrial function, increased Bcl-2 expression but reduced Bax expression, inhibited caspase-3 activation, and improved cell survival.	betulinic acid	65-67	BCL2-associated X protein	Mus musculus	219-222
26454207-5	2016	In cultures of myofibers and myoblasts isolated from dysf(-/-) mice, halofuginone reduced Bax and induced Bcl2 expression levels and induced Akt phosphorylation in a time-dependent manner.	halofuginone	69-81	BCL2-associated X protein	Mus musculus	90-93
27141616-0	2016	[Electroacupuncture Intervention Inhibits the Decline of Learning-memory Ability and Overex- pression of Cleaved Caspase-3 and Bax in Hippocampus Induced by Isoflurane in APPswe/PS 1].	Isoflurane	157-167	BCL2-associated X protein	Mus musculus	127-130
26099903-7	2016	We found that FTY720 administration after TBI improved neurobehavioral function, alleviated brain edema, accompanied by modulation of apoptotic indicators such as Bcl-2, Bcl-xL, Bax, and cytochrome c. In experiment 2, ICR mice were also divided into four groups: sham group, TBI + vehicle group, TBI + FTY720 group, and TBI + FTY720 + inhibitors group.	Fingolimod Hydrochloride	14-20	BCL2-associated X protein	Mus musculus	178-181
28119929-7	2016	Furthermore, aspirin induced the apoptosis of acinar cells by TUNEL assay, and the expression of Bax and caspase 3 was increased and the expression of Bcl-2 was decreased.	Aspirin	13-20	BCL2-associated X protein	Mus musculus	97-100
26828432-0	2016	Doxycycline Protects Thymic Epithelial Cells from Mitomycin C-Mediated Apoptosis In Vitro via Trx2-NF-kappaB-Bcl-2/Bax Axis.	Mitomycin	50-61	BCL2-associated X protein	Mus musculus	115-118
26828432-10	2016	Meanwhile, Dox also increased the expression of Bcl-2, partially reduced the expression of Bax, and normalized the ratio of Bcl-2 to Bax.	Doxycycline	11-14	BCL2-associated X protein	Mus musculus	91-94
26828432-10	2016	Meanwhile, Dox also increased the expression of Bcl-2, partially reduced the expression of Bax, and normalized the ratio of Bcl-2 to Bax.	Doxycycline	11-14	BCL2-associated X protein	Mus musculus	133-136
26828432-11	2016	CONCLUSION: Dox exerts an anti-apoptosis function via the NF-kappaB-Bcl-2/Bax and Trx2-ASK1/JNK pathways in vitro.	Doxycycline	12-15	BCL2-associated X protein	Mus musculus	74-77
27643515-10	2016	Moreover, DMDD protected against PA-induced Min6 cells apoptosis and the expression of Cleaved-Caspase-3, -8 and -9 were down-regulated and the Bcl-2/Bax ratio was increased in DMDD-pretreated Min6 cells.	2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione	10-14	BCL2-associated X protein	Mus musculus	150-153
27643515-10	2016	Moreover, DMDD protected against PA-induced Min6 cells apoptosis and the expression of Cleaved-Caspase-3, -8 and -9 were down-regulated and the Bcl-2/Bax ratio was increased in DMDD-pretreated Min6 cells.	Palmitic Acid	33-35	BCL2-associated X protein	Mus musculus	150-153
27643515-10	2016	Moreover, DMDD protected against PA-induced Min6 cells apoptosis and the expression of Cleaved-Caspase-3, -8 and -9 were down-regulated and the Bcl-2/Bax ratio was increased in DMDD-pretreated Min6 cells.	2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione	177-181	BCL2-associated X protein	Mus musculus	150-153
25577170-10	2016	Furthermore, atorvastatin decreased the levels of cytosolic cytochrome C, Bax, cleaved caspase-9, and cleaved caspase-3, which are associated with death in oxidative stress-injured NSC-34D cells.	Atorvastatin	13-25	BCL2-associated X protein	Mus musculus	74-77
27119348-0	2016	Gambogic Acid Inhibits Malignant Melanoma Cell Proliferation Through Mitochondrial p66shc/ROS-p53/Bax-Mediated Apoptosis.	gambogic acid	0-13	BCL2-associated X protein	Mus musculus	98-101
27119348-9	2016	GA concentration-dependently upregulated p53 and Bax expression in A375 cells.	gambogic acid	0-2	BCL2-associated X protein	Mus musculus	49-52
26807019-7	2016	Western blot analysis showed that CA abrogated APAP-induced cleaved caspase-3, Bax and phosphorylated JNK protein expression.	Acetaminophen	47-51	BCL2-associated X protein	Mus musculus	79-82
26784930-8	2016	TUNEL staining showed that the goblet cell apoptosis rate was much higher in the short-term gefinitib treatment group compared with the asthma and chronic gefitinib treatment group which was accompanied by a decrease in Bcl-2 levels and an increase in Bax expression in goblet cells.	gefinitib	92-101	BCL2-associated X protein	Mus musculus	252-255
26828432-0	2016	Doxycycline Protects Thymic Epithelial Cells from Mitomycin C-Mediated Apoptosis In Vitro via Trx2-NF-kappaB-Bcl-2/Bax Axis.	Doxycycline	0-11	BCL2-associated X protein	Mus musculus	115-118
27189473-4	2016	Blockage of sigma -1R significantly inhibited the increased pro-apoptotic proteins such as Bax, Caspase-3 and Caspase-9 induced by methamphetamine.	Methamphetamine	131-146	BCL2-associated X protein	Mus musculus	91-94
26930476-2	2016	Treatment with cocaine resulted in significant increases in malondialdehyde, protein carbonyl, and pro-apoptotic Bax expression and decreases in the ratio of glutathione (GSH) and its oxidized form (GSSG), GSH-dependent enzymes, and anti-apoptotic factors in the kidney.	Cocaine	15-22	BCL2-associated X protein	Mus musculus	113-116
26484597-3	2016	Treatment with samples significantly ameliorated the depletion of both DA and TH-, Bcl-2- and Bax-positive neurons in MPTP-induced PD mice, DF1 showed the highest activity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	118-122	BCL2-associated X protein	Mus musculus	94-97
28105250-6	2016	3,5-diCQA may prevent neuronal apoptosis through the protection of mitochondrial activities and the repression of apoptotic signaling molecules such as p-Akt, BAX, and p-tau (Ser 404).	3,5-dicaffeoylquinic acid	0-9	BCL2-associated X protein	Mus musculus	159-162
27738547-7	2016	Furthermore, Sal could increase the phosphorylation level of Akt and GSK3beta, upregulate the ratio of Bcl-2/Bax, and inhibit the activation of caspase-3, caspase-6, and caspase-9.	rhodioloside	13-16	BCL2-associated X protein	Mus musculus	109-112
26825069-5	2016	Therefore a series of mixed polyphenol-heterocyclic molecules, were rationally designed by molecular docking as Bax/Bcl-xL inhibitors.	Polyphenols	28-38	BCL2-associated X protein	Mus musculus	112-115
26718146-10	2016	CONCLUSIONS: We concluded that hyperoxia induces ROS production and cell death in lung tissues through a cell-type specific mechanism involving the upregulation of c-Myc/Bax, and caspase-8 and -3/7 activation-dependent pathways, thereby leading to the development of DAD.	Reactive Oxygen Species	49-52	BCL2-associated X protein	Mus musculus	170-173
26756818-7	2016	As a result of formononetin treatment, anti-apoptotic Bcl-2 was up-regulated, whereas pro-apoptotic Bax and p53 were down-regulated, resulting in a decrease of caspase-3 activation.	formononetin	15-27	BCL2-associated X protein	Mus musculus	100-103
26805733-16	2016	CONCLUSION: The combination of Olaprib and fractionated radiotherapy can markedly improve the radiobiological effects on lewis cells and xenografts, which may be induced by promoting the formation of DNA double strand break and upregulating the expression of Bax/Bcl-2 pro-apoptotic proteins.	olaprib	31-38	BCL2-associated X protein	Mus musculus	259-262
26560700-7	2015	Importantly, caffeine-cocaine combination potentiated the cocaine-induced germ cell loss, and induced pro-apoptotic BAX protein expression and diminished adenosine receptor A1 mRNA levels.	Caffeine	13-21	BCL2-associated X protein	Mus musculus	116-119
26585277-5	2015	Specifically, we find that when ESCs are stimulated to differentiate, a subpopulation fails to do so and instead upregulates FAS in a p53-dependent manner to trigger Bax/Bak-dependent apoptosis.	ammonium ferrous sulfate	125-128	BCL2-associated X protein	Mus musculus	166-169
25977985-8	2015	In the developed adult brains from vitamin C-deficient Gulo(-/-) mice, the levels of glutathione, MDA, nitrate, IL-6, TNF-alpha, and Bax were increased and the expression of the GABRA6 and calbindin-28k was decreased.	Ascorbic Acid	35-44	BCL2-associated X protein	Mus musculus	133-136
25808346-10	2015	An increased Bcl-2/Bax transcript ratio contributed to cellular proliferation, and this was maintained in the MPA-treated environment.	Mycophenolic Acid	110-113	BCL2-associated X protein	Mus musculus	19-22
26471208-8	2015	Treatment of pre-B cells with ACY-738 decreased the Bcl-2:Bax ratio leading to a pro-apoptotic environment.	N-hydroxy-2-(1-phenylcycloproylamino)pyrimidine-5-carboxamide	30-37	BCL2-associated X protein	Mus musculus	58-61
26411262-11	2015	Notably, treatment with fisetin significantly (P<0.05) reduced Abeta aggregation, ASK-1, p-JNK, p53, cytochrome c, caspase-9 and 3 protein expressions and modulated Bax/Bcl-2 ratio.	fisetin	24-31	BCL2-associated X protein	Mus musculus	165-168
26685797-7	2015	Further mechanism study suggested that the up-regulation of Bax and Calpain-2, rather than the Caspase-3, should be responsible for the asymmetry in the MNU induced photoreceptor degeneration.	Methylnitrosourea	153-156	BCL2-associated X protein	Mus musculus	60-63
26112963-8	2015	Expression levels of Bcl-2 decreased, while those of Bax and caspase-3 increased following MTX treatment.	Methotrexate	91-94	BCL2-associated X protein	Mus musculus	53-56
26112963-12	2015	In conclusion chrysin inhibits MTX-triggered cardiomyocyte apoptosis via multiple pathways, including decrease of the Bax/Bcl-2 ratio and caspase-3 expression along with preservation of the desmin disarray.	Methotrexate	31-34	BCL2-associated X protein	Mus musculus	118-121
26527380-9	2015	In addition, melatonin enhanced autophagy after TBI, which was accompanied by a decrease in both the translocation of Bax to mitochondria and the release of cytochrome C to cytoplasm.	Melatonin	13-22	BCL2-associated X protein	Mus musculus	118-121
26343046-9	2015	RESULTS: Fenofibrate precondition can significantly alleviate the renal dysfunction, the pathological change, up-regulate the expression of p-PPAR-alpha, Bcl-2, Bcl-xl, Caspase3 and down-regulate the expression of p-JAK2, p-STAT3, p53, p21, CytC and Bax induced by renal IR injury.	Fenofibrate	9-20	BCL2-associated X protein	Mus musculus	250-253
26560700-7	2015	Importantly, caffeine-cocaine combination potentiated the cocaine-induced germ cell loss, and induced pro-apoptotic BAX protein expression and diminished adenosine receptor A1 mRNA levels.	Cocaine	22-29	BCL2-associated X protein	Mus musculus	116-119
26330141-7	2015	Curcumin treatment inhibited palmitate-induced apoptosis, relieved mitochondrial depolarization and up-regulated Bcl-2/Bax ratio.	Curcumin	0-8	BCL2-associated X protein	Mus musculus	119-122
26526304-6	2015	Furthermore, administration with DADS prevented radiation-induced Tap73/DeltaNp73 expression and consequently down regulated Bax/Bcl-2 ratio, cytochrome c release and caspase-3 expression, indicating that the balance between Tap73 and DeltaNp73 had potential to activate p53 responsive genes.	diallyl disulfide	33-37	BCL2-associated X protein	Mus musculus	125-128
26330141-7	2015	Curcumin treatment inhibited palmitate-induced apoptosis, relieved mitochondrial depolarization and up-regulated Bcl-2/Bax ratio.	Palmitates	29-38	BCL2-associated X protein	Mus musculus	119-122
26648012-13	2015	An anti-apoptotic property of piperine was identified by maintaining the balance of Bcl-2/Bax.	piperine	30-38	BCL2-associated X protein	Mus musculus	90-93
26316359-7	2015	Although prophylactic and acute resveratrol delivery reduced infarct volume and enhanced blood-brain-barrier integrity at 2 days post-ischemia by elevating resveratrol"s downstream signal sirtuin-1, increasing cell survival signals (phosphorylated Akt, heme oxygenase-1, Bcl-2) and decreasing cell death signals (Bax, activated caspase-3), a sustained reduction of infarct size on day 28 was not observed in any of the three experimental conditions.	Resveratrol	32-43	BCL2-associated X protein	Mus musculus	313-316
26424772-10	2015	Flavocoxid administration reduced, in a time-dependent way, p-ERK 1/2, TNF-alpha, COX-2, 5-LOX, MDA, Bax, FSH, LH, TGF-beta3, augmented Bcl-2, testosterone, inhibin B, occludin, N-Cadherin, and improved the structural organization of the testis and the blood-testis barrier.	flavocoxid	0-10	BCL2-associated X protein	Mus musculus	101-104
26586942-6	2015	EGCG and TF-NPs were also found to be more effective than bulk TF/EGCG in inducing the cleavage of caspase-3 and caspase-9 and Bax/Bcl2 ratio in favor of apoptosis.	theaflavin	9-11	BCL2-associated X protein	Mus musculus	127-130
26586942-6	2015	EGCG and TF-NPs were also found to be more effective than bulk TF/EGCG in inducing the cleavage of caspase-3 and caspase-9 and Bax/Bcl2 ratio in favor of apoptosis.	epigallocatechin gallate	66-70	BCL2-associated X protein	Mus musculus	127-130
28959548-9	2016	Furthermore, treatments with the mucoadhesive formulation containing BP/CL up modulated Ki-67 and Bcl-2 expression while reduced pro-apoptotic regulator Bax.	Benzo(a)pyrene	69-71	BCL2-associated X protein	Mus musculus	153-156
26297476-8	2015	Piceatannol significantly increased apoptotic cells and expression of both Bax and cleaved caspase-3 but reduced Bcl-2 expression in tumor tissues.	3,3',4,5'-tetrahydroxystilbene	0-11	BCL2-associated X protein	Mus musculus	75-78
26586942-6	2015	EGCG and TF-NPs were also found to be more effective than bulk TF/EGCG in inducing the cleavage of caspase-3 and caspase-9 and Bax/Bcl2 ratio in favor of apoptosis.	epigallocatechin gallate	0-4	BCL2-associated X protein	Mus musculus	127-130
26512966-5	2015	Damage of mitochondrial function and metabolism, as predicted by bioinformatics analyses, was observed: BPA exposure led to a time-dependent decrease in mitochondrial membrane potential, to an increase of ROS cellular levels and, finally, to an induction of apoptosis, attributable to the bigger Bax/Bcl-2 ratio owing to activation of NF-kappaB pathway.	bisphenol A	104-107	BCL2-associated X protein	Mus musculus	296-299
26413814-8	2015	The level of anti-apoptotic protein Bcl-2 was increased and the pro-apoptotic protein Bax was reduced in VPA treated normal cells.	Valproic Acid	105-108	BCL2-associated X protein	Mus musculus	86-89
26279331-7	2015	Nicorandil also increased the expression of Bcl-2 and decreased the expression of Bax, while increasing p-Akt level.	Nicorandil	0-10	BCL2-associated X protein	Mus musculus	82-85
26187689-11	2015	(Val8)GLP-1-glu-PAL showed good effects in preventing the MPTP-induced motor impairment (Rotarod, open field locomotion, swim test), reduction in tyrosine hydroxylase levels (dopamine synthesis) in the substantia nigra, a reduction of activated caspase 3 levels, of TUNEL positive cell numbers, of the pro-apoptotic signaling molecule BAX and an increase in the growth signaling molecule Bcl-2.	Glutamic Acid	12-15	BCL2-associated X protein	Mus musculus	335-338
26442822-3	2015	The Bax/Bcl-2 ratio increased when garcinol was applied to PC-3 cells indicating a presence of apoptosis.	garcinol	35-43	BCL2-associated X protein	Mus musculus	4-7
26283170-3	2015	The DAPG induced apoptosis in cancer cells by intrinsic and extrinsic pathways via the release of cytochrome-C, upregulation of Bax and the activation of caspases and also, exhibited anti-inflammatory activity by the inhibition of LPS-inflammed cell proliferation of macrophage (Raw 264.7), monocytic cells (THP-1) and peripheral blood mononuclear cells (PBMCs).	2,4-diacetylphloroglucinol	4-8	BCL2-associated X protein	Mus musculus	128-131
26253170-0	2015	A New Fungal Diterpene Induces VDAC1-dependent Apoptosis in Bax/Bak-deficient Cells.	Diterpenes	13-22	BCL2-associated X protein	Mus musculus	60-63
25609004-7	2015	In all analyzed tissues, Bax immunopositivity has been withdrawn by highest dose of silymarin concomitant with reversal of Bcl-2 intensity at a level comparable with control.	Silymarin	84-93	BCL2-associated X protein	Mus musculus	25-28
26722406-14	2015	Severe apoptosis in doxorubicin group was verified by a set of markers including Bax, Bcl-2, cytosolic cytochrome c and caspase-3 up-regulation expression.	Doxorubicin	20-31	BCL2-associated X protein	Mus musculus	81-84
26421001-7	2015	Jacaric acid also triggered apoptosis as reflected by induction of DNA fragmentation, phosphatidylserine externalization, mitochondrial membrane depolarization, up-regulation of pro-apoptotic Bax protein and down-regulation of anti-apoptotic Bcl-2 and Bcl-xL proteins.	jacaric acid	0-12	BCL2-associated X protein	Mus musculus	192-195
25968954-6	2015	Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity.	Tunicamycin	10-21	BCL2-associated X protein	Mus musculus	105-108
25856413-0	2015	Transient activation of microglia following acute alcohol exposure in developing mouse neocortex is primarily driven by BAX-dependent neurodegeneration.	Alcohols	50-57	BCL2-associated X protein	Mus musculus	120-123
25856413-7	2015	Alcohol-induced microglial activation and pro-inflammatory factor expression were largely abolished in BAX null mice lacking neuroapoptosis, indicating that microglial activation is primarily triggered by apoptosis rather than the alcohol.	Alcohols	0-7	BCL2-associated X protein	Mus musculus	103-106
26253170-0	2015	A New Fungal Diterpene Induces VDAC1-dependent Apoptosis in Bax/Bak-deficient Cells.	bakuchiol	64-67	BCL2-associated X protein	Mus musculus	60-63
26253170-3	2015	Upon screening a fungal secondary metabolite library for compounds inducing apoptosis in Bax/Bak-deficient mouse embryonic fibroblasts, we identified cyathin-R, a new cyathane diterpenoid compound able to activate apoptosis in the absence of Bax/Bak via promotion of the VDAC1 oligomerization that mediates cytochrome c release.	cyathin-r	150-159	BCL2-associated X protein	Mus musculus	89-92
26253170-3	2015	Upon screening a fungal secondary metabolite library for compounds inducing apoptosis in Bax/Bak-deficient mouse embryonic fibroblasts, we identified cyathin-R, a new cyathane diterpenoid compound able to activate apoptosis in the absence of Bax/Bak via promotion of the VDAC1 oligomerization that mediates cytochrome c release.	cyathin-r	150-159	BCL2-associated X protein	Mus musculus	242-245
26253170-7	2015	Finally, cyathin-R effectively attenuated tumor growth and induced apoptosis in Bax/Bak-deficient cells implanted into a xenograft mouse model.	cyathin-r	9-18	BCL2-associated X protein	Mus musculus	80-83
26395757-5	2015	Meanwhile, two different zincs inhibited the ZEA-induced loss of mitochondrial membrane potential and elevation of late-stage apoptosis via activating the mitochondrial apoptotic pathway by recovering the mRNA and protein expression of pro-apoptotic genes (Bax, Casp3, Casp9).	Zinc	25-30	BCL2-associated X protein	Mus musculus	257-260
26404244-5	2015	An increase in ROS generation with a concomitant increase in the gene expression of the tumor suppressor gene p53, the pro-apoptotic gene Bcl-2 and a decrease in the anti-apoptosis gene Bax, suggested that a mitochondria mediated pathway was involved in CdTe QDs" induced apoptosis.	Reactive Oxygen Species	15-18	BCL2-associated X protein	Mus musculus	186-189
26404244-5	2015	An increase in ROS generation with a concomitant increase in the gene expression of the tumor suppressor gene p53, the pro-apoptotic gene Bcl-2 and a decrease in the anti-apoptosis gene Bax, suggested that a mitochondria mediated pathway was involved in CdTe QDs" induced apoptosis.	cadmium telluride	254-258	BCL2-associated X protein	Mus musculus	186-189
26395757-5	2015	Meanwhile, two different zincs inhibited the ZEA-induced loss of mitochondrial membrane potential and elevation of late-stage apoptosis via activating the mitochondrial apoptotic pathway by recovering the mRNA and protein expression of pro-apoptotic genes (Bax, Casp3, Casp9).	Zearalenone	45-48	BCL2-associated X protein	Mus musculus	257-260
29124200-1	2015	A Bax-dependent increase of reactive oxygen species (ROS) and other reactive species (RS) occurs after withdrawing NGF from mouse sympathetic neurons in cell culture.	Reactive Oxygen Species	28-51	BCL2-associated X protein	Mus musculus	2-5
25935694-10	2015	Furthermore, farnesol treatment reduced the expression of Bax and antagonized LPS-induced decrease in anti-apoptotic Bcl-2.	Farnesol	13-21	BCL2-associated X protein	Mus musculus	58-61
26197224-8	2015	ATX also increased the mitochondrial expression of AIF, Cyto-c as well as Bax while decreased Bcl-2.	astaxanthine	0-3	BCL2-associated X protein	Mus musculus	74-77
26379247-8	2015	Mechanistically, SS-31 treatment suppressed pro-inflammatory responses by decreasing the levels of NF-kappaB, NLRP3, caspase 1, IL-1beta, and TNF-alpha; and inhibited the apoptotic pathway by decreasing the Bax/Bcl-2 ratio, reducing the release of cytochrome C, and blocking the cleavage of caspase 3.	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	17-22	BCL2-associated X protein	Mus musculus	207-210
26141845-11	2015	Both liraglutide and lixisenatide showed effects in preventing the MPTP-induced motor impairment (Rotarod, open-field locomotion, catalepsy test), reduction in tyrosine hydroxylase (TH) levels (dopamine synthesis) in the substantia nigra and basal ganglia, a reduction of the pro-apoptotic signaling molecule BAX and an increase in the anti-apoptotic signaling molecule B-cell lymphoma-2.	lixisenatide	21-33	BCL2-associated X protein	Mus musculus	309-312
29124200-1	2015	A Bax-dependent increase of reactive oxygen species (ROS) and other reactive species (RS) occurs after withdrawing NGF from mouse sympathetic neurons in cell culture.	Reactive Oxygen Species	53-56	BCL2-associated X protein	Mus musculus	2-5
29124200-3	2015	We previously demonstrated that deletion of Bax or caspase 3 from these cells reduces ROS/RS production to near baseline levels indicating a central role for both Bax and caspase 3 in generating the ROS/RS.	Reactive Oxygen Species	86-89	BCL2-associated X protein	Mus musculus	44-47
29124200-3	2015	We previously demonstrated that deletion of Bax or caspase 3 from these cells reduces ROS/RS production to near baseline levels indicating a central role for both Bax and caspase 3 in generating the ROS/RS.	Reactive Oxygen Species	86-89	BCL2-associated X protein	Mus musculus	163-166
29124200-3	2015	We previously demonstrated that deletion of Bax or caspase 3 from these cells reduces ROS/RS production to near baseline levels indicating a central role for both Bax and caspase 3 in generating the ROS/RS.	Reactive Oxygen Species	199-202	BCL2-associated X protein	Mus musculus	44-47
29124200-3	2015	We previously demonstrated that deletion of Bax or caspase 3 from these cells reduces ROS/RS production to near baseline levels indicating a central role for both Bax and caspase 3 in generating the ROS/RS.	Reactive Oxygen Species	199-202	BCL2-associated X protein	Mus musculus	163-166
29124200-6	2015	ROS/RS was highest in bax wild-type cells, lowest in bax knockout cells, and at an intermediate level in the bax hemizygous cells.	Reactive Oxygen Species	0-3	BCL2-associated X protein	Mus musculus	22-25
29124200-6	2015	ROS/RS was highest in bax wild-type cells, lowest in bax knockout cells, and at an intermediate level in the bax hemizygous cells.	Reactive Oxygen Species	0-3	BCL2-associated X protein	Mus musculus	53-56
29124200-6	2015	ROS/RS was highest in bax wild-type cells, lowest in bax knockout cells, and at an intermediate level in the bax hemizygous cells.	Reactive Oxygen Species	0-3	BCL2-associated X protein	Mus musculus	53-56
29124200-6	2015	ROS/RS was highest in bax wild-type cells, lowest in bax knockout cells, and at an intermediate level in the bax hemizygous cells.	rs	4-6	BCL2-associated X protein	Mus musculus	22-25
29124200-6	2015	ROS/RS was highest in bax wild-type cells, lowest in bax knockout cells, and at an intermediate level in the bax hemizygous cells.	rs	4-6	BCL2-associated X protein	Mus musculus	53-56
29124200-6	2015	ROS/RS was highest in bax wild-type cells, lowest in bax knockout cells, and at an intermediate level in the bax hemizygous cells.	rs	4-6	BCL2-associated X protein	Mus musculus	53-56
29124200-7	2015	These and our previous findings indicate that Bax and caspase 3 are necessary for the increased ROS/RS after withdrawing NGF from these cells and that little or none of the increased ROS/RS are secondary to a depletion of cytochrome c from the electron transport chain.	Reactive Oxygen Species	96-99	BCL2-associated X protein	Mus musculus	46-49
29124200-7	2015	These and our previous findings indicate that Bax and caspase 3 are necessary for the increased ROS/RS after withdrawing NGF from these cells and that little or none of the increased ROS/RS are secondary to a depletion of cytochrome c from the electron transport chain.	rs	100-102	BCL2-associated X protein	Mus musculus	46-49
25979689-5	2015	RESULTS: Although treatment of diabetic mice with hydrogen water did not significantly affect blood glucose level, it significantly attenuated cardiac hypertrophy and reduced expression of atrial natriuretic factor and beta-myosin heavy chain; it alleviated cardiac fibrosis and reduced expression of collagen I and III, transforming growth factor beta, alpha-smooth muscle actin, and osteopontin; it reduced cardiac caspase-3 activity and ratio of bax/bcl-2.	hydrogen water	50-64	BCL2-associated X protein	Mus musculus	449-452
26464676-0	2015	Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer.	Curcumin	10-18	BCL2-associated X protein	Mus musculus	32-35
26212257-5	2015	Resveratrol+curcumin combination caused apoptosis by increasing Bax/Bcl-xL ratio, Cytochrome C release, cleaved product of PARP and caspase 3 in cells.	Resveratrol	0-11	BCL2-associated X protein	Mus musculus	64-67
26212257-5	2015	Resveratrol+curcumin combination caused apoptosis by increasing Bax/Bcl-xL ratio, Cytochrome C release, cleaved product of PARP and caspase 3 in cells.	Curcumin	12-20	BCL2-associated X protein	Mus musculus	64-67
26094939-15	2015	Additionally, melatonin upregulated the expression of SIRT1 and Bcl-2 and downregulated the expression of Ac-FoxO1, Ac-p53, Ac-NF-kappaB, and Bax.	Melatonin	14-23	BCL2-associated X protein	Mus musculus	142-145
26142126-5	2015	Furthermore, we found that rasagiline upregulated expression levels of the synaptic plasticity markers brain-derived neurotrophic factor, tyrosine kinase-B receptor, and synapsin-1, increased Bcl-2 to Bax antiapoptotic ratio and the activity of the antioxidant enzyme, catalase in brain of aged mice.	rasagiline	27-37	BCL2-associated X protein	Mus musculus	201-204
26290634-12	2015	Western blot analysis revealed that DHI antagonised LPS-stimulated decrease of Bcl-2 and increase of Bax protein expression.	dehydrosoyasaponin I	36-39	BCL2-associated X protein	Mus musculus	101-104
26113535-6	2015	We show that Foxc2 reduces the expression of Bax, caspase-9, and caspase-3 in both serum-starved and palmitic acid-induced cell apoptotic models, which confirms the anti-apoptotic role of Foxc2.	Palmitic Acid	101-114	BCL2-associated X protein	Mus musculus	45-48
26135032-12	2015	Western blot analysis and immunofluorescence staining revealed a marked decrease in caspase-3 expression and an increase in the Bcl-2/Bax ratio in the group pre-treated with matrine (30 mg/kg) as compared with the vehicle-treated group.	matrine	174-181	BCL2-associated X protein	Mus musculus	134-137
26260377-6	2015	Moreover, tBHQ treatment restored Bcl-2 and Bax expression and reduced caspase-3 cleavage, suggesting the protective effect of tBHQ treatment in ameliorating brain injury after SAH.	2-tert-butylhydroquinone	10-14	BCL2-associated X protein	Mus musculus	44-47
26108789-6	2015	Moreover, PFOA exposure up-regulated p-p53 and BAX expression and down-regulated BCL-2 expression in the testis.	3-O-(N-(p-fluorobenzenesulfonyl)carbamoyl)oleanolic acid	10-14	BCL2-associated X protein	Mus musculus	47-50
26059977-7	2015	Targeted LC/MS analysis revealed elevated levels of additional sphingadiene-containing ceramides (d18:2-Cers) in BAX, BAK-double knockout MEFs.	sphingadiene	63-75	BCL2-associated X protein	Mus musculus	113-116
26059977-7	2015	Targeted LC/MS analysis revealed elevated levels of additional sphingadiene-containing ceramides (d18:2-Cers) in BAX, BAK-double knockout MEFs.	Ceramides	87-96	BCL2-associated X protein	Mus musculus	113-116
26464676-3	2015	This study aimed to explore the curcumin induced prostate cancer cell apoptosis and apoptosis related proteins Bcl-2 and Bax expression.	Curcumin	32-40	BCL2-associated X protein	Mus musculus	121-124
26464676-13	2015	Curcumin could inhibit PC-3 growth, decrease tumor volume, reduce tumor weight, and induce cell apoptosis under the skin of nude mice by up-regulating Bax and down-regulating Bcl-2.	Curcumin	0-8	BCL2-associated X protein	Mus musculus	151-154
26226833-10	2015	These results demonstrated that fatty acid oxidation resulted in ROS generation, activating P53/Bax-mediated mitochondrial apoptosis, leading to reduction of osteogenic differentiation and bone loss in T2DM.	Fatty Acids	32-42	BCL2-associated X protein	Mus musculus	96-99
25128030-8	2015	Bucladesine also decreased production of caspase-3 as well as Bax and increased Bcl-2 levels.	Bucladesine	0-11	BCL2-associated X protein	Mus musculus	62-65
26226833-10	2015	These results demonstrated that fatty acid oxidation resulted in ROS generation, activating P53/Bax-mediated mitochondrial apoptosis, leading to reduction of osteogenic differentiation and bone loss in T2DM.	ros	65-68	BCL2-associated X protein	Mus musculus	96-99
26222683-9	2015	Moreover, baicalein preserved mitochondrial respiratory enzyme activities and inhibited cisplatin-induced apoptosis by suppressing p53 expression, Bax/Bcl-2 imbalance, cytochrome c release and activation of caspase-9, caspase-3 and PARP.	baicalein	10-19	BCL2-associated X protein	Mus musculus	147-150
25869780-9	2015	Furthermore, flupirtine (10mg/kg and 25mg/kg) treatment significantly decreased the expression of Bax and increased the p-Akt and p-GSK-3beta, and flupirtine (25mg/kg) treatment up-regulated the p-Erk1/2 in the hippocampus of CRS mice.	flupirtine	13-23	BCL2-associated X protein	Mus musculus	98-101
26149967-4	2015	MCD sensitizes MCF-7 and Hepa1-6 cells to DOX, Combination of MCD and marginal dose of DOX reduces the cell viability, and promoted apoptosis through induction of pro-apoptotic protein, Bax, activation of caspase-8 and caspase-7, down regulation of anti-apoptotic protein Bcl-2 and finally promoting PARP cleavage.	Doxorubicin	87-90	BCL2-associated X protein	Mus musculus	186-189
26135924-9	2015	However, initial cell viability, cell recovery after culture, and PCNA expression were significantly lower in MEF cells, and the BAX/BCL2 protein ratio was elevated in mBMCs cryopreserved in D10O20.	mbmcs	168-173	BCL2-associated X protein	Mus musculus	129-132
25959028-4	2015	In addition to reactive oxygen species scavenging activity in Dex-induced splenocytes, BA administration up-regulated antioxidant enzymes, decreased lipid peroxidation, restored mitochondrial function, decreased the expression of pro-apoptotic protein Bax, prevented the decline of anti-apoptotic protein Bcl-2, inhibited caspase-9 and caspase-3 activation, and improved cell survival.	betulinic acid	87-89	BCL2-associated X protein	Mus musculus	252-255
26148186-7	2015	Furthermore, combined UVB and quercetin treatment decreased the ratio of Bcl-2 to that of Bax, and upregulated the expression of Bim and apoptosis inducing factor (AIF).	Quercetin	30-39	BCL2-associated X protein	Mus musculus	90-93
25862283-6	2015	Interestingly, cells overexpressing Bcl-xL were more sensitive to apoptosis upon treatment with the BH3-mimetic ABT-737, suggesting that despite its role in Bax inhibition, Bcl-xL also primes mitochondria to permeabilization and cytochrome c release.	BH 3	100-103	BCL2-associated X protein	Mus musculus	157-160
25862283-6	2015	Interestingly, cells overexpressing Bcl-xL were more sensitive to apoptosis upon treatment with the BH3-mimetic ABT-737, suggesting that despite its role in Bax inhibition, Bcl-xL also primes mitochondria to permeabilization and cytochrome c release.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	112-115	BCL2-associated X protein	Mus musculus	157-160
26151119-9	2015	Results showed that procyanidin B2 significantly inhibited CCl4-induced hepatocyte apoptosis, markedly suppressed the upregulation of Bax expression and restored the downregulation of Bcl-xL expression.	procyanidin B2	20-34	BCL2-associated X protein	Mus musculus	134-137
25849952-9	2015	At the same time, our result demonstrates that myricitrin treatment optimizes the balance of pro/anti-apoptosis proteins, including Bax, Bad, XIAP, cIAP-2, and survivin.	myricitrin	47-57	BCL2-associated X protein	Mus musculus	132-135
26198964-6	2015	LPS significantly increased the myocardial Bax expression and slightly decreased Bcl-2 expression; quercetin pretreatment decreased Bax expression to the control level and significantly lowered Bax/Bcl-2 ratio as compared with the LPS group.	Quercetin	99-108	BCL2-associated X protein	Mus musculus	132-135
26198964-6	2015	LPS significantly increased the myocardial Bax expression and slightly decreased Bcl-2 expression; quercetin pretreatment decreased Bax expression to the control level and significantly lowered Bax/Bcl-2 ratio as compared with the LPS group.	Quercetin	99-108	BCL2-associated X protein	Mus musculus	132-135
25815636-0	2015	A nonapoptotic role for BAX and BAK in eicosanoid metabolism.	Eicosanoids	39-49	BCL2-associated X protein	Mus musculus	24-27
25815636-4	2015	We used an unbiased lipidomics strategy to reveal that the proapoptotic proteins BAX, and to a lesser extent BAK, regulate the cellular inflammatory response by mediating COX-2 expression and prostaglandin biosynthesis.	Prostaglandins	192-205	BCL2-associated X protein	Mus musculus	81-84
25639863-6	2015	The 4-MC significantly upregulated the mRNA level of Bax gene and considerably downregulated the Bcl-2 gene expression in a concentration-dependent manner.	4-methylcatechol	4-8	BCL2-associated X protein	Mus musculus	53-56
25839806-4	2015	Moreover, TRP administration increased the levels of the proapoptotic Bax protein and decreased the level of the antiapoptotic Bcl-2 protein, thus resulting in a rise of Bax/Bcl-2 ratio.	Tryptophan	10-13	BCL2-associated X protein	Mus musculus	70-73
25839806-4	2015	Moreover, TRP administration increased the levels of the proapoptotic Bax protein and decreased the level of the antiapoptotic Bcl-2 protein, thus resulting in a rise of Bax/Bcl-2 ratio.	Tryptophan	10-13	BCL2-associated X protein	Mus musculus	170-173
25639863-7	2015	Results showed that 4-MC could induce TM4 Sertoli cell apoptosis, and the cytotoxic effect of 4-MC on TM4 Sertoli cells may be associated with upregulated Bax gene expression, which induced caspase cascade activation.	4-methylcatechol	20-24	BCL2-associated X protein	Mus musculus	155-158
25639863-7	2015	Results showed that 4-MC could induce TM4 Sertoli cell apoptosis, and the cytotoxic effect of 4-MC on TM4 Sertoli cells may be associated with upregulated Bax gene expression, which induced caspase cascade activation.	4-methylcatechol	94-98	BCL2-associated X protein	Mus musculus	155-158
25391371-12	2015	Thiostrepton also induced dose- and time-dependent apoptosis of LSCC cells by down-regulation of Bcl-2, up-regulation of Bax and p53, and inducing release of cytochrome c accompanied by activation of cleaved caspase-9, cleaved caspase-3 and cleaved PARP.	Thiostrepton	0-12	BCL2-associated X protein	Mus musculus	121-124
25824411-4	2015	Our results demonstrated that 4-ACGC possessed notable anti-tumor activity on lung cancer in vivo and in vitro; the mechanisms were involved in inducing mitochondria-mediated apoptosis via up-regulations of caspase-3, caspase-9, Bad and Bax, and down-regulation of Bcl-2.	4-acgc	30-36	BCL2-associated X protein	Mus musculus	237-240
25808759-6	2015	The forsythiaside-A group also showed a 60% increase in the Bcl-2/Bax ratio, which is a factor related to mitochondrial apoptosis.	Forsythoside?A	4-19	BCL2-associated X protein	Mus musculus	66-69
25985365-6	2015	Consequently, miR-200-induced T2D is suppressed by interfering with the signaling of Trp53 and Bax, a proapoptotic member of the B cell lymphoma 2 protein family.	mir-200	14-21	BCL2-associated X protein	Mus musculus	95-98
25962180-10	2015	Both the inhibition of Bag-1 by miR-138 and the silencing of Bag-1 by siRNA led to alterations of apoptosis-related proteins such as Bcl-2 and Bax.	mir-138	32-39	BCL2-associated X protein	Mus musculus	143-146
26125762-7	2015	Further study on gene expression indicated that ABX can partially impair the function of cisplatin by upregulating the expression of VEGFA and downregulating the expression of BAX and CDKN1B.	CHEMBL369125	48-51	BCL2-associated X protein	Mus musculus	176-179
26125762-7	2015	Further study on gene expression indicated that ABX can partially impair the function of cisplatin by upregulating the expression of VEGFA and downregulating the expression of BAX and CDKN1B.	Cisplatin	89-98	BCL2-associated X protein	Mus musculus	176-179
25736991-6	2015	Our experimental evidence suggests that ATO exposure induces apoptotic cell deathby the activation of caspase-3 and reciprocal regulation of Bcl-2/Bax with the concomitant reduction of mitochondrial membrane potential and increased level of cytosolic cytochrome c, Apaf1, caspase-9.	Atorvastatin	40-43	BCL2-associated X protein	Mus musculus	147-150
25709011-6	2015	Data showed that radiation-induced apoptosis of thymocytes could be reversed by SP through inducing upregulation of Bcl-2 expression and downregulation of Fas and Bax levels.	sp	80-82	BCL2-associated X protein	Mus musculus	163-166
25760015-10	2015	SP600125 significantly downregulated expression of Bax and caspase-3 but upregulated Bcl-2 expression in MC3T3-E1 cells stimulated by LPS.	pyrazolanthrone	0-8	BCL2-associated X protein	Mus musculus	51-54
25849616-9	2015	Using transient expression assays in N. benthamiana, we found that Ha-ANNEXIN could suppress programmed cell death triggered by the pro-apoptotic mouse protein BAX and the induction of marker genes of PAMP-triggered immunity (PTI) in N. benthamiana.	ha-annexin	67-77	BCL2-associated X protein	Mus musculus	160-163
25619546-4	2015	Hiporfin-PDT increased the expression of cleaved-caspase-3, cleaved PARP-1, Bax and RIP1 while it decreased the expression of Bcl-2; in addition, low concentration of hiporfin increased LC3 conversion.	hiporfin	167-175	BCL2-associated X protein	Mus musculus	76-79
25619546-4	2015	Hiporfin-PDT increased the expression of cleaved-caspase-3, cleaved PARP-1, Bax and RIP1 while it decreased the expression of Bcl-2; in addition, low concentration of hiporfin increased LC3 conversion.	hiporfin	0-8	BCL2-associated X protein	Mus musculus	76-79
25889084-0	2015	SapC-DOPS nanovesicles induce Smac- and Bax-dependent apoptosis through mitochondrial activation in neuroblastomas.	sapc-dops	0-9	BCL2-associated X protein	Mus musculus	40-43
25889084-8	2015	The mechanisms underlying the induction of apoptosis by SapC-DOPS were addressed through measurements of cell viability, mitochondrial membrane potential (DeltaPsiM), flow cytometric DNA fragmentation assays and by immunoblot analysis of second mitochondria-derived activator of caspases (Smac), Bax, Cytochrome c (Cyto c) and Caspase-3 in the cytosol or in mitochondrial fractions of cultured neuroblastoma cells.	sapc-dops	56-65	BCL2-associated X protein	Mus musculus	296-299
25889084-11	2015	ShRNA-mediated Smac knockdown and V5 peptide-mediated Bax inhibition decreased cytosolic Smac and Cyto c release along with caspase activation and abrogated apoptosis, indicating that Smac and Bax are critical mediators of SapC-DOPS action.	sapc-dops	223-232	BCL2-associated X protein	Mus musculus	54-57
25889084-11	2015	ShRNA-mediated Smac knockdown and V5 peptide-mediated Bax inhibition decreased cytosolic Smac and Cyto c release along with caspase activation and abrogated apoptosis, indicating that Smac and Bax are critical mediators of SapC-DOPS action.	sapc-dops	223-232	BCL2-associated X protein	Mus musculus	193-196
25889084-14	2015	CONCLUSIONS: Taken together, our results indicate that SapC-DOPS acts through a mitochondria-mediated pathway accompanied by an early release of Smac and Bax.	sapc-dops	55-64	BCL2-associated X protein	Mus musculus	154-157
25680694-13	2015	Finally, we found that exposure to Nano-ZnO caused increased ER stress-associated apoptotic protein levels, such as caspase-3, caspase-9, caspase-12, phosphorylation of JNK, and CHOP/GADD153, and up-regulation of pro-apoptotic genes (chop and bax).	Zinc Oxide	40-43	BCL2-associated X protein	Mus musculus	243-246
25617233-5	2015	The expression of Bcl-2-associated X protein (Bax) an apoptotic marker protein was two times higher in brain compared to liver at an exposure level of 0.5mgL(-1) CdCl2.	Cadmium Chloride	162-167	BCL2-associated X protein	Mus musculus	18-44
25680506-4	2015	The hepatic expression of Bax and Fas, representative intrinsic and extrinsic apoptotic molecules, respectively, was significantly increased by dosing with DOX.	Doxorubicin	156-159	BCL2-associated X protein	Mus musculus	26-29
25680506-5	2015	However, the elevation in the hepatic expression of Bax, but not Fas, was suppressed to control levels by theanine.	theanine	106-114	BCL2-associated X protein	Mus musculus	52-55
25892964-7	2015	Second, insulin pre-administration could significantly reduce apoptosis and ameliorate mitochondrial dysfunction in liver of mice exposed to ethanol, supporting by decreasing caspases-3 activities and the ratio of Bax/Bcl-2, increasing mitochondrial viability and mitochondrial oxygen consumption, inhibition of the decline of ATP levels and mitochondrial ROS accumulation.	Ethanol	141-148	BCL2-associated X protein	Mus musculus	214-217
25155888-5	2015	Additionally, pretreatment with dieckol potentiated the CoCl2-induced decrease of Bcl-2 expression and attenuated the CoCl2-induced increase in the expression of Bax and caspase-3.	dieckol	32-39	BCL2-associated X protein	Mus musculus	162-165
25155888-5	2015	Additionally, pretreatment with dieckol potentiated the CoCl2-induced decrease of Bcl-2 expression and attenuated the CoCl2-induced increase in the expression of Bax and caspase-3.	cobaltous chloride	118-123	BCL2-associated X protein	Mus musculus	162-165
25155888-7	2015	In addition, dieckol and SB203580 (p38 MAPK inhibitor) increased the CoCl2-induced decrease of Bcl-2 expression and decreased the CoCl2-induced increase of Bax and caspase-3 expressions.	dieckol	13-20	BCL2-associated X protein	Mus musculus	156-159
25155888-7	2015	In addition, dieckol and SB203580 (p38 MAPK inhibitor) increased the CoCl2-induced decrease of Bcl-2 expression and decreased the CoCl2-induced increase of Bax and caspase-3 expressions.	SB 203580	25-33	BCL2-associated X protein	Mus musculus	156-159
25155888-7	2015	In addition, dieckol and SB203580 (p38 MAPK inhibitor) increased the CoCl2-induced decrease of Bcl-2 expression and decreased the CoCl2-induced increase of Bax and caspase-3 expressions.	cobaltous chloride	130-135	BCL2-associated X protein	Mus musculus	156-159
25617233-5	2015	The expression of Bcl-2-associated X protein (Bax) an apoptotic marker protein was two times higher in brain compared to liver at an exposure level of 0.5mgL(-1) CdCl2.	Cadmium Chloride	162-167	BCL2-associated X protein	Mus musculus	46-49
26281601-7	2015	(2) RT-PCR results: Bax (Bcl-2 associated x protein) mRNA expression shows that compared with model control group, the treatment group has increased (P &lt; 0.01), and the cisplatin combined CDQD group compared with the other group is the highest, there was significant difference with the rest of the treatment group (P &lt; 0.01).	Cisplatin	172-181	BCL2-associated X protein	Mus musculus	20-23
25861418-13	2015	In addition, the combination of AHCC and 5-FU further up-regulated the expression of Bcl-2 associated X protein (Bax) (P &lt; 0.01), while it down-regulated the expression of B cell lymphoma 2 (Bcl-2) (P &lt; 0.01).	Active Hexose Correlated Compound	32-36	BCL2-associated X protein	Mus musculus	113-116
25861418-13	2015	In addition, the combination of AHCC and 5-FU further up-regulated the expression of Bcl-2 associated X protein (Bax) (P &lt; 0.01), while it down-regulated the expression of B cell lymphoma 2 (Bcl-2) (P &lt; 0.01).	Fluorouracil	41-45	BCL2-associated X protein	Mus musculus	113-116
25737433-7	2015	CFZ and z-VAD-fmk treatments resulted in higher levels of caspase-3 and BAX and lower level of BCL-XL in gastrocnemius muscles and altered the level of proteins in the renin-angiotensin system.	carfilzomib	0-3	BCL2-associated X protein	Mus musculus	72-75
25737433-7	2015	CFZ and z-VAD-fmk treatments resulted in higher levels of caspase-3 and BAX and lower level of BCL-XL in gastrocnemius muscles and altered the level of proteins in the renin-angiotensin system.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	8-17	BCL2-associated X protein	Mus musculus	72-75
26281601-9	2015	(Western blot shows: compared with model control group, the Bax protein of treatment group has increased expression (P &lt; 0.01), the expression of Bax protein in cisplatin combined CDQD group is the highest(P &lt; 0.01).	Cisplatin	164-173	BCL2-associated X protein	Mus musculus	60-63
26281601-9	2015	(Western blot shows: compared with model control group, the Bax protein of treatment group has increased expression (P &lt; 0.01), the expression of Bax protein in cisplatin combined CDQD group is the highest(P &lt; 0.01).	Cisplatin	164-173	BCL2-associated X protein	Mus musculus	149-152
26281601-12	2015	CONCLUSION: The effect of CDQD on subcutaneous transplantation ovarian tumor has promoting apoptosis function, its mechanism may be related to downgrade the Bcl-2 expression, higher expression of bax, stimulation on the apoptosis of tumor cells; cisplatin combined CDQD have synergistic effect.	cdqd	26-30	BCL2-associated X protein	Mus musculus	196-199
25773147-6	2015	The protective effect of 1,25(OH)2D3 was associated with significantly elevated expression of Beclin1, increased Bcl-2/Bax ratio, and decreased LC3-II accumulation.	Calcitriol	25-36	BCL2-associated X protein	Mus musculus	119-122
25826786-6	2015	In addition, we found that hispidin can suppress cleavage of caspase-3, expression of Bax, and NF-kappaB translocation.	hispidin	27-35	BCL2-associated X protein	Mus musculus	86-89
25542456-3	2015	Resveratrol was found to significantly increase the expressions of p53, p21, Atf3, smac/Diablo, Bax, Bak1, Bok, and Noxa mRNA in the embryos, whereas Cullin 3 and Cdk1 expressions were decreased.	Resveratrol	0-11	BCL2-associated X protein	Mus musculus	96-99
25781218-5	2015	The endometrium decidual tissue of the folate deficiency group expressed less Bax compared to the normal diet group while they had nearly equal expression of Bcl2 protein.	Folic Acid	39-45	BCL2-associated X protein	Mus musculus	78-81
25645943-4	2015	Previous reports have indicated those knockout mice with Bcl-2 associated protein X (Bax) or caspase-2, two mitochondrial outer membrane permeabilization inducers, are resistant to MPTP administration, suggesting that mitochondria are involved in MPP(+)-triggered apoptosis.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	181-185	BCL2-associated X protein	Mus musculus	57-83
25762107-9	2015	Kirenol treatment upregulated Bax,downregulated Bcl-2,and increased activation of caspase-3 and release of cytochrome c, indicating that a mitochondrial pathway was involved in kirenol induced apoptosis.	kirenol	0-7	BCL2-associated X protein	Mus musculus	30-33
25645943-4	2015	Previous reports have indicated those knockout mice with Bcl-2 associated protein X (Bax) or caspase-2, two mitochondrial outer membrane permeabilization inducers, are resistant to MPTP administration, suggesting that mitochondria are involved in MPP(+)-triggered apoptosis.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	181-185	BCL2-associated X protein	Mus musculus	85-88
25438952-0	2015	Rapamycin protects against apoptotic neuronal death and improves neurologic function after traumatic brain injury in mice via modulation of the mTOR-p53-Bax axis.	Sirolimus	0-9	BCL2-associated X protein	Mus musculus	153-156
25438952-9	2015	RESULTS: Rapamycin administration after TBI was associated with an increased number of neurons, decreased apoptosis index, and improved neurobehavioral function, which was potentially mediated by inactivation of the mTOR-p53-Bax axis.	Sirolimus	9-18	BCL2-associated X protein	Mus musculus	225-228
26417363-6	2015	The results demonstrate that the isolated SP containing plentiful fucose and sulfated group contents has the anticancer effect on colon cancer cells via regulation of Bcl-2/Bax signal pathway.	TFF2 protein, human	42-44	BCL2-associated X protein	Mus musculus	173-176
25640758-8	2015	KEY FINDINGS: The administration of rotigotine significantly improved the Parkinsonism score, protected dopaminergic neurons with antioxidants, reduced microglial cell activation and the release of neuroinflammatory cytokines, and balanced the expression of Bcl-2 and Bax in MPTP-treated mice.	rotigotine	36-46	BCL2-associated X protein	Mus musculus	268-271
25916440-0	2015	[The effect of nickel-smelting fumes on the expression of bcl-2 and bax in NIH/3T3 cells].	Nickel	15-21	BCL2-associated X protein	Mus musculus	68-71
25916440-9	2015	And the expression of bax significantly decreased in group of 6.25 microg/ml nickel-smelting fumes (0.58 +- 0.00) and increased in groups of 50.00, 100.00 microg/m nickel-smelting fumes (0.71 +- 0.01 and 0.78 +- 0.02) as compared with that of the control group (P &lt; 0.05).	Nickel	77-83	BCL2-associated X protein	Mus musculus	22-25
25916440-9	2015	And the expression of bax significantly decreased in group of 6.25 microg/ml nickel-smelting fumes (0.58 +- 0.00) and increased in groups of 50.00, 100.00 microg/m nickel-smelting fumes (0.71 +- 0.01 and 0.78 +- 0.02) as compared with that of the control group (P &lt; 0.05).	Nickel	164-170	BCL2-associated X protein	Mus musculus	22-25
25326673-5	2015	Administration of sodium phenylbutyrate induced accumulation of acetylated histone H3 at lysine 9 and lysine 18 in round spermatids, together with spermatid morphological abnormalities and induction of apoptosis through a Bax-related pathway.	4-phenylbutyric acid	18-39	BCL2-associated X protein	Mus musculus	222-225
25619640-4	2015	6-Shogaol reduced the mitochondrial membrane potential (MMP) and released cytochrome c from mitochondria to cytosol via Bax activation.	shogaol	0-9	BCL2-associated X protein	Mus musculus	120-123
25359171-4	2015	Interestingly, separate as well as combined supplementation of curcumin (60 mg/kg body weight) and quercetin (40 mg/kg body weight) to BP-treated animals resulted in a significant decrease in the protein expression of Bcl-2 but caused a significant increase in the protein expression of Bax along with a noticeable improvement in the number of apoptotic cells.	Curcumin	63-71	BCL2-associated X protein	Mus musculus	287-290
24837741-0	2015	Benzo(a)pyrene-7,8-diol-9,10-epoxide induced p53-independent necrosis via the mitochondria-associated pathway involving Bax and Bak activation.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	0-36	BCL2-associated X protein	Mus musculus	120-123
24837741-4	2015	The results showed that BPDE could induce Bax and Bak activation, cytochrome c release, caspases activation, and necrotic cell death in the BMK cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	24-28	BCL2-associated X protein	Mus musculus	42-45
24837741-5	2015	Bax and Bak, two key molecules of mitochondrial permeability transition pore, were interdependently activated by BPDE, with Bax and Bak translocation to and Bax/Bak homo-oligomerization in mitochondria, release of cytochrome c was induced.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	113-117	BCL2-associated X protein	Mus musculus	0-3
24837741-5	2015	Bax and Bak, two key molecules of mitochondrial permeability transition pore, were interdependently activated by BPDE, with Bax and Bak translocation to and Bax/Bak homo-oligomerization in mitochondria, release of cytochrome c was induced.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	113-117	BCL2-associated X protein	Mus musculus	124-127
24837741-5	2015	Bax and Bak, two key molecules of mitochondrial permeability transition pore, were interdependently activated by BPDE, with Bax and Bak translocation to and Bax/Bak homo-oligomerization in mitochondria, release of cytochrome c was induced.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	113-117	BCL2-associated X protein	Mus musculus	124-127
24837741-8	2015	Together the findings suggested that BPDE-induced necrosis was modulated by the p53-independent pathway, which was related to the translocation of Bax and Bak to mitochondria, release of cytochrome c, and activation of caspases.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	37-41	BCL2-associated X protein	Mus musculus	147-150
25457551-8	2015	Notably, PUMA contributed to neuronal apoptosis through competitive binding of apoptosis repressor with caspase recruitment domain to activate caspase-8 that cleaved Bid into tBid to accelerate Bax mitochondrial translocation, revealing a novel pathway of Bax activation by PUMA to mediate Abeta-induced neuronal apoptosis.	tBID	175-179	BCL2-associated X protein	Mus musculus	194-197
25359171-4	2015	Interestingly, separate as well as combined supplementation of curcumin (60 mg/kg body weight) and quercetin (40 mg/kg body weight) to BP-treated animals resulted in a significant decrease in the protein expression of Bcl-2 but caused a significant increase in the protein expression of Bax along with a noticeable improvement in the number of apoptotic cells.	Quercetin	99-108	BCL2-associated X protein	Mus musculus	287-290
25359171-4	2015	Interestingly, separate as well as combined supplementation of curcumin (60 mg/kg body weight) and quercetin (40 mg/kg body weight) to BP-treated animals resulted in a significant decrease in the protein expression of Bcl-2 but caused a significant increase in the protein expression of Bax along with a noticeable improvement in the number of apoptotic cells.	Benzo(a)pyrene	135-137	BCL2-associated X protein	Mus musculus	287-290
25629230-7	2015	The IHC results showed that the protein expression of Bcl-2, VEGF, HIF-1alpha, and survivin were consistently downregulated, whereas that of Bax was upregulated after myricanol treatment.	myricanol	167-176	BCL2-associated X protein	Mus musculus	141-144
25483100-6	2015	In addition, we found that HS-543 induced apoptosis with the loss of mitochondrial membrane potential by decreasing the expression of Mcl-1 and survivin, together with increasing that of Bax.	hs-543	27-33	BCL2-associated X protein	Mus musculus	187-190
25632145-2	2015	We report here that deficiency in bax exerted broad neuroprotection against excitotoxic injury and oxygen/glucose deprivation in mouse neocortical neuron cultures and reduced infarct size, necrotic injury, and cerebral edema formation after middle cerebral artery occlusion in mice.	Oxygen	99-105	BCL2-associated X protein	Mus musculus	34-37
25632145-3	2015	Neuronal Ca(2+) and mitochondrial membrane potential (Deltapsim) analysis during excitotoxic injury revealed that bax-deficient neurons showed significantly reduced Ca(2+) transients during the NMDA excitation period and did not exhibit the deregulation of Deltapsim that was observed in their wild-type (WT) counterparts.	N-Methylaspartate	194-198	BCL2-associated X protein	Mus musculus	114-117
25632145-7	2015	However, when Ca(2+) uptake into the sarco/endoplasmic reticulum was blocked with the Ca(2+)-ATPase inhibitor thapsigargin, bax-deficient neurons showed strongly elevated cytosolic Ca(2+) levels during NMDA excitation, suggesting that the ability of Bax to support dynamic ER Ca(2+) handling is critical for cell death signaling during periods of neuronal overexcitation.	Thapsigargin	110-122	BCL2-associated X protein	Mus musculus	124-127
25632145-7	2015	However, when Ca(2+) uptake into the sarco/endoplasmic reticulum was blocked with the Ca(2+)-ATPase inhibitor thapsigargin, bax-deficient neurons showed strongly elevated cytosolic Ca(2+) levels during NMDA excitation, suggesting that the ability of Bax to support dynamic ER Ca(2+) handling is critical for cell death signaling during periods of neuronal overexcitation.	Thapsigargin	110-122	BCL2-associated X protein	Mus musculus	250-253
25632145-7	2015	However, when Ca(2+) uptake into the sarco/endoplasmic reticulum was blocked with the Ca(2+)-ATPase inhibitor thapsigargin, bax-deficient neurons showed strongly elevated cytosolic Ca(2+) levels during NMDA excitation, suggesting that the ability of Bax to support dynamic ER Ca(2+) handling is critical for cell death signaling during periods of neuronal overexcitation.	N-Methylaspartate	202-206	BCL2-associated X protein	Mus musculus	124-127
25478867-3	2015	DMBA treatment suppressed Bax, Bax/Bcl-2 ratio, release of cyt c, Apaf1, caspase-9, -3 mediated apoptosis.	9,10-Dimethyl-1,2-benzanthracene	0-4	BCL2-associated X protein	Mus musculus	26-29
25629230-8	2015	Myricanol also significantly upregulated the mRNA expression of Bax and downregulated that of Bcl-2, VEGF, HIF-1alpha, and survivin in a dose-dependent manner (p &lt; 0.05 to 0.001).	myricanol	0-9	BCL2-associated X protein	Mus musculus	64-67
25478867-3	2015	DMBA treatment suppressed Bax, Bax/Bcl-2 ratio, release of cyt c, Apaf1, caspase-9, -3 mediated apoptosis.	9,10-Dimethyl-1,2-benzanthracene	0-4	BCL2-associated X protein	Mus musculus	31-34
25615615-7	2015	We further showed that induction of apoptosis by DON in Myc-overexpressing cancers is via the pro-apoptotic factor Bax.	Diazooxonorleucine	49-52	BCL2-associated X protein	Mus musculus	115-118
25478867-5	2015	Simultaneous application of BA, NA and CAG induced a mitochondria-mediated apoptosis, characterized by a rise in the Bax, Bax/Bcl-2 ratio, release of cyt c, upregulation of Apaf1 with down-stream activation of caspase-9, -3.	Butyric Acid	28-30	BCL2-associated X protein	Mus musculus	117-120
25478867-5	2015	Simultaneous application of BA, NA and CAG induced a mitochondria-mediated apoptosis, characterized by a rise in the Bax, Bax/Bcl-2 ratio, release of cyt c, upregulation of Apaf1 with down-stream activation of caspase-9, -3.	Butyric Acid	28-30	BCL2-associated X protein	Mus musculus	122-125
25478867-5	2015	Simultaneous application of BA, NA and CAG induced a mitochondria-mediated apoptosis, characterized by a rise in the Bax, Bax/Bcl-2 ratio, release of cyt c, upregulation of Apaf1 with down-stream activation of caspase-9, -3.	Glucaric Acid	39-42	BCL2-associated X protein	Mus musculus	117-120
25478867-5	2015	Simultaneous application of BA, NA and CAG induced a mitochondria-mediated apoptosis, characterized by a rise in the Bax, Bax/Bcl-2 ratio, release of cyt c, upregulation of Apaf1 with down-stream activation of caspase-9, -3.	Glucaric Acid	39-42	BCL2-associated X protein	Mus musculus	122-125
25613943-12	2015	Meanwhile, TO90 suppressed the elevation of apoptosis factors caspase-3 and bax induced by NMDA and upregulated the level of an antiapoptotic factor bcl-2.	N-Methylaspartate	91-95	BCL2-associated X protein	Mus musculus	76-79
25785006-5	2015	Furthermore, ALA significantly inhibited TNBS-induced apoptosis, which partly due to up-regulation of Bcl-2 expression, reduction of Bax expression and caspase-3, caspase-9 activity.	Thioctic Acid	13-16	BCL2-associated X protein	Mus musculus	133-136
25301748-8	2015	Furthermore, our findings suggest that the increased nigral iron content exacerbates the oxidative stress levels, promoting apoptosis through the Bcl-2/Bax pathway and the activated caspase-3 pathway in the brain.	Iron	60-64	BCL2-associated X protein	Mus musculus	152-155
25785006-5	2015	Furthermore, ALA significantly inhibited TNBS-induced apoptosis, which partly due to up-regulation of Bcl-2 expression, reduction of Bax expression and caspase-3, caspase-9 activity.	Trinitrobenzenesulfonic Acid	41-45	BCL2-associated X protein	Mus musculus	133-136
26514497-6	2015	Interestingly, simvastatin treatment of P3NS1 cells increased the intracellular ROS production and decreased antioxidant enzyme activity with increased P53, Bax and Caspase3 gene expression while that of Bcl2 was decreased.	Simvastatin	15-26	BCL2-associated X protein	Mus musculus	157-160
25429088-5	2015	Diosgenin significantly inhibited apoptosis, as reflected by decreased percentage of TUNEL-positive cells; decreased expression of Bax (Bcl-2-associated X protein), AIF (apoptosis-inducing factor), and cleaved caspases 3 and 9; and increased expression of Bcl-2 (B-cell lymphoma 2).	Diosgenin	0-9	BCL2-associated X protein	Mus musculus	131-134
25715028-3	2015	Here we report that the BH3 mimetic, ABT-737, induces autophagy in parallel with disruption of BCL2-BECN1 binding in 2 different apoptosis-deficient cell types lacking BAX and BAK1, namely in mouse embryonic fibroblasts cells and in human colon cancer HCT116 cells.	BH 3	24-27	BCL2-associated X protein	Mus musculus	168-171
25715028-3	2015	Here we report that the BH3 mimetic, ABT-737, induces autophagy in parallel with disruption of BCL2-BECN1 binding in 2 different apoptosis-deficient cell types lacking BAX and BAK1, namely in mouse embryonic fibroblasts cells and in human colon cancer HCT116 cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	37-40	BCL2-associated X protein	Mus musculus	168-171
25429088-5	2015	Diosgenin significantly inhibited apoptosis, as reflected by decreased percentage of TUNEL-positive cells; decreased expression of Bax (Bcl-2-associated X protein), AIF (apoptosis-inducing factor), and cleaved caspases 3 and 9; and increased expression of Bcl-2 (B-cell lymphoma 2).	Diosgenin	0-9	BCL2-associated X protein	Mus musculus	136-162
26064905-10	2015	10 mg/kg NaB treatment also remarkably inhibited the apoptosis, decreasing the levels of caspase-3 and Bax and increasing the levels of Bcl-2, p-Akt, and BDNF.	nab	9-12	BCL2-associated X protein	Mus musculus	103-106
25401748-7	2015	The melatonin-induced upregulation of SIRT1 was also associated with an increase in the anti-apoptotic factor, Bcl2, and a reduction in the pro-apoptotic factor Bax.	Melatonin	4-13	BCL2-associated X protein	Mus musculus	161-164
26406155-4	2015	Results demonstrated that Sirt 1 and Bcl-2 were inhibited, whereas p53 acetylation, Bax, and caspase 9 were promoted by H2O2, as was aggravated by the Sirt 1 inhibitor, EX-527.	Hydrogen Peroxide	120-124	BCL2-associated X protein	Mus musculus	84-87
25997722-9	2015	The levels of p-Akt (Ser 473) and Bcl-2 were significantly increased while Bax and cleaved caspase-3 were decreased by hydrogen treatment on the model of H/R.	Hydrogen	119-127	BCL2-associated X protein	Mus musculus	75-78
25968939-5	2015	Meanwhile, ginkgetin dramatically inhibited cell apoptosis induced by MPP+ through the caspase-3 and Bcl2/Bax pathway.	ginkgetin	11-20	BCL2-associated X protein	Mus musculus	106-109
25968939-5	2015	Meanwhile, ginkgetin dramatically inhibited cell apoptosis induced by MPP+ through the caspase-3 and Bcl2/Bax pathway.	mangion-purified polysaccharide (Candida albicans)	70-74	BCL2-associated X protein	Mus musculus	106-109
26090427-5	2015	In EAE treatment group, the volume of xenograft was significantly reduced compared with the control group (P &lt; 0.05) and the protein expressions of CyclinD1, bcl-2, and MMP-9 were reduced, while those of bax, caspase-3, and nm23-H1 were increased.	EAE	3-6	BCL2-associated X protein	Mus musculus	207-210
25967874-15	2015	Finally, Resveratrol treatment also may suppress apoptosis of myocardium in cold-treated mouse hearts via inhibiting Bax and caspase-3 activation.	Resveratrol	9-20	BCL2-associated X protein	Mus musculus	117-120
26156438-9	2015	In addition, sesamol pre-treatment reduced the radiation-induced pattern of expression of p53 and Bax apoptotic proteins in the bone marrow, spleen, and GI.	sesamol	13-20	BCL2-associated X protein	Mus musculus	98-101
25787108-0	2015	Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl-2/Bax pathway.	Arsenic	23-30	BCL2-associated X protein	Mus musculus	106-109
25787108-12	2015	However, the expressions of the Bax gene and its protein, and the expression ratio of Bax/Bcl-2 in the hippocampus were significantly higher in the groups exposed to As than in the control group (p&lt;0.05).	Arsenic	166-168	BCL2-associated X protein	Mus musculus	32-35
25787108-12	2015	However, the expressions of the Bax gene and its protein, and the expression ratio of Bax/Bcl-2 in the hippocampus were significantly higher in the groups exposed to As than in the control group (p&lt;0.05).	Arsenic	166-168	BCL2-associated X protein	Mus musculus	86-89
24963915-5	2015	In vitro, high glucose-conditioned renal proximal tubular cells showed higher apoptosis and caspase activation following ATP depletion and hypoxic injury, accompanied by a heightened mitochondrial accumulation of Bax and release of cytochrome c. In response to injury, both glucose-conditioned renal proximal tubular cells and diabetic kidney tissues showed markedly higher p53 induction.	Glucose	15-22	BCL2-associated X protein	Mus musculus	213-216
25481089-7	2015	Rotenone-treated mice showed impairment in locomotor behavior and a significant reduction in brain dopamine, serotonin, norepinephrine, GSH levels, and paraoxonase activity, whereas a significant increase was observed in brain malondialdehyde, tumor necrosis factor-alpha, interleukin-beta levels besides DNA damage, and over-expression of caspase-3, Bax, and Bcl-2 genes.	Rotenone	0-8	BCL2-associated X protein	Mus musculus	351-354
25798044-4	2015	Additionally, H2O2 treatment increased Bax, decreased Bcl-2, and promoted PARP-1 cleavage in a dose-dependent manner.	Hydrogen Peroxide	14-18	BCL2-associated X protein	Mus musculus	39-42
25798044-8	2015	Furthermore, H2O2-induced increase of Bax, decrease of Bcl-2, and PARP-1 cleavage was also inhibited by BHA.	Hydrogen Peroxide	13-17	BCL2-associated X protein	Mus musculus	38-41
25355463-9	2015	Furthermore, this converse oxaliplatin-inducing apoptosis exerted through the functional gap junction was correlated with the mitochondrial pathway-related protein Bcl-2/Bax and caspase-3/9.	Oxaliplatin	27-38	BCL2-associated X protein	Mus musculus	170-173
25563365-5	2015	Compared to the PBS or the NC mice, levels of Bax mRNA and protein in tumor xenografts were significantly upregulated in p65 siRNA-treated mice.	Lead	16-19	BCL2-associated X protein	Mus musculus	46-49
25453207-8	2015	The findings suggest that activated GSK3beta orchestrated neurodegenerative alterations following KA treatment and its inhibition by TDZD-8 affords a distinct neuroprotective profile by activating Akt/GSK3beta pathway which might act upstream of Bax/Bcl2 and caspase-3 pathways.	4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione	133-139	BCL2-associated X protein	Mus musculus	246-249
25661164-10	2015	In cultured murine podocytes, ADR stimulated the expression of Bax/Bcl-2 and apoptosis as determined by Hoechst 33342 staining.	bisbenzimide ethoxide trihydrochloride	104-117	BCL2-associated X protein	Mus musculus	63-66
25384499-0	2015	Chidamide, a histone deacetylase inhibitor, functions as a tumor inhibitor by modulating the ratio of Bax/Bcl-2 and P21 in pancreatic cancer.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	0-9	BCL2-associated X protein	Mus musculus	102-105
25857436-8	2015	RESULTS: Our histological findings revealed that MPTP administration enhanced Bax/Bcl2 ratio and microglial cells activation reflecting induction of apoptosis and inflammation, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	49-53	BCL2-associated X protein	Mus musculus	78-81
25384499-9	2015	The in vitro and in vivo studies found that Chidamide treatment significantly decreased the expression of type I HDACs, uncleaved Caspase-3 and p21 and increased the ratio of Bax/Bcl-2 expression.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	44-53	BCL2-associated X protein	Mus musculus	175-178
25810725-5	2015	We observed that Lin(-)BMCs integrated into outer retinal layers improving morphological retinal structure and induced molecular changes such as downregulation of proapoptotic caspase-3 gene, a decrease in BAX/BCL-2 gene ratio, and significant elevation of BDNF expression.	S-benzyl-N-malonylcysteine	23-27	BCL2-associated X protein	Mus musculus	206-209
25264132-7	2015	PFOS was also observed to down-regulate the protein expression of Bcl-2 and to up-regulate that of Bax.	perfluorooctane sulfonic acid	0-4	BCL2-associated X protein	Mus musculus	99-102
25237909-8	2015	CONCLUSIONS: Luteolin + Gem promoted apoptotic cell death in pancreatic tumor cells in vivo through inhibition of the K-ras/GSK-3beta/NF-kappaB signaling pathway, leading to a reduction in the Bcl-2/Bax ratio, release of cytochrome c, and activation of caspase 3.	luteolin + gem	13-27	BCL2-associated X protein	Mus musculus	199-202
25445441-9	2014	KEY FINDINGS: Geniposide alleviated mammary gland apoptosis, down-regulated Bax expression, inhibited Caspase-3 cleavage and p53 phosphorylation and up-regulated Bcl-2 expression in vivo.	geniposide	14-24	BCL2-associated X protein	Mus musculus	76-79
25516522-3	2014	We found that: (1) melatonin resulted in reductions of tumor"s volume and weight in the gastric cancer-bearing mice and thus showed anti-cancer effect; (2) melatonin reduced Bcl-2 expression, but increased the expression of Bax, p53 and p21 in tumor tissue.	Melatonin	19-28	BCL2-associated X protein	Mus musculus	224-227
25516522-3	2014	We found that: (1) melatonin resulted in reductions of tumor"s volume and weight in the gastric cancer-bearing mice and thus showed anti-cancer effect; (2) melatonin reduced Bcl-2 expression, but increased the expression of Bax, p53 and p21 in tumor tissue.	Melatonin	156-165	BCL2-associated X protein	Mus musculus	224-227
25406029-7	2014	In addition, we observed that AAI markedly increases the expression of pro-apoptotic proteins, including Bax, caspase-3, caspase-9, and poly(ADP) ribose polymerase (PARP).	aristolochic acid I	30-33	BCL2-associated X protein	Mus musculus	105-108
25397718-4	2014	According to Western blotting data, overexpressions of cleaved forms of caspase-9, caspase-3, and PARP-1 and pro-apoptotic Bax and Bad, accompanied by underexpressed anti-apoptotic Bcl-2 and Bcl-xL indicate that GA induces B16F10 cell apoptosis via mitochondrial pathway.	Gallic Acid	212-214	BCL2-associated X protein	Mus musculus	123-126
25445441-11	2014	Geniposide inhibited Bax expression and Caspase-3 cleavage, and up-regulated the expression of Bcl-2.	geniposide	0-10	BCL2-associated X protein	Mus musculus	21-24
25445441-13	2014	SIGNIFICANCE: These results demonstrate that the anti-apoptotic property of geniposide is due to its modulation of TLR4 and apoptosis-related factors (p53, Bax, Bcl-2 and Caspase-3) in LPS-induced mouse mastitis.	geniposide	76-86	BCL2-associated X protein	Mus musculus	156-159
24132498-4	2014	Further study indicated that TBrC not only enhances the protein levels of Bax, cytosolic cytochrome c, caspase-3 and PARP-1 but also reduces the protein expressions of Bcl-2, cyclin D1, VEGFR1 and NF-kappaB as well as inhibits the phosphorylation and expressions of VEGFR2 and Akt in the cancer cells.	TBrC	29-33	BCL2-associated X protein	Mus musculus	74-77
24748476-7	2014	The study in primary embryonic cell lines showed that the apoptosis after incubation with DOX was reduced in cells overexpressing Hsp70 (Tg/Tg), while the apoptotic pathway that was activated by DOX administration involved activated protein factors such as p53, Bax, caspase-9, caspase-3, and PARP-1.	Doxorubicin	90-93	BCL2-associated X protein	Mus musculus	262-265
25211405-0	2014	Methylsulfonylmethane modulates apoptosis of LPS/IFN-gamma-activated RAW 264.7 macrophage-like cells by targeting p53, Bax, Bcl-2, cytochrome c and PARP proteins.	dimethyl sulfone	0-21	BCL2-associated X protein	Mus musculus	119-122
25458503-7	2014	Melamine-related toxicity promoted the expression of Bax mRNA, and suppressed the expression of Bcl-2 mRNA in spleen of the treated mice.	melamine	0-8	BCL2-associated X protein	Mus musculus	53-56
25075795-7	2014	Furthermore, oridonin promoted apoptosis by increasing terminal dUTP nick end labeling-positive cells as well as the ratio of Bax/Bcl-2 in xenograft mice.	oridonin	13-21	BCL2-associated X protein	Mus musculus	126-129
24748476-7	2014	The study in primary embryonic cell lines showed that the apoptosis after incubation with DOX was reduced in cells overexpressing Hsp70 (Tg/Tg), while the apoptotic pathway that was activated by DOX administration involved activated protein factors such as p53, Bax, caspase-9, caspase-3, and PARP-1.	Doxorubicin	195-198	BCL2-associated X protein	Mus musculus	262-265
25543474-7	2014	Meanwhile, quercetin could down-regulate the expression of BCL-2 and NF-kappaB gene, and up-regulate the expression of BAX gene.	Quercetin	11-20	BCL2-associated X protein	Mus musculus	119-122
25050737-7	2014	Rottlerin inhibited the expression of Bcl-2, cyclin D1, CDK2 and CDK6, and induced the expression of Bax in tumor tissues compared to untreated control.	rottlerin	0-9	BCL2-associated X protein	Mus musculus	101-104
25111896-0	2014	Cell death induced by 2-phenylethynesulfonamide uncovers a pro-survival function of BAX.	2-phenylacetylenesulfonamide	22-47	BCL2-associated X protein	Mus musculus	84-87
25111661-6	2014	PQ also induced more apoptosis in pneumocytes from MT(-/-) mice, and the expressions of apoptosis-related proteins Bax, Bcl-2, cleaved-caspase-3, and the ratio of Bax/Bcl-2 were all more significantly increased in PQ-treated MT(-/-) mice.	Paraquat	0-2	BCL2-associated X protein	Mus musculus	115-118
25111661-6	2014	PQ also induced more apoptosis in pneumocytes from MT(-/-) mice, and the expressions of apoptosis-related proteins Bax, Bcl-2, cleaved-caspase-3, and the ratio of Bax/Bcl-2 were all more significantly increased in PQ-treated MT(-/-) mice.	Paraquat	0-2	BCL2-associated X protein	Mus musculus	163-166
25176185-7	2014	The coumarin-copper drug also significantly induced LA795 cell apoptosis in a time-dependent manner (P&lt;0.05), which was accompanied by upregulation p35 and B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax), and downregulation of Bcl-2.	coumarin	4-12	BCL2-associated X protein	Mus musculus	207-210
25176185-7	2014	The coumarin-copper drug also significantly induced LA795 cell apoptosis in a time-dependent manner (P&lt;0.05), which was accompanied by upregulation p35 and B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax), and downregulation of Bcl-2.	Copper	13-19	BCL2-associated X protein	Mus musculus	207-210
25176185-9	2014	In conclusion, the coumarin-copper drug may inhibit the proliferation of LA795 cells through the induction of cell apoptosis, which may be associated with the upregulation of p53 and Bax, with concurrent downregulation of Bcl-2.	coumarin	19-27	BCL2-associated X protein	Mus musculus	183-186
25176185-9	2014	In conclusion, the coumarin-copper drug may inhibit the proliferation of LA795 cells through the induction of cell apoptosis, which may be associated with the upregulation of p53 and Bax, with concurrent downregulation of Bcl-2.	Copper	28-34	BCL2-associated X protein	Mus musculus	183-186
25361902-5	2014	RESULTS: Our results showed that ivabradine treatment attenuated the expression and staining score of matrix metalloproteinase (MMP)-2, induced the dephosphorylation of caspase 3, BAX and MMP-2, and enhanced the phosphorylation of NF-kappaB.	Ivabradine	33-43	BCL2-associated X protein	Mus musculus	180-183
25333616-5	2014	We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels.	Glucose	59-66	BCL2-associated X protein	Mus musculus	164-167
25431364-5	2014	Moreover, 2,4,6-TCP alters the mitochondrial membrane potential and increases the apoptosis rate, the caspase 3 activity, and the Bax/Bcl-2 ratio, demonstrating that the mitochondrial pathway is involved in the 2,4,6-TCP-induced apoptosis.	2,4,6-trichlorophenol	10-19	BCL2-associated X protein	Mus musculus	130-133
25431364-5	2014	Moreover, 2,4,6-TCP alters the mitochondrial membrane potential and increases the apoptosis rate, the caspase 3 activity, and the Bax/Bcl-2 ratio, demonstrating that the mitochondrial pathway is involved in the 2,4,6-TCP-induced apoptosis.	2,4,6-trichlorophenol	211-220	BCL2-associated X protein	Mus musculus	130-133
24965756-8	2014	Nano-EGCG also inhibited proliferation (Ki-67 and PCNA) and induced apoptosis (Bax, PARP) in tumors harvested from the treated mice.	epigallocatechin gallate	5-9	BCL2-associated X protein	Mus musculus	79-82
25333616-5	2014	We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels.	Leucine	14-21	BCL2-associated X protein	Mus musculus	164-167
25333616-5	2014	We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels.	Tyrosine	23-31	BCL2-associated X protein	Mus musculus	164-167
25333616-5	2014	We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels.	Arginine	33-41	BCL2-associated X protein	Mus musculus	164-167
25333616-5	2014	We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels.	Homoarginine	43-55	BCL2-associated X protein	Mus musculus	164-167
25336920-6	2014	Moreover, pretreatment with R-LA stimulated the activation of PI3K-Akt through mTORC1 and mTORC2 components (mTOR, rictor and raptor) and production of antiinflammatory cytokine, IL-10 which led to the inactivation of glycogen synthase kinase-3beta (GSK-3beta) and reduction of both Bax/Bcl2 and Bax/Bcl-xL ratios, accompanied by inhibition of the cleaved caspase-3.	Thioctic Acid	28-32	BCL2-associated X protein	Mus musculus	283-286
25336920-6	2014	Moreover, pretreatment with R-LA stimulated the activation of PI3K-Akt through mTORC1 and mTORC2 components (mTOR, rictor and raptor) and production of antiinflammatory cytokine, IL-10 which led to the inactivation of glycogen synthase kinase-3beta (GSK-3beta) and reduction of both Bax/Bcl2 and Bax/Bcl-xL ratios, accompanied by inhibition of the cleaved caspase-3.	Thioctic Acid	28-32	BCL2-associated X protein	Mus musculus	296-299
25290208-8	2014	Perindopril significantly decreased caspase-3 and caspase-9 activities, and elevated Bcl-2/Bax ratio in the hippocampus.	Perindopril	0-11	BCL2-associated X protein	Mus musculus	91-94
25080441-8	2014	Immunostaining and western blotting showed that DOC induces activation of intrinsic, type II apoptosis in ovarian somatic cells; increasing the levels of cleaved caspase 3, cleaved caspase 8, Bax and cleaved poly(ADP-ribose) polymerase, while also inducing movement of cytochrome C from mitochondria into the cytosol.	Docetaxel	48-51	BCL2-associated X protein	Mus musculus	192-195
25084483-10	2014	Rutin significantly reversed ethanol-increased Bax, cytochrome c expression and caspase 3 activity, and decreased Bcl-2 and Bcl-xL protein expression in HT22 cells.	Ethanol	29-36	BCL2-associated X protein	Mus musculus	47-50
24716481-12	2014	In addition, phloroglucinol attenuated the UVB-induced expression of the pro-apoptotic proteins, Bax protein, and activated caspase-3.	Phloroglucinol	13-27	BCL2-associated X protein	Mus musculus	97-100
25090966-6	2014	Furthermore, the overexpression of Sirt3 attenuated the release of cytochrome c, the increase in the Bax/Bcl-2 ratio, as well as caspase-9/caspase-3 activity induced by H(2)O(2), and eventually inhibited apoptotic neuronal cell death.	Hydrogen Peroxide	169-177	BCL2-associated X protein	Mus musculus	101-104
25264893-13	2014	In addition, JNK, p-JNK, Bax, TNF-alpha, NF-kappaB, IL2, IL6 and levels were also decreased in NAC-treated mice.	Acetylcysteine	95-98	BCL2-associated X protein	Mus musculus	25-28
25109418-8	2014	Celecoxib also increased the abundance of the pro-apoptotic protein Bax and reduced the levels of the anti-apoptotic protein Bcl-2.	Celecoxib	0-9	BCL2-associated X protein	Mus musculus	68-71
24932975-9	2014	Consistently, phloretin enhanced bcl-2 induction but diminished bax expression.	Phloretin	14-23	BCL2-associated X protein	Mus musculus	64-67
25222049-10	2014	Moreover, Bazhen decoction down-regulate acetaminophen-induced Bax/Bcl-2 ratio, caspase 3, caspase 8 and caspase 9.	Acetaminophen	41-54	BCL2-associated X protein	Mus musculus	63-66
25225718-6	2014	Dap significantly inhibited the neuronal apoptosis by regulating balance of Bcl-2 and Bax expression.	daphnetin	0-3	BCL2-associated X protein	Mus musculus	86-89
24699224-10	2014	In addition, guanabenz increased the protein levels of anti-apoptotic B cell lymphoma/lewkmia-2 (Bcl-2), and down-regulated the pro-apoptotic protein levels of C/EBP homologous protein (CHOP), Bcl-2-associated X protein (BAX) and cytochrome C in SOD1 G93A mice.	Guanabenz	13-22	BCL2-associated X protein	Mus musculus	193-219
24699224-10	2014	In addition, guanabenz increased the protein levels of anti-apoptotic B cell lymphoma/lewkmia-2 (Bcl-2), and down-regulated the pro-apoptotic protein levels of C/EBP homologous protein (CHOP), Bcl-2-associated X protein (BAX) and cytochrome C in SOD1 G93A mice.	Guanabenz	13-22	BCL2-associated X protein	Mus musculus	221-224
25400823-6	2014	We also found that under high glucose conditions miR-378 activated the PI3K/Akt signaling pathway and down regulated pro-apoptotic CytC, Apaf-1 and Bax proteins via the PI3K/Akt pathway.	Glucose	30-37	BCL2-associated X protein	Mus musculus	148-151
24995576-5	2014	The administration of MPTP (30 mg/kg for four successive days) significantly induced motor impairments as determined by behavioral studies (narrow beam test, catalepsy and akinesia), lowered dopamine levels and up-regulated the expressions of the inflammatory and apoptotic markers (tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, inducible nitric oxide synthase, glial fibrillary acidic protein, cyclooxygenase-2 and Bax).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	22-26	BCL2-associated X protein	Mus musculus	433-436
25183508-13	2014	In the Naltrexone plus TM group, gene expression of Bax/Bcl-2 ratio and caspase3 significantly lowered compared with the TM group.	Naltrexone	7-17	BCL2-associated X protein	Mus musculus	52-55
24908354-11	2014	The DFO and ATO can up-regulate the expression of Caspase-3 and Bax, and down-regulate the expression of NF-kappaBp65 and survivin, especially for their combination.	Deferoxamine	4-7	BCL2-associated X protein	Mus musculus	64-67
25028793-9	2014	Moreover, adiponectin treatment prevented palmitate-induced apoptosis by inhibition of caspase-9 activation, but not of caspase-8, and induced an upregulation of BCL-2 and a downregulation of Bax in protein level.	Palmitates	42-51	BCL2-associated X protein	Mus musculus	192-195
24908354-11	2014	The DFO and ATO can up-regulate the expression of Caspase-3 and Bax, and down-regulate the expression of NF-kappaBp65 and survivin, especially for their combination.	Arsenic Trioxide	12-15	BCL2-associated X protein	Mus musculus	64-67
25113976-5	2014	The expression of DNA repair genes p53, PARP1 and BAX were up-regulated in testes of mice killed after 3 and 24h of last administration of 4 mg/kg/day Aroclor 1254.	Aroclors	151-158	BCL2-associated X protein	Mus musculus	50-53
24850187-9	2014	Down-regulation of bax and caspase-3 protein, and up-regulation of nephrin and podocin protein were observed in the glomeruli of diabetic mice after administration of rapamycin.	Sirolimus	167-176	BCL2-associated X protein	Mus musculus	19-22
24352031-10	2014	Triptolide and chemotherapeutics treatment also induced Bax expression, and inhibited Bcl-2 expression.	triptolide	0-10	BCL2-associated X protein	Mus musculus	56-59
25074826-6	2014	We found that fluoride exposure affected the expression levels of stress response factors, signal transduction components, and apoptosis-related proteins, including caspase-3/caspase-9, B-cell lymphoma 2 (Bcl-2), and Bax.	Fluorides	14-22	BCL2-associated X protein	Mus musculus	217-220
25178635-8	2014	Sensitization to tamoxifen was associated with down regulation of antiapoptotic protein Bcl-2, up-regulation of proapoptotic protein Bax, reduced caveolin-1 (Cav-1) and decreased pAkt/pERK levels.	Tamoxifen	17-26	BCL2-associated X protein	Mus musculus	133-136
25337186-8	2014	The caspase-3 activity of PLLA-DOX/pDA group was the highest using biochemical techniques, and the Bax: Bcl-2 ratio increased significantly in PLLA-DOX/pDA group through qRT-PCR analysis.	Doxorubicin	148-151	BCL2-associated X protein	Mus musculus	99-102
25210696-9	2014	The ratio of Bax to Bcl-2 was higher in the MK-801-induced schizophrenia mice than the normal mice.	Dizocilpine Maleate	44-50	BCL2-associated X protein	Mus musculus	13-16
24991917-8	2014	Western blot analysis showed that GlcNAc-Sal pretreatment decreased the expression of caspase-3 and increased the expression of Bcl-2 (B-cell lymphoma 2)/Bax (Bcl-2-associated X protein) induced by GCI-R treatment.	2-acetamido-2-deoxy-4-O-(beta-2-acetamid-2-deoxyglucopyranosyl)glucopyranose	34-40	BCL2-associated X protein	Mus musculus	154-157
24827147-5	2014	Interestingly, the Bax translocation was dependent on Ca(2+) mobilization from IP3 receptors because pre-incubation with xestospongin C, a selective IP3 receptor inhibitor, abolished this response.	xestospongin C	121-135	BCL2-associated X protein	Mus musculus	19-22
24583196-7	2014	Chalcones R7 and R13 induced an increase of pro-apoptotic proteins Bax, Bid and Bak (only chalcone R13), as well as a decrease in anti-apoptotic Bcl-2 expression.	Chalcones	0-9	BCL2-associated X protein	Mus musculus	67-70
25010671-8	2014	Aged septic Mttp-IKO mice exhibited increased gut epithelial apoptosis, increased jejunal Bax/Bcl-2 and Bax/Bcl-XL ratios yet simultaneously demonstrated increased crypt proliferation and villus length.	O(4)-methylthymidine triphosphate	12-16	BCL2-associated X protein	Mus musculus	90-93
25010671-8	2014	Aged septic Mttp-IKO mice exhibited increased gut epithelial apoptosis, increased jejunal Bax/Bcl-2 and Bax/Bcl-XL ratios yet simultaneously demonstrated increased crypt proliferation and villus length.	O(4)-methylthymidine triphosphate	12-16	BCL2-associated X protein	Mus musculus	104-107
24835026-6	2014	Further, the H2O2 induced cell death was arrested in the presence of CWC through the inhibition of CDC42 mediated SAPK/JNK pathways and activation of other molecules of apoptotic pathways, including Bax and caspase3.	Hydrogen Peroxide	13-17	BCL2-associated X protein	Mus musculus	199-202
24835026-6	2014	Further, the H2O2 induced cell death was arrested in the presence of CWC through the inhibition of CDC42 mediated SAPK/JNK pathways and activation of other molecules of apoptotic pathways, including Bax and caspase3.	CHEMBL3425950	69-72	BCL2-associated X protein	Mus musculus	199-202
24800927-8	2014	Mechanistically, CXCL4mab reduced the apoptosis of the crypt epithelia by suppression of the 5-FU-induced expression of p53 and Bax through its receptor CXCR3.	Fluorouracil	93-97	BCL2-associated X protein	Mus musculus	128-131
25197333-8	2014	EGCG also inhibited the expression of the ligand of death receptor Fas (Fas-L), apoptosis regulator BAX (Bax) and tumor-suppressor protein p53, and increased the expression of B-cell lymphoma 2 (Bcl-2).	epigallocatechin gallate	0-4	BCL2-associated X protein	Mus musculus	80-103
25197333-8	2014	EGCG also inhibited the expression of the ligand of death receptor Fas (Fas-L), apoptosis regulator BAX (Bax) and tumor-suppressor protein p53, and increased the expression of B-cell lymphoma 2 (Bcl-2).	epigallocatechin gallate	0-4	BCL2-associated X protein	Mus musculus	105-108
25197333-9	2014	These findings suggest that EGCG can ameliorate CP-induced apoptosis in the kidney by regulating death receptor Fas conducted extrinsic pathway, and the expression of Bax and Bcl-2.	epigallocatechin gallate	28-32	BCL2-associated X protein	Mus musculus	167-170
24991917-8	2014	Western blot analysis showed that GlcNAc-Sal pretreatment decreased the expression of caspase-3 and increased the expression of Bcl-2 (B-cell lymphoma 2)/Bax (Bcl-2-associated X protein) induced by GCI-R treatment.	sal	41-44	BCL2-associated X protein	Mus musculus	154-157
25143814-7	2014	These results suggest that paeonol exhibits antitumor effects and the mechanism of the inhibition is via induction of apoptosis, regulation of Bcl-2 and Bax expression, and activation of caspase 8 and caspase 3.	paeonol	27-34	BCL2-associated X protein	Mus musculus	153-156
24795386-9	2014	Urothelial tumors of the licofelone-fed mice showed an increase in apoptosis (p53, p21, Bax, and caspase3) with a decrease in proliferation, inflammation, and angiogenesis markers (proliferating cell nuclear antigen, COX-2, 5-LOX, prostaglandin E synthase 1, FLAP, and VEGF).	licofelone	25-35	BCL2-associated X protein	Mus musculus	88-91
24703880-5	2014	Halofuginone treatment of mdx mice reduced the apoptotic nuclei number in the diaphragm, together with reduction in Bax and induction in Bcl2 levels in myofibers isolated from these mice.	halofuginone	0-12	BCL2-associated X protein	Mus musculus	116-119
24703880-8	2014	Inhibition of apoptosis or staurosporine-induced apoptosis by halofuginone in mdx primary myoblasts and C2 myogenic cell line, respectively, was reflected by less pyknotic/apoptotic cells and reduced Bax expression.	Staurosporine	27-40	BCL2-associated X protein	Mus musculus	200-203
24703880-8	2014	Inhibition of apoptosis or staurosporine-induced apoptosis by halofuginone in mdx primary myoblasts and C2 myogenic cell line, respectively, was reflected by less pyknotic/apoptotic cells and reduced Bax expression.	halofuginone	62-74	BCL2-associated X protein	Mus musculus	200-203
24438098-0	2014	Pseudomonas aeruginosa homoserine lactone triggers apoptosis and Bak/Bax-independent release of mitochondrial cytochrome C in fibroblasts.	homoserine lactone	23-41	BCL2-associated X protein	Mus musculus	69-72
24438098-6	2014	A DKO MEF line that was relatively unaffected by the Bak/Bax-dependent proapoptotic stimulants staurosporine and etoposide responded to C12 similarly to WT MEF: activation of caspase 3/7, depolarization of Deltapsimito and release of cytochrome C and cell death.	Staurosporine	95-108	BCL2-associated X protein	Mus musculus	57-60
24830635-7	2014	Addition of nicotine to HFD further resulted in an increase in the incidence of hepatocellular apoptosis and was associated with activation of caspase 2, induction of inducible nitric oxide synthase (iNOS), and perturbation of the BAX/BCL-2 ratio.	Nicotine	12-20	BCL2-associated X protein	Mus musculus	231-234
24739012-9	2014	Western blot analysis revealed elevated TNF-alpha, Bax, Bcl-2, Bip, caspase 8 and caspase 9 in ob/ob mice with various degrees of reversal by lenalidomide treatment.	Lenalidomide	142-154	BCL2-associated X protein	Mus musculus	51-54
24952344-5	2014	In addition, DON could significantly increase the protein levels of p53 and Bax/Bcl-2 ratio in MTEC1 cells.	deoxynivalenol	13-16	BCL2-associated X protein	Mus musculus	76-79
24807380-9	2014	Treatment with muscone also reduced myocardial apoptosis by enhancing Bcl-2 and suppressing Bax expression.	muscone	15-22	BCL2-associated X protein	Mus musculus	92-95
25221579-6	2014	Pretreatment with Asiaticoside decreased neuronal cell loss in a concentration-dependent manner and restored changes in expression of apoptotic-related proteins Bcl-2 and Bax.	asiaticoside	18-30	BCL2-associated X protein	Mus musculus	171-174
24789513-9	2014	Quantitative polymerase chain reaction confirmed that pingyangmycin significantly upregulated the expression of p53, p53-induced protein with death domain, Bax, p53 upregulated modulator of apoptosis and p53 inducible gene 3, and downregulated the expression of murine double minute 2.	bleomycetin	54-67	BCL2-associated X protein	Mus musculus	156-159
24768735-0	2014	Gene expression regulation of Bcl2, Bax and cytochrome-C by geraniol on chronic MPTP/probenecid induced C57BL/6 mice model of Parkinson"s disease.	geraniol	60-68	BCL2-associated X protein	Mus musculus	36-39
24682241-11	2014	OGD induced cell apoptosis, the expression of Bax and the activation of caspase-3 and ERK, inhibited the expression of Bcl-2 and increased the expression of MMP-9, while these effects were reversed by treatment with resveratrol.	Resveratrol	216-227	BCL2-associated X protein	Mus musculus	46-49
24685508-8	2014	Oxidative species generation including the influence of iNOS, nitrotyrosine tissue expression and cell apoptotic death pathway was also evaluated resulting in a lower Bax/Bcl-2 unbalance.	3-nitrotyrosine	62-75	BCL2-associated X protein	Mus musculus	167-170
24718383-0	2014	Paris saponin I induces apoptosis via increasing the Bax/Bcl-2 ratio and caspase-3 expression in gefitinib-resistant non-small cell lung cancer in vitro and in vivo.	calenduloside E	6-15	BCL2-associated X protein	Mus musculus	53-56
24682241-13	2014	Treatment with U0126 inhibited MMP-9 and Bax expression and caspase-3 activation, while it further promoted the expression of the anti-apoptotic molecule Bcl-2, suggesting that resveratrol inhibits MMP-9 expression and cell apoptosis by attenuating the activation of ERK1/2.	U 0126	15-20	BCL2-associated X protein	Mus musculus	41-44
24885625-0	2014	High glucose increases LPS-induced DC apoptosis through modulation of ERK1/2, AKT and Bax/Bcl-2.	Glucose	5-12	BCL2-associated X protein	Mus musculus	86-89
24885625-8	2014	CONCLUSIONS: These results suggest that high glucose concentrations might prime dendritic cells for apoptosis induced by LPS in the intestinal tract through upregulating the expression of Bax and downregulating the expression of AKT, ERK and Bcl-2.	Glucose	45-52	BCL2-associated X protein	Mus musculus	188-191
24801481-6	2014	Fenofibrate decreased the activity of phosphatidylinositol-3 kinase (PI3K)-Akt phosphorylation and FoxO3a phosphorylation in kidneys, increasing the B cell leukaemia/lymphoma 2 (BCL-2)/BCL-2-associated X protein (BAX) ratio and superoxide dismutase (SOD) 1 levels.	Fenofibrate	0-11	BCL2-associated X protein	Mus musculus	185-223
24686337-7	2014	Furthermore, pharmacological BAX channel inhibition is able to prevent LMP, restore lysosomal levels, reverse AP accumulation, and attenuate mitochondrial permeabilization and overall nigrostriatal degeneration caused by MPTP, both in vitro and in vivo.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	221-225	BCL2-associated X protein	Mus musculus	29-32
24686182-10	2014	While, the effect of Apelin-13 on Bax, Bcl-2, caspase-3 and cleaved caspase-3 was attenuated by LY294002 and PD98059.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	96-104	BCL2-associated X protein	Mus musculus	34-37
24686182-10	2014	While, the effect of Apelin-13 on Bax, Bcl-2, caspase-3 and cleaved caspase-3 was attenuated by LY294002 and PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	109-116	BCL2-associated X protein	Mus musculus	34-37
24581239-8	2014	RESULTS: The elevation of apoptotic DNA fragmentation and number of TUNEL-positive nuclei were accompanied with the upregulation of Bax in muscle after exposure to doxorubicin, but all these changes were neither seen in the muscle treated with acylated ghrelin nor unacylated ghrelin after doxorubicin exposure.	Doxorubicin	164-175	BCL2-associated X protein	Mus musculus	132-135
24781573-13	2014	remifentanil inhibited cortical Bax protein expression, caspase-9 activity, and preserved mitochondrial integrity, whereas it had no effect on caspase-8 activity.	Remifentanil	0-12	BCL2-associated X protein	Mus musculus	32-35
24707974-6	2014	ACE and AITC elevated Bcl2 and inhibited Bax expressions in MG-induced Neuro-2A cells.	Pyruvaldehyde	60-62	BCL2-associated X protein	Mus musculus	41-44
24632094-10	2014	In addition, JNK phosphorylations were involved in activating the mitochondria-dependent apoptotic pathway following Ang II stimulation, as pre-treatment of JNK-specific inhibitor SP600125 could rescue osteoblast cells from apoptosis by enhancing the anti-apoptotic protein Bcl-2 expressions, suppressing the translocation of Bax from cytosol into mitochondria, blocking cytochrome C release and caspase-3 activation.	pyrazolanthrone	180-188	BCL2-associated X protein	Mus musculus	326-329
24560902-6	2014	Moreover, ligustilide-treated groups exhibited a significant increase in the bcl-2/bax ratio, pro-caspase 3 and pro-caspase 8 compared with the TNF-alpha-control group in a dose-dependent manner.	ligustilide	10-21	BCL2-associated X protein	Mus musculus	83-86
24362790-6	2014	The absence of Bax and Bak in mouse embryonic fibroblasts rendered them resistant to cisplatin-induced apoptosis and consequently to the sensitizing action of the RasGAP-derived peptide.	Cisplatin	85-94	BCL2-associated X protein	Mus musculus	15-18
24851101-6	2014	Our findings suggest that NR4A1 expression and mitochondrial translocation of Bax are related to simvastatin-induced apoptosis in LPS-activated RAW 264.7 macrophages.	Simvastatin	97-108	BCL2-associated X protein	Mus musculus	78-81
24560905-9	2014	In addition, garcinol obviously reduced the induction of Bax but did not alter the level of Bcl-2.	garcinol	13-21	BCL2-associated X protein	Mus musculus	57-60
24682087-8	2014	Furthermore, prazosin and yohimbine protected against restraint-induced hepatocytes apoptosis through attenuating the activation of caspases-9 and -3 and reducing the Bax/Bcl-2 ratio.	Prazosin	13-21	BCL2-associated X protein	Mus musculus	167-170
24561153-5	2014	Western blot analysis showed that CS increased the expression of Bax-to-Bcl-2 ratio and activated caspase-8 and caspase-3 to induce apoptosis.	Cesium	34-36	BCL2-associated X protein	Mus musculus	65-68
23893732-6	2014	Moreover, naloxone increased anti-apoptotic Bcl-2 expression, attenuated apoptotic protein (Bax, cytochrome c, and caspase) expression and decreased apoptotic death.	Naloxone	10-18	BCL2-associated X protein	Mus musculus	92-95
24658098-6	2014	We found that the Wnt5a supplement promoted the vertical and horizontal migration of mMSCs, ameliorated the cell death and the reduction of Bcl-2/Bax induced by H2O2.	Hydrogen Peroxide	161-165	BCL2-associated X protein	Mus musculus	146-149
24682087-8	2014	Furthermore, prazosin and yohimbine protected against restraint-induced hepatocytes apoptosis through attenuating the activation of caspases-9 and -3 and reducing the Bax/Bcl-2 ratio.	Yohimbine	26-35	BCL2-associated X protein	Mus musculus	167-170
24595063-9	2014	We also observed that VASH2 overexpression downregulated wild-type p53, as well as suppressed the expression of the pro-apoptotic protein BCL2-associated X protein (Bax) and cleaved caspase-3 (CC-3) after treatment by CDDP.	Cisplatin	218-222	BCL2-associated X protein	Mus musculus	138-163
24647338-5	2014	Combined melatonin and ER stress significantly reduced Bcl-2 protein and augmented Bax protein compared to melatonin-only treatment.	Melatonin	9-18	BCL2-associated X protein	Mus musculus	83-86
24469707-3	2014	Results showed that treatment of Taxol could increase the inhibition rate of tumour growth, positive expression levels of Caspase-3, Bax and decrease positive expression levels of Bcl-2 and Bcl-2/Bax, expression levels of HGF, MACC1 and C-met proteins and MACC1 mRNA in tumour tissue of CC mice.	Paclitaxel	33-38	BCL2-associated X protein	Mus musculus	133-136
24378639-9	2014	Glutamate treatment induced the loss of BV-2 cell viability, which was associated with an increase in the apoptotic rate, as well as an increase in the Bax/Bcl-2 ratio and the extracellular levels of cleaved caspase-3.	Glutamic Acid	0-9	BCL2-associated X protein	Mus musculus	152-155
24469707-3	2014	Results showed that treatment of Taxol could increase the inhibition rate of tumour growth, positive expression levels of Caspase-3, Bax and decrease positive expression levels of Bcl-2 and Bcl-2/Bax, expression levels of HGF, MACC1 and C-met proteins and MACC1 mRNA in tumour tissue of CC mice.	Paclitaxel	33-38	BCL2-associated X protein	Mus musculus	196-199
24469707-4	2014	It can be concluded that inhibitory activity of Taxol against tumour growth in CC mice is closely associated with its modulating positive expression of Bcl-2, Bax, Caspase-3, expression of HGF, MACC1, Caspase-3 and C-met proteins and MACC1 mRNA in tumour of CC mice.	Paclitaxel	48-53	BCL2-associated X protein	Mus musculus	159-162
24399025-7	2014	Further exploration demonstrated that nicotine efficiently abolished cisplatin-promoted mitochondria translocation of Bax and the release of cytochrome c. The pretreatment of alpha-bungarotoxin and tubocurarine chloride significantly attenuated nicotine-augmented cell viability, abolished caspase-3 activation and alpha7 nAChR upregulation.	Nicotine	38-46	BCL2-associated X protein	Mus musculus	118-121
24399025-7	2014	Further exploration demonstrated that nicotine efficiently abolished cisplatin-promoted mitochondria translocation of Bax and the release of cytochrome c. The pretreatment of alpha-bungarotoxin and tubocurarine chloride significantly attenuated nicotine-augmented cell viability, abolished caspase-3 activation and alpha7 nAChR upregulation.	Cisplatin	69-78	BCL2-associated X protein	Mus musculus	118-121
24399025-7	2014	Further exploration demonstrated that nicotine efficiently abolished cisplatin-promoted mitochondria translocation of Bax and the release of cytochrome c. The pretreatment of alpha-bungarotoxin and tubocurarine chloride significantly attenuated nicotine-augmented cell viability, abolished caspase-3 activation and alpha7 nAChR upregulation.	Tubocurarine	198-219	BCL2-associated X protein	Mus musculus	118-121
24523936-11	2014	Pentoxifylline treatment reduced expression levels of BNP, bcl2 and bax.	Pentoxifylline	0-14	BCL2-associated X protein	Mus musculus	68-71
24486958-3	2014	Excessive glutamate induces oxidative and endoplasmic reticulum (ER) stress, gradually increasing ER-related pro-apoptotic transcription factor C/EBP homologous protein (CHOP) expression, and eventually up-regulating expression of the pro-apoptotic factor Bax.	Glutamic Acid	10-19	BCL2-associated X protein	Mus musculus	256-259
24486958-4	2014	Cordycepin inhibits CHOP and Bax expressions, as well as p-ERK, p-JNK, and p-p38, all of which are involved in oxidative or ER stress-induced apoptosis.	cordycepin	0-10	BCL2-associated X protein	Mus musculus	29-32
24559268-11	2014	Increased apoptotic cell death and a high ratio of B cell leukaemia/lymphoma 2 (Bcl-2)-associated X protein (Bax) to Bcl-2 in CsA-treated mice were also significantly ameliorated by OA treatment.	Cyclosporine	126-129	BCL2-associated X protein	Mus musculus	109-112
24326424-9	2014	Doxorubicin induced fibrosis (accumulated collagen deposition and increased CTGF), activated apoptosis (increased TUNEL index, apoptotic DNA fragmentation, and caspase-3 activity and decreased Bcl-2/Bax ratio), and suppressed phosphorylation status of prosurvival signals (ERK1/2 and Akt) in ventricular muscles.	Doxorubicin	0-11	BCL2-associated X protein	Mus musculus	199-202
24352880-5	2014	BIM exerts its pro-death function via its alpha-helical BH3 death domain that has the dual capacity to inhibit antiapoptotic proteins such as BCL-2 and MCL-1 and directly trigger proapoptotic proteins such as the mitochondrial executioner protein BAX.	BH 3	56-59	BCL2-associated X protein	Mus musculus	247-250
23955895-9	2014	Pro-apoptosis-related gene expression levels of Bax, caspase 3 were expressed lower than control in MII stage oocytes derived from M-CSS group; anti apoptosis-related genes, survivin and heat shock factor-1 (Hsf-1) were slightly increased.	m-css	131-136	BCL2-associated X protein	Mus musculus	48-51
24072771-8	2014	In tumor tissues of mice treated with Chit-nanoEGCG, compared with groups treated with EGCG and controls, there was significant (i) induction of poly (ADP-ribose) polymerases cleavage, (ii) increase in the protein expression of Bax with concomitant decrease in Bcl-2, (iii) activation of caspases and (iv) reduction in Ki-67 and proliferating cell nuclear antigen.	chit	38-42	BCL2-associated X protein	Mus musculus	228-231
24072771-8	2014	In tumor tissues of mice treated with Chit-nanoEGCG, compared with groups treated with EGCG and controls, there was significant (i) induction of poly (ADP-ribose) polymerases cleavage, (ii) increase in the protein expression of Bax with concomitant decrease in Bcl-2, (iii) activation of caspases and (iv) reduction in Ki-67 and proliferating cell nuclear antigen.	nanoegcg	43-51	BCL2-associated X protein	Mus musculus	228-231
24072771-8	2014	In tumor tissues of mice treated with Chit-nanoEGCG, compared with groups treated with EGCG and controls, there was significant (i) induction of poly (ADP-ribose) polymerases cleavage, (ii) increase in the protein expression of Bax with concomitant decrease in Bcl-2, (iii) activation of caspases and (iv) reduction in Ki-67 and proliferating cell nuclear antigen.	epigallocatechin gallate	47-51	BCL2-associated X protein	Mus musculus	228-231
24550650-7	2014	Significantly less apoptosis, a lower ratio of Bax to Bcl-2 expression and fewer apoptotic cells in TUNEL staining, and decreased expression of transforming growth factor-beta1 were observed in the obstructed kidneys from tempol-treated mice compared with those from control mice.	tempol	222-228	BCL2-associated X protein	Mus musculus	47-50
24398778-7	2014	Moreover, PD173074 also significantly increased the ratio of Bax/Bcl-2.	PD 173074	10-18	BCL2-associated X protein	Mus musculus	61-64
22223438-7	2014	Therefore, a possible signaling pathway in TBT-induced apoptosis in mouse livers involves PP2A inhibition and ROS elevation serving a pivotal function as upstream activators of MAPKs; activation of MAPKs in turn leads to an increase in the Bax/Bcl-2 ratio, ultimately leading to the activation of caspase-3.	tributyltin	43-46	BCL2-associated X protein	Mus musculus	240-243
22223438-7	2014	Therefore, a possible signaling pathway in TBT-induced apoptosis in mouse livers involves PP2A inhibition and ROS elevation serving a pivotal function as upstream activators of MAPKs; activation of MAPKs in turn leads to an increase in the Bax/Bcl-2 ratio, ultimately leading to the activation of caspase-3.	Reactive Oxygen Species	110-113	BCL2-associated X protein	Mus musculus	240-243
24475141-7	2014	In SHP knockdown by small interfering RNA, cisplatin-induced activation of TGF-beta1, p-JNK and Bax/Bcl-2 ratio was not attenuated, while SHP overexpression and FXR ligand inhibited expression of these proteins in cisplatin-pretreated HK2 cells.	Cisplatin	43-52	BCL2-associated X protein	Mus musculus	96-99
24405628-12	2014	Treatment with DHA significantly reduced: (1) the degree of spinal cord inflammation and tissue injury, (2) pro-inflammatory cytokine expression (TNF-alpha), (3) nitrotyrosine formation, (4) glial fibrillary acidic protein (GFAP) expression, and (5) apoptosis (Fas-L, Bax, and Bcl-2 expression).	Docosahexaenoic Acids	15-18	BCL2-associated X protein	Mus musculus	268-271
24388981-0	2014	Polyglutamine expansion disturbs the endoplasmic reticulum formation, leading to caspase-7 activation through Bax.	polyglutamine	0-13	BCL2-associated X protein	Mus musculus	110-113
24388981-3	2014	This study reveals that polyglutamine oligomers augmented at ER induce insertion of Bax into the ER membrane, thereby activating caspase-7.	polyglutamine	24-37	BCL2-associated X protein	Mus musculus	84-87
24393202-8	2014	Additionally, significantly less inflammatory cell infiltration, a lower ratio of Bax to Bcl-2 expression, and fewer apoptotic cells on TUNEL staining were observed in the obstructed kidneys of oleanolic acid-treated mice.	Oleanolic Acid	194-208	BCL2-associated X protein	Mus musculus	82-85
24568162-4	2014	We observed inhibition of NF-kappaB nuclear translocation, up-regulation of Bax and down-regulation of Bcl-2, as well as increased caspase-3 and caspase-9 expression after baicalin treatment in vitro and in vivo, which indicates that the mitochondrial pathway was involved in baicalin-induced apoptosis.	baicalin	172-180	BCL2-associated X protein	Mus musculus	76-79
24335837-7	2014	Furthermore, WS0701 administration significantly reduced the stress-induced apoptosis of hippocampal neurons, and increased the Bcl-2/Bax ratio in the hippocampus.	3,4-dihydroxy-5-(6-((4-hydroxy-3-methoxybenzyl)amino)-9H-purin-9-yl)tetrahydrofuran-2-yl)methyl decanoate	13-19	BCL2-associated X protein	Mus musculus	134-137
24849190-4	2014	Western blot analysis was also used to measure the expression level of Bcl-2, Bax, caspase 9, and caspase 3 proteins in H2O2-treated RGC-5 cells.	Hydrogen Peroxide	120-124	BCL2-associated X protein	Mus musculus	78-81
25146619-15	2014	The expression of Ang1 and Bcl-2 was improved, while the expression of ICAM-1 and Bax was inhibited, in melatonin-treated SCI mice.	Melatonin	104-113	BCL2-associated X protein	Mus musculus	82-85
23906530-14	2014	Cardiomyocyte apoptosis and induction of Bax in response to AB were suppressed by puerarin.	puerarin	82-90	BCL2-associated X protein	Mus musculus	41-44
24849190-6	2014	MDHB also obstructed H2O2-induced apoptosis by regulating the expression of Bcl-2 and Bax, as well as suppressing the activation of caspase 9 and caspase 3.	methyl 3,4-dihydroxybenzoate	0-4	BCL2-associated X protein	Mus musculus	86-89
24849190-6	2014	MDHB also obstructed H2O2-induced apoptosis by regulating the expression of Bcl-2 and Bax, as well as suppressing the activation of caspase 9 and caspase 3.	Hydrogen Peroxide	21-25	BCL2-associated X protein	Mus musculus	86-89
24141792-6	2014	Vit significantly inhibited the neuronal apoptosis induced by NMDA exposure by regulating balance of Bcl-2 and Bax expression and the cleavages of poly (ADP-ribose) polymerase and pro-caspase 3.	N-Methylaspartate	62-66	BCL2-associated X protein	Mus musculus	111-114
23922174-5	2014	Besides, LJSP induced apoptosis of transplanted tumor tissues by increasing the ratio of Bax/Bcl-2.	ljsp	9-13	BCL2-associated X protein	Mus musculus	89-92
24945996-8	2014	Pu-erh tea also significantly induced apoptosis in tissues of mice (P &lt; 0.05) by upregulating Bax and downregulating Bcl-2.	pu-erh	0-6	BCL2-associated X protein	Mus musculus	97-100
24349043-10	2013	Moreover, we demonstrated that nifedipine treatment reduced mRNA levels of pro-oxidative/nitrosative (iNOS and gp91(phox)/p47(phox) NOX2 subunits) and pro-apoptotic (Bax) genes in mdx diaphragm muscles and lowered serum creatine kinase (CK) levels.	Nifedipine	31-41	BCL2-associated X protein	Mus musculus	166-169
24336083-12	2013	Indeed, knockdown of PATZ1 in p53-null osteosarcoma cells upregulates BAX expression and decreases survival of 5FU-treated cells, then suggesting an anti-apoptotic role of PATZ1 in p53-null cancer cells.	Fluorouracil	111-114	BCL2-associated X protein	Mus musculus	70-73
24165291-8	2013	Curcumin suppressed cell proliferation, colony formation, migration, and induced apoptosis which was mediated partly through the mitochondrial pathway after an increase in the ratio of Bax to Bcl2.	Curcumin	0-8	BCL2-associated X protein	Mus musculus	185-188
24161766-13	2013	Testosterone may have reduced HSP10 expression in GCs, leading to reduced Bcl-2 expression and increased Bax expression.	Testosterone	0-12	BCL2-associated X protein	Mus musculus	105-108
24092928-7	2013	Treatment with a DPP-4 inhibitor, alogliptin (AG), significantly reduced CP-induced renal injury and reduced the renal mRNA expression ratios of Bax/Bcl-2 and Bim/Bcl-2.	alogliptin	34-44	BCL2-associated X protein	Mus musculus	145-148
24012889-6	2013	In addition, the levels of Bcl-2 and full-length Bid were protected, and that of mitochondrial Bax was reduced by liquiritigenin.	liquiritigenin	114-128	BCL2-associated X protein	Mus musculus	95-98
25566426-4	2013	Treadmill exercise ameliorated cognitive function in water maze test and significantly increased the level of Bcl-2/Bax ratio and HSP-70 in Tg-exe group compared to Tg-con group; on the other hand, it significantly decreased the expression of caspase-3 and COX-2 in Tg-exe group compared to Tg-con group.	Thioguanine	140-142	BCL2-associated X protein	Mus musculus	116-119
24259976-10	2013	Furthermore, CMN treatment efficiently protected against APAP-induced apoptosis via increasing Bcl-2/Bax ratio.	Acetaminophen	57-61	BCL2-associated X protein	Mus musculus	101-104
24092818-4	2013	Renal mitochondrial Bax induction following cisplatin treatment was significantly decreased by treatment of mice with AR9273 and these antiapoptotic effects involved p38 mitogen-activated protein kinase signaling.	Cisplatin	44-53	BCL2-associated X protein	Mus musculus	20-23
24095822-0	2013	Mangiferin attenuates MPTP induced dopaminergic neurodegeneration and improves motor impairment, redox balance and Bcl-2/Bax expression in experimental Parkinson"s disease mice.	mangiferin	0-10	BCL2-associated X protein	Mus musculus	121-124
24095822-6	2013	MPTP treatment leads to enhanced oxidative stress, induction of apoptosis (upregulates the expression of Bax, proapoptotic protein and downregulates the expression of anti-apoptotic marker Bcl-2), and loss of dopominergic neurons which results in motor impairments.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	BCL2-associated X protein	Mus musculus	105-108
24262283-10	2013	Expressions of Bax and Bcl2 along with GFAP did show significant variations (p &lt; 0.05) on MPTP treatment when compared to control animals and the changes were found to be reversed significantly (p &lt; 0.05) after treatment with asiaticoside.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	93-97	BCL2-associated X protein	Mus musculus	15-18
24262283-10	2013	Expressions of Bax and Bcl2 along with GFAP did show significant variations (p &lt; 0.05) on MPTP treatment when compared to control animals and the changes were found to be reversed significantly (p &lt; 0.05) after treatment with asiaticoside.	asiaticoside	232-244	BCL2-associated X protein	Mus musculus	15-18
24227720-6	2013	Disruption of Bax:Bcl-xL binding by BH3-mimetic ABT 737 caused rapid apoptosis of cerebellar progenitors and primary murine medulloblastoma cells.	BH 3	36-39	BCL2-associated X protein	Mus musculus	14-17
24227720-6	2013	Disruption of Bax:Bcl-xL binding by BH3-mimetic ABT 737 caused rapid apoptosis of cerebellar progenitors and primary murine medulloblastoma cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	48-51	BCL2-associated X protein	Mus musculus	14-17
24008345-6	2013	After exposure to ALDO, the mouse pancreatic beta-cell line MIN6 exhibited decreased viability and increased caspase-3 activity, as well as reduced expression of Bcl-2/Bax and p-AKT, even if mineralocorticoid receptor was completely suppressed with small interfering RNA.	Aldosterone	18-22	BCL2-associated X protein	Mus musculus	168-171
24209962-4	2013	We found that fluvastatin treatment enhanced the activation of pro-apoptotic members such as caspase-3 and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells.	Fluvastatin	14-25	BCL2-associated X protein	Mus musculus	107-110
24139803-6	2013	The recruitment of Bcl-2 to the BAP31-CDIP1 complex, as well as CDIP1-dependent truncated Bid (tBid) and caspase-8 activation, contributes to BAX oligomerization.	tBID	95-99	BCL2-associated X protein	Mus musculus	142-145
22674879-6	2013	Increased expression of p21 and Bcl-2 as well as decreased expression of Bax were observed after cisplatin treatment by Western blotting.	Cisplatin	97-106	BCL2-associated X protein	Mus musculus	73-76
24085658-5	2013	We showed that 3-NP-induced apoptosis, which was accompanied by Bax and Beclin-1 upregulation, was dependent on acidic vesicular organelle (AVO) formation after a continuous exposure to 3-NP for 12 h. The upregulation of Bax and Beclin-1 as well as AVO formation were normalized 24 h after 3-NP exposure.	3-nitropropionic acid	15-19	BCL2-associated X protein	Mus musculus	64-67
24085658-5	2013	We showed that 3-NP-induced apoptosis, which was accompanied by Bax and Beclin-1 upregulation, was dependent on acidic vesicular organelle (AVO) formation after a continuous exposure to 3-NP for 12 h. The upregulation of Bax and Beclin-1 as well as AVO formation were normalized 24 h after 3-NP exposure.	3-nitropropionic acid	15-19	BCL2-associated X protein	Mus musculus	221-224
24085658-5	2013	We showed that 3-NP-induced apoptosis, which was accompanied by Bax and Beclin-1 upregulation, was dependent on acidic vesicular organelle (AVO) formation after a continuous exposure to 3-NP for 12 h. The upregulation of Bax and Beclin-1 as well as AVO formation were normalized 24 h after 3-NP exposure.	3-nitropropionic acid	186-190	BCL2-associated X protein	Mus musculus	64-67
24085658-5	2013	We showed that 3-NP-induced apoptosis, which was accompanied by Bax and Beclin-1 upregulation, was dependent on acidic vesicular organelle (AVO) formation after a continuous exposure to 3-NP for 12 h. The upregulation of Bax and Beclin-1 as well as AVO formation were normalized 24 h after 3-NP exposure.	3-nitropropionic acid	186-190	BCL2-associated X protein	Mus musculus	221-224
24085658-5	2013	We showed that 3-NP-induced apoptosis, which was accompanied by Bax and Beclin-1 upregulation, was dependent on acidic vesicular organelle (AVO) formation after a continuous exposure to 3-NP for 12 h. The upregulation of Bax and Beclin-1 as well as AVO formation were normalized 24 h after 3-NP exposure.	3-nitropropionic acid	186-190	BCL2-associated X protein	Mus musculus	64-67
24085658-5	2013	We showed that 3-NP-induced apoptosis, which was accompanied by Bax and Beclin-1 upregulation, was dependent on acidic vesicular organelle (AVO) formation after a continuous exposure to 3-NP for 12 h. The upregulation of Bax and Beclin-1 as well as AVO formation were normalized 24 h after 3-NP exposure.	3-nitropropionic acid	186-190	BCL2-associated X protein	Mus musculus	221-224
24051269-8	2013	Proapoptotic Bax protein expression increased in breast tumor by solanine compared with its respective control group (P&lt;0.05).	Solanine	65-73	BCL2-associated X protein	Mus musculus	13-16
24146755-5	2013	Surprisingly, tyrosine phosphorylation of YAP was detected which coincided with increased nuclear p73 association, Bax-driven epithelial cell death and p53 accumulation resulting in enhanced apoptosis and poor survival of DSS-treated Rassf1a knockout mice.	Tyrosine	14-22	BCL2-associated X protein	Mus musculus	115-118
24146755-8	2013	These observations suggest that tyrosine phosphorylation of YAP (to drive p73 association and up-regulation of pro-apoptotic genes such as Bax) and accumulation of p53 are consequences of inflammation-induced injury in DSS-treated Rassf1a(-/-) mice.	Tyrosine	32-40	BCL2-associated X protein	Mus musculus	139-142
24146755-8	2013	These observations suggest that tyrosine phosphorylation of YAP (to drive p73 association and up-regulation of pro-apoptotic genes such as Bax) and accumulation of p53 are consequences of inflammation-induced injury in DSS-treated Rassf1a(-/-) mice.	dss	219-222	BCL2-associated X protein	Mus musculus	139-142
23747734-3	2013	Intraperitoneal administration of CAP (10mg/kg body weight) to Swiss albino mice suppressed the development of lung carcinoma by amending the protein expressions of apoptotic regulators p53, Bcl-2, Bax and caspase-3.	Capsaicin	34-37	BCL2-associated X protein	Mus musculus	198-201
23997041-5	2013	However, simultaneous supplementation with quercetin (75 mg/kg) attenuated the toxicity induced by PNP through renewal of the antioxidant enzyme"s status, alleviating apoptosis by regulating the expressions of Bax and Bcl-xl, XBP-1 and HO-1mRNAs, and the regulation of caspase-3 activity.	Quercetin	43-52	BCL2-associated X protein	Mus musculus	210-213
23891578-3	2013	Results showed that following exposure to MC-LR, expression of Bax, caspase 3 and caspase 8 was up-regulated.	cyanoginosin LR	42-47	BCL2-associated X protein	Mus musculus	63-66
23590664-5	2013	The results showed that GDNF pretreatment blocked the apoptotic effects induced by 6-OHDA, with the upregulation of the antiapoptotic protein, Bcl-2 and Bcl-w, as well as the downregulation of the proapoptotic proteins, Bax and Bad.	Oxidopamine	83-89	BCL2-associated X protein	Mus musculus	220-223
23891578-6	2013	In conclusion, p53, Bcl-2, Bax, Caspase 3 and Caspase 8 are involved in the regulation of MC-LR-induced apoptosis of testicular cells.	cyanoginosin LR	90-95	BCL2-associated X protein	Mus musculus	27-30
23877198-6	2013	In addition, the Bax/Bcl-2 gene and protein expression ratios were significantly increased in the MPTP-exposed mice, and this effect was reversed by selegiline.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	BCL2-associated X protein	Mus musculus	17-20
23877198-6	2013	In addition, the Bax/Bcl-2 gene and protein expression ratios were significantly increased in the MPTP-exposed mice, and this effect was reversed by selegiline.	Selegiline	149-159	BCL2-associated X protein	Mus musculus	17-20
23590664-7	2013	These results indicated that GDNF could protect MN9D cells from apoptosis induced by 6-OHDA via upregulating Bcl-2 and Bcl-w expressions and downregulating Bax and Bad expressions.	Oxidopamine	85-91	BCL2-associated X protein	Mus musculus	156-159
24124281-9	2013	Disruption of the mitochondrial membrane potential (DeltaPsim), activation of the pro-apoptotic proteins Bid and Bax, and cytochrome c release in response to glutamate-induced oxidative stress were reduced.	Glutamic Acid	158-167	BCL2-associated X protein	Mus musculus	113-116
23897984-13	2013	Mouse lung tissues respond to long-term Cd exposure increased p-Tyr, downregulated LC3-II, and accumulated full-length Bax and procaspase-3.	Cadmium	40-42	BCL2-associated X protein	Mus musculus	119-122
24066113-4	2013	In the present study, we showed low glucose to induce a decrease of BCL2 and BCL-XL anti-apoptotic proteins expression, leading to an increase of free pro-apoptotic BAX.	Glucose	36-43	BCL2-associated X protein	Mus musculus	165-168
25206541-8	2013	We further found that expression of pro-apoptotic Bax and caspase-3 were significantly decreased while anti-apoptotic Bcl-2 was greatly increased in H2O2 damaged RGC-5 cells with oligomeric proanthocyanidin by western blot assay.	Hydrogen Peroxide	149-153	BCL2-associated X protein	Mus musculus	50-53
24146535-12	2013	Consistent with these effects, TFF treatment decreased the Bax expression level and, concurrently, increased the ratio of Bcl-2 to Bax.	trofosfamide	31-34	BCL2-associated X protein	Mus musculus	59-62
24146535-12	2013	Consistent with these effects, TFF treatment decreased the Bax expression level and, concurrently, increased the ratio of Bcl-2 to Bax.	trofosfamide	31-34	BCL2-associated X protein	Mus musculus	131-134
24146535-13	2013	CONCLUSIONS: TFF attenuated diabetes-induced apoptosis in retinal neurons by inhibiting Bax expression and increasing the ratio of Bcl-2 to Bax, which suggests that TFF might prevent retinal neuronal damage in diabetes mellitus.	trofosfamide	13-16	BCL2-associated X protein	Mus musculus	88-91
24146535-13	2013	CONCLUSIONS: TFF attenuated diabetes-induced apoptosis in retinal neurons by inhibiting Bax expression and increasing the ratio of Bcl-2 to Bax, which suggests that TFF might prevent retinal neuronal damage in diabetes mellitus.	trofosfamide	13-16	BCL2-associated X protein	Mus musculus	140-143
24146535-13	2013	CONCLUSIONS: TFF attenuated diabetes-induced apoptosis in retinal neurons by inhibiting Bax expression and increasing the ratio of Bcl-2 to Bax, which suggests that TFF might prevent retinal neuronal damage in diabetes mellitus.	trofosfamide	165-168	BCL2-associated X protein	Mus musculus	140-143
25206541-8	2013	We further found that expression of pro-apoptotic Bax and caspase-3 were significantly decreased while anti-apoptotic Bcl-2 was greatly increased in H2O2 damaged RGC-5 cells with oligomeric proanthocyanidin by western blot assay.	proanthocyanidin	190-206	BCL2-associated X protein	Mus musculus	50-53
23726868-9	2013	Consistently, decrease in tumor necrosis factor-alpha level, up-regulation of Bcl-2, and down-regulation of BAX and the downstream executioner caspase-3, also occurred in the hippocampus of 3xTg-AD mice after treatment with Tabiano"s spa-water, thus suggesting that it is also able to modulate inflammation and apoptosis.	spa	145-148	BCL2-associated X protein	Mus musculus	108-111
23816832-0	2013	gamma-Tocotrienol induced cell cycle arrest and apoptosis via activating the Bax-mediated mitochondrial and AMPK signaling pathways in 3T3-L1 adipocytes.	plastochromanol 8	0-17	BCL2-associated X protein	Mus musculus	77-80
23640013-12	2013	Vitamin C and CPA administration increased the expression of anti-apoptotic protein Bcl-2 and decreased the expression of pro-apoptotic protein Bax in the ischemic mice.	Ascorbic Acid	0-9	BCL2-associated X protein	Mus musculus	144-147
23640013-12	2013	Vitamin C and CPA administration increased the expression of anti-apoptotic protein Bcl-2 and decreased the expression of pro-apoptotic protein Bax in the ischemic mice.	N(6)-cyclopentyladenosine	14-17	BCL2-associated X protein	Mus musculus	144-147
23726868-9	2013	Consistently, decrease in tumor necrosis factor-alpha level, up-regulation of Bcl-2, and down-regulation of BAX and the downstream executioner caspase-3, also occurred in the hippocampus of 3xTg-AD mice after treatment with Tabiano"s spa-water, thus suggesting that it is also able to modulate inflammation and apoptosis.	Water	238-243	BCL2-associated X protein	Mus musculus	108-111
23991283-4	2013	Loss of Bax/Bak reduced outer mitochondrial membrane permeability and conductance without altering inner membrane MPTP function, resulting in resistance to mitochondrial calcium overload and necrotic cell death.	Calcium	170-177	BCL2-associated X protein	Mus musculus	8-11
23791694-11	2013	Furthermore, DON induced apoptosis in spleen, MLNs, and PPs, and DON-induced apoptosis was promoted by increased expression of Bax and decreased expression of Bcl-2.	deoxynivalenol	13-16	BCL2-associated X protein	Mus musculus	127-130
23639522-11	2013	The resulting significantly increased bcl-2/bax ratio indicates that myricitrin may prevent the apoptosis induced by oxidative stress injury.	myricitrin	69-79	BCL2-associated X protein	Mus musculus	44-47
23791694-11	2013	Furthermore, DON induced apoptosis in spleen, MLNs, and PPs, and DON-induced apoptosis was promoted by increased expression of Bax and decreased expression of Bcl-2.	deoxynivalenol	65-68	BCL2-associated X protein	Mus musculus	127-130
23605481-0	2013	AICAR induces Bax/Bak-dependent apoptosis through upregulation of the BH3-only proteins Bim and Noxa in mouse embryonic fibroblasts.	AICA ribonucleotide	0-5	BCL2-associated X protein	Mus musculus	14-17
23598363-8	2013	While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the cisplatin-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.	Imatinib Mesylate	118-126	BCL2-associated X protein	Mus musculus	258-261
23598363-8	2013	While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the cisplatin-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.	Cisplatin	141-150	BCL2-associated X protein	Mus musculus	258-261
23598363-11	2013	The expression kinetics of TAp63, c-Abl and TAp73 suggest that cisplatin activates TAp63-dependent expression of c-Abl and TAp73 and, in turn, the activation of TAp73 by c-Abl-induced BAX expression.	Cisplatin	63-72	BCL2-associated X protein	Mus musculus	184-187
23598363-12	2013	Our findings indicate that imatinib protects oocytes from cisplatin-induced cell death by inhibiting c-Abl kinase, which would otherwise activate TAp73-BAX-mediated apoptosis.	Imatinib Mesylate	27-35	BCL2-associated X protein	Mus musculus	152-155
23686134-9	2013	Impaired glucose utilization was found and was associated with ER stress and apoptosis, associated with the upregulation of Bim and Bax; downregulation of Bim protected against apoptosis during differentiation.	Glucose	9-16	BCL2-associated X protein	Mus musculus	132-135
23598363-12	2013	Our findings indicate that imatinib protects oocytes from cisplatin-induced cell death by inhibiting c-Abl kinase, which would otherwise activate TAp73-BAX-mediated apoptosis.	Cisplatin	58-67	BCL2-associated X protein	Mus musculus	152-155
21786383-6	2013	Western blot analysis demonstrated that propofol promoted Fas, cytochrome c, caspase-9 and -3 active form and Bax levels, but inhibited Bcl-xl protein level which led to cell apoptosis.	Propofol	40-48	BCL2-associated X protein	Mus musculus	110-113
23723062-9	2013	The number of deoxynucleotidyl transferase-mediated dUTP nick end-labelling positive nuclei was markedly increased in SMP30-KO mice with activation of caspase-3, increases in the Bax to Bcl-2 ratio and phosphorylation of c-Jun N-terminal kinase compared with WT mice.	deoxyuridine triphosphate	52-56	BCL2-associated X protein	Mus musculus	179-182
23603105-8	2013	Pretreatment with selenium partially blocked Cd-induced ROS generation, inhibited Cd induced mitochondrial membrane potential collapse, prevented cytochrome c release, inhibited caspase activation and changed the level of VDAC, Bcl-2 and Bax.	Selenium	18-26	BCL2-associated X protein	Mus musculus	238-241
23603105-8	2013	Pretreatment with selenium partially blocked Cd-induced ROS generation, inhibited Cd induced mitochondrial membrane potential collapse, prevented cytochrome c release, inhibited caspase activation and changed the level of VDAC, Bcl-2 and Bax.	Cadmium	45-47	BCL2-associated X protein	Mus musculus	238-241
23935943-6	2013	Cardiac AT1aR, Bax, and IGF-1 mRNA expression was significantly increased by DEX compared to SAL at E17.5.	Dexamethasone	77-80	BCL2-associated X protein	Mus musculus	15-18
23611870-5	2013	At 4 hours postinjury, bcl-2/bax ratio mRNA expression was increased in p55 (-/-) compared with p75 (-/-) mice and was associated with reduced DNA damage terminal deoxynucleotidyl transferaseYmediated dUTP nick end labeling (TUNEL-positivity), reduced CD11b expression and increased Ym1 expression at 24 hours postinjury in p55 (-/-) compared with p75 (-/-) mice, indicative of a protective M/M response.	deoxyuridine triphosphate	201-205	BCL2-associated X protein	Mus musculus	29-32
23819597-1	2013	The hypothesis that mitochondrial dysfunction and increased superoxide levels in thymocytes over expressing Bax (Lck-Bax1 and Lck-Bax38&amp;1) contributes to lymphomagenesis after low-dose radiation was tested.	Superoxides	60-70	BCL2-associated X protein	Mus musculus	108-111
23819597-4	2013	In Lck-Bax38&amp;1 mice, a 100 cGy dose of high-LET iron ions caused a significant dose dependent acceleration of lymphomagenesis in both males and females that was not seen with silicon ions.	Iron	52-56	BCL2-associated X protein	Mus musculus	3-18
23846222-7	2013	Ssd also proved to be a potent cytotoxic agent in apoptosis-defective or apoptosis-resistant mouse embryonic fibroblast cells, which either lack caspases 3, 7 or 8 or had the Bax-Bak double knockout.	bakuchiol	179-182	BCL2-associated X protein	Mus musculus	175-178
23688867-11	2013	Pro-apoptotic protein Bax expression was up-regulated in the 3-MC treated skin of transgenic mice.	Methylcholanthrene	61-65	BCL2-associated X protein	Mus musculus	22-25
23824039-14	2013	Collectively, MPTQ-induced neuro 2a cell death is mediated by ATM and p53 activation, and Bax-mediated activation of caspase-dependent and caspase-independent mitochondrial apoptosis pathways.	8-methoxypyrimido(4',5'-4,5)thieno(2,3-b)quinoline-4(3H)-one	14-18	BCL2-associated X protein	Mus musculus	90-93
23584725-8	2013	Delphinidin attenuated the hypoxia-induced increase in Bax, cleaved caspase-9, cleaved caspase-3, and decrease in Bcl-2, which were diminished by pretreatment of Akt inhibitor.	delphinidin	0-11	BCL2-associated X protein	Mus musculus	55-58
23541438-5	2013	Also, geraniin inhibited apoptosis in radiosensitive splenocytes by reducing the expression level and immunoreactivity of proapoptotic p53 and Bax and increasing those of anti-apoptotic Bcl-2.	Geraniin	6-14	BCL2-associated X protein	Mus musculus	143-146
23430060-7	2013	GP7 or etoposide induced sub-G(1) peak, apoptotic DNA fragmentation, activations of caspase-3, -8, -9, and DNA fragmentation factor, downregulation of Bcl-2 and Bcl-xL, upregulation of Bax and Bak, and cytochrome-c release from mitochondria in both mouse and human OS cells.	Etoposide	7-16	BCL2-associated X protein	Mus musculus	185-188
23506954-9	2013	In addition, renal tissues of Cis/WT and Cis-treated MPTCs displayed enhanced phosphorylation of p53 and Bax expression.	mptcs	53-58	BCL2-associated X protein	Mus musculus	105-108
23605050-0	2013	Effects of high iron and glucose concentrations over the relative expression of Bcl2, Bax, and Mfn2 in MIN6 cells.	Glucose	25-32	BCL2-associated X protein	Mus musculus	86-89
23605050-3	2013	The purpose of this study was to describe the effect of different iron and/or glucose concentrations over Mfn2, Bax, and Bcl2 expressions in a beta-pancreatic cell line (MIN6 cells).	Iron	66-70	BCL2-associated X protein	Mus musculus	112-115
23605050-6	2013	The Bcl2/Bax ratio increased and Mfn2 expression decreased in MIN6 cells after glucose stimulation.	Glucose	79-86	BCL2-associated X protein	Mus musculus	9-12
23605050-9	2013	Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis.	Glucose	29-36	BCL2-associated X protein	Mus musculus	101-104
23605050-9	2013	Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis.	Iron	37-39	BCL2-associated X protein	Mus musculus	101-104
23506274-5	2013	Under 20% oxygen, but not 1.5% or 5%, NGF decreased apoptosis in mouse ovaries by down-regulating the pro-apoptotic genes Bax and p53.	Oxygen	10-16	BCL2-associated X protein	Mus musculus	122-125
23417833-10	2013	Cardiomyocyte apoptosis and induction of Bax and cleaved caspase3 in response to AB were suppressed by paeoniflorin.	peoniflorin	103-115	BCL2-associated X protein	Mus musculus	41-44
23522402-7	2013	Moreover, duloxetine reduced Bax and p53 expression in the hippocampus, and Bad expression in the cerebral cortex.	Duloxetine Hydrochloride	10-20	BCL2-associated X protein	Mus musculus	29-32
23522402-8	2013	Mirtazapine decreased Bcl-xL and Bax expression in the hippocampus, and Bad and p53 expression in both the hippocampus and cerebral cortex.	Mirtazapine	0-11	BCL2-associated X protein	Mus musculus	33-36
23865328-13	2013	Bax protein level in control group((942+/-104)/mm2) was also significantly lower than that in midazolam group((1839+/-160)/mm2, P&lt;0.	Midazolam	94-103	BCL2-associated X protein	Mus musculus	0-3
23865328-15	2013	05); Bax/Bcl-2 ratio in midazolam group(0.	Midazolam	24-33	BCL2-associated X protein	Mus musculus	5-8
23546223-5	2013	Expression levels of the proapoptotic genes transcriptionally regulated by CHOP (BIM, BAX, DR5 and TRB3) were all enhanced by combined treatment with BZ plus CAM, compared with treatment with each reagent alone.	Clarithromycin	158-161	BCL2-associated X protein	Mus musculus	86-89
23499928-3	2013	CRS induced a large, moderately significant increase in protein levels of Bax 1 h following stress.	3-cresol	0-3	BCL2-associated X protein	Mus musculus	74-77
23499928-10	2013	Therefore, exercise protects against CRS-induced increases in levels of Bax in the cortex, and microglial/macrophage expression of Cox-2 in the hippocampus.	3-cresol	37-40	BCL2-associated X protein	Mus musculus	72-75
23619570-12	2013	In addition, immunohistochemistry staining showed that the expression of Bax was significantly increased in Meth and Meth-F group compared with the N-control group.	Methamphetamine	108-112	BCL2-associated X protein	Mus musculus	73-76
23619570-12	2013	In addition, immunohistochemistry staining showed that the expression of Bax was significantly increased in Meth and Meth-F group compared with the N-control group.	meth-f	117-123	BCL2-associated X protein	Mus musculus	73-76
23528870-7	2013	Down-regulation of Bax and up-regulation of Bcl-xl protein expressions were observed in liver tissues of the dieckol administered groups.	dieckol	109-116	BCL2-associated X protein	Mus musculus	19-22
23546223-5	2013	Expression levels of the proapoptotic genes transcriptionally regulated by CHOP (BIM, BAX, DR5 and TRB3) were all enhanced by combined treatment with BZ plus CAM, compared with treatment with each reagent alone.	Bortezomib	150-152	BCL2-associated X protein	Mus musculus	86-89
23340267-0	2013	NFAT2 mediates high glucose-induced glomerular podocyte apoptosis through increased Bax expression.	Glucose	20-27	BCL2-associated X protein	Mus musculus	84-87
23397978-8	2013	Expressions of Bcl-2, Bax, and catalase proteins were low under fluid shear stress plus 1 mM melatonin compared with only fluid shear stress alone, whereas Mn-SOD expression was high compared with conditions of no fluid shear stress.	Melatonin	93-102	BCL2-associated X protein	Mus musculus	22-25
23364800-7	2013	Similarly, the induction of apoptosis was higher in tunicamycin-treated male mice, as measured by the activation of Bax and caspase-3.	Tunicamycin	52-63	BCL2-associated X protein	Mus musculus	116-119
23384965-7	2013	DMTU reduced the expression levels of TNF-alpha, Bax and c-fos and increased the expression levels of IL-6, Bcl-xL and Nrf2 in WT mice.	1,3-dimethylthiourea	0-4	BCL2-associated X protein	Mus musculus	49-52
23384965-9	2013	In IL-6(-/-) mice, DMTU also improved cisplatin-induced renal dysfunction and reduced expression levels of TNF-alpha, Bax and c-fos, but not Bcl-xL and Nrf2.	1,3-dimethylthiourea	19-23	BCL2-associated X protein	Mus musculus	118-121
23435943-4	2013	We observed an increase in levels of antiapoptotic Bcl-2, Bcl-XL mRNA and a decrease in levels of proapoptotic Bax mRNA following reynosin treatment of hepatocytes.	reynosin	130-138	BCL2-associated X protein	Mus musculus	111-114
23435943-8	2013	Bcl-2 and Bcl-XL mRNA levels were increased, and the Bax mRNA level was decreased in reynosin-treated mice.	reynosin	85-93	BCL2-associated X protein	Mus musculus	53-56
23324999-2	2013	This is attributed to induced antioxidant and antiapoptotic state, which among other factors results from induction of Bcl-2 and reduction of Bax, however, cDNA microarray reveals that this represents only one cascade of lithium targets.	Lithium	221-228	BCL2-associated X protein	Mus musculus	142-145
23302291-9	2013	delta-Tocotrienol also induced biomarkers of apoptosis such as Bax and activated caspase 3 along with an increase in plasma levels of CK18.	tocotrienol, delta	0-17	BCL2-associated X protein	Mus musculus	63-66
23354124-10	2013	Overabundance of 14-3-3zeta sequestered BAD-BCL2-associated X protein (BAX) from mitochondria, attenuated Dp5 (also known as Hrk) and Puma (also known as Bbc3) induction, and increased survival in response to pro-inflammatory cytokines or thapsigargin.	Thapsigargin	239-251	BCL2-associated X protein	Mus musculus	71-74
23391769-7	2013	RESULTS: Simvastatin reduced stroke-induced spleen atrophy and splenic apoptosis via increased mitochrondrial antiapoptotic Bcl-2 expression and decreased proapoptotic Bax translocation from cytosol into mitochondria.	Simvastatin	9-20	BCL2-associated X protein	Mus musculus	168-171
22965195-10	2013	The in vivo effects of O-1602 on PCNA, BAX, and p53 were also observed in colon cancer cells.	mk-1602	23-29	BCL2-associated X protein	Mus musculus	39-42
23376140-7	2013	However, after 12h CdCl2 treatment, cell viability diminished in 50%, accompanied by a drastic decrease of metallothionein-II production, and an increase in p53 activation and the pro-apoptotic protein Bax.	12-hydroxydodecanoic acid	15-18	BCL2-associated X protein	Mus musculus	202-205
23376140-7	2013	However, after 12h CdCl2 treatment, cell viability diminished in 50%, accompanied by a drastic decrease of metallothionein-II production, and an increase in p53 activation and the pro-apoptotic protein Bax.	Cadmium Chloride	19-24	BCL2-associated X protein	Mus musculus	202-205
23429506-6	2013	AG14361 was also applied to p53 and Bax knockout cultures and mice and combined with the JNK inhibitor SP600125.	1-(4-dimethylaminomethylphenyl)-8,9-dihydro-7H-2,7,9a-benzo(cd)azulen-6-one	0-7	BCL2-associated X protein	Mus musculus	36-39
23429506-11	2013	AG14361 reduced ischemic cell death in wild-type and p53 or Bax knockout cultures and animals but had no additional effect in PRX2-overexpressing mice.	1-(4-dimethylaminomethylphenyl)-8,9-dihydro-7H-2,7,9a-benzo(cd)azulen-6-one	0-7	BCL2-associated X protein	Mus musculus	60-63
23319265-7	2013	rSj16 treatment induced an increase in the activity of caspase 3, 6, and 9, and expression of pro-apoptotic Bax.	rsj16	0-5	BCL2-associated X protein	Mus musculus	108-111
23386286-9	2013	In addition, rosuvastatin administration decreased the pro-apoptotic proteins Bim and Bax, and increased the anti-apoptotic proteins Bcl-xL and Bcl-2.	Rosuvastatin Calcium	13-25	BCL2-associated X protein	Mus musculus	86-89
23036022-10	2013	Western blot analysis revealed that VPA notably down-regulated the expression of Caspase-3, Caspase-9 and Caspase-12, reduced the level of cytochrome C and Bax.	Valproic Acid	36-39	BCL2-associated X protein	Mus musculus	156-159
23050834-4	2013	Treatment with the electron transport chain complex III inhibitor, antimycin A, but not the complex I inhibitor, rotenone, caused increased cytosolic superoxide through release from the mitochondrial intermembrane space via voltage-dependent anion or Bax channels, but inhibition of these channels did not affect contraction-induced increases in cytosolic superoxide.	Antimycin A	67-78	BCL2-associated X protein	Mus musculus	251-254
23369986-10	2013	Ropinirole increased the Bcl-2/Bax ratio, transcription factor A, and nuclear respiratory factor 1 and inhibited cytosolic cytochrome c release and caspase-3 activity, indicating that ropinirole inhibited the apoptotic cascade.	ropinirole	0-10	BCL2-associated X protein	Mus musculus	31-34
23369986-10	2013	Ropinirole increased the Bcl-2/Bax ratio, transcription factor A, and nuclear respiratory factor 1 and inhibited cytosolic cytochrome c release and caspase-3 activity, indicating that ropinirole inhibited the apoptotic cascade.	ropinirole	184-194	BCL2-associated X protein	Mus musculus	31-34
23449454-4	2013	Statins (atorvastatin, fluvastatin and simvastatin) treatment enhanced the DNA fragmentation and the activation of proapoptotic members such as caspase-3, PARP and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells, which was accompanied by inhibition of cell survival.	Atorvastatin	9-21	BCL2-associated X protein	Mus musculus	164-167
23449454-4	2013	Statins (atorvastatin, fluvastatin and simvastatin) treatment enhanced the DNA fragmentation and the activation of proapoptotic members such as caspase-3, PARP and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells, which was accompanied by inhibition of cell survival.	Fluvastatin	23-34	BCL2-associated X protein	Mus musculus	164-167
23449454-4	2013	Statins (atorvastatin, fluvastatin and simvastatin) treatment enhanced the DNA fragmentation and the activation of proapoptotic members such as caspase-3, PARP and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells, which was accompanied by inhibition of cell survival.	Simvastatin	39-50	BCL2-associated X protein	Mus musculus	164-167
23050834-4	2013	Treatment with the electron transport chain complex III inhibitor, antimycin A, but not the complex I inhibitor, rotenone, caused increased cytosolic superoxide through release from the mitochondrial intermembrane space via voltage-dependent anion or Bax channels, but inhibition of these channels did not affect contraction-induced increases in cytosolic superoxide.	Superoxides	150-160	BCL2-associated X protein	Mus musculus	251-254
23123599-13	2013	Transfection of WT macrophages with miR-125b mimics attenuated H/R-induced caspase-3/7 and -8 activities and H/R-decreased viability, and prevented H/R-increased p-53, Bak-1 and Bax expression.	mir-125b	36-44	BCL2-associated X protein	Mus musculus	178-181
23213199-6	2013	In addition, it was observed that H(2)O(2) induced translocation of Bax to mitochondria; however, in the presence of the steroid this effect was abrogated suggesting that members of the Bcl-2 family may be regulated by E(2) to exert an antiapoptotic effect.	Hydrogen Peroxide	34-42	BCL2-associated X protein	Mus musculus	68-71
23213199-6	2013	In addition, it was observed that H(2)O(2) induced translocation of Bax to mitochondria; however, in the presence of the steroid this effect was abrogated suggesting that members of the Bcl-2 family may be regulated by E(2) to exert an antiapoptotic effect.	Steroids	121-128	BCL2-associated X protein	Mus musculus	68-71
23409868-9	2013	RESULTS: Combined treatment protected cells against vanadate-induced cell death with decreasing B cell lymphoma 2-associated X protein (Bax) levels.	Vanadates	52-60	BCL2-associated X protein	Mus musculus	96-134
23231952-8	2013	Sorafenib also blocks Mcl-1 and cyclin D1 translation, which promotes an imbalance between pro- and antiapoptotic proteins and facilitates Bax release from cyclin D1, leading to the induction of mitochondrial apoptosis and caspase-dependent and -independent mechanisms.	Sorafenib	0-9	BCL2-associated X protein	Mus musculus	139-142
23403521-11	2013	Using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting, the purple bamboo salt group demonstrated an increase in Bcl-2-associated X protein (Bax) and a decrease in B cell lymphoma-2 (Bcl-2), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, compared with the sea salt and control groups.	Salts	103-107	BCL2-associated X protein	Mus musculus	142-168
22516481-9	2013	Furthermore, upregulation of the Bax/Bcl-2 ratio in gastric mucosa was clearly depressed by propofol.	Propofol	92-100	BCL2-associated X protein	Mus musculus	33-36
23403521-11	2013	Using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting, the purple bamboo salt group demonstrated an increase in Bcl-2-associated X protein (Bax) and a decrease in B cell lymphoma-2 (Bcl-2), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, compared with the sea salt and control groups.	Salts	103-107	BCL2-associated X protein	Mus musculus	170-173
23103613-9	2013	Pretreatment with NAC and specific p38-MAPK inhibitor (SB203580), but not JNK inhibitor (SP600125) effectively abrogated the phosphorylation of p38-MAPK and attenuated the apoptotic signals (including: decrease in cytotoxicity, caspase-3/-7 activation, the cytosolic cytochrome c release, and the reversed alteration of Bcl-2 and Bax mRNA) in CA-treated Neuro-2a cells.	Acetylcysteine	18-21	BCL2-associated X protein	Mus musculus	330-333
23229920-5	2013	The             positive rates of Bcl-2 and Bax proteins which were treated by ar-turmerone did             not show marked differences compared to the control group, but the Bax protein             in the Glivec-treated group increased compared to the control group.	ar-turmerone	79-91	BCL2-associated X protein	Mus musculus	44-47
23103613-9	2013	Pretreatment with NAC and specific p38-MAPK inhibitor (SB203580), but not JNK inhibitor (SP600125) effectively abrogated the phosphorylation of p38-MAPK and attenuated the apoptotic signals (including: decrease in cytotoxicity, caspase-3/-7 activation, the cytosolic cytochrome c release, and the reversed alteration of Bcl-2 and Bax mRNA) in CA-treated Neuro-2a cells.	SB 203580	55-63	BCL2-associated X protein	Mus musculus	330-333
23336516-5	2013	Compared with the groups treated with empty ME and drug solution, the mRNA levels of Bax and caspase-3 were up-regulated, and the mRNA and protein levels of Bcl-2 were down-regulated in H22 cells treated with TanIIA ME in a dose-dependent manner.	methionylglutamic acid	44-46	BCL2-associated X protein	Mus musculus	85-88
23336516-5	2013	Compared with the groups treated with empty ME and drug solution, the mRNA levels of Bax and caspase-3 were up-regulated, and the mRNA and protein levels of Bcl-2 were down-regulated in H22 cells treated with TanIIA ME in a dose-dependent manner.	methionylglutamic acid	216-218	BCL2-associated X protein	Mus musculus	85-88
23127512-7	2013	Our findings suggest that by specifically activating LPA(2) receptors GRI977143 activates the ERK1/2 prosurvival pathway, effectively reduces Bax translocation to the mitochondrion, attenuates the activation of initiator and effector caspases, reduces DNA fragmentation, and inhibits PARP-1 cleavage associated with gamma-irradiation-induced apoptosis.	GRI 1665	70-79	BCL2-associated X protein	Mus musculus	142-145
24335166-8	2013	TUNEL staining presented that AZA reduced apoptotic cells due to attenuated caspase activation and increased Bcl-2/Bax ratio.	Acetazolamide	30-33	BCL2-associated X protein	Mus musculus	115-118
23090186-8	2013	Furthermore, resveratrol decreased the activity of phosphatidylinositol-3 kinase (PI3K)-Akt phosphorylation and class O forkhead box (FOXO)3a phosphorylation, which resulted in a decrease in B cell leukaemia/lymphoma 2 (BCL-2)-associated X protein (BAX) and increases in BCL-2, superoxide dismutase (SOD)1 and SOD2 production.	Resveratrol	13-24	BCL2-associated X protein	Mus musculus	249-252
23182907-8	2013	A lanata treatment resulted in downregulation of bcl-2 and cyclin-D1 expression and upregulation of p53, bax, caspase-9, caspase-3, p21, and p27 gene expression in B16F-10 cells.	lanata	2-8	BCL2-associated X protein	Mus musculus	105-108
22878015-6	2013	Moreover, SB203580 inhibited the translocation of Bax from the cytosol to the mitochondria.	SB 203580	10-18	BCL2-associated X protein	Mus musculus	50-53
22878015-7	2013	Taken together, these results suggest that NO-induced apoptosis in mES cells was mediated through p38 MAP kinase/ERK signaling pathway by triggering caspases activation and Bax translocation from the cytosol to the mitochondria.	2-(N-morpholino)ethanesulfonic acid	67-70	BCL2-associated X protein	Mus musculus	173-176
24454506-7	2013	LBP also shows significant positive effects on the expression of Bcl-2/Bax in BPA treated mice.	bisphenol A	78-81	BCL2-associated X protein	Mus musculus	71-74
23059190-6	2013	Furthermore, we demonstrated that COS-S led to an increase in the Bcl-2/Bax mRNA expression ratio and the inhibition of Caspase-3 mRNA expression in H(2)O(2)-stimulated MIN6 cells.	oligochitosan	34-39	BCL2-associated X protein	Mus musculus	72-75
23064251-5	2013	Compared with empty ME and drug solution groups, the mRNA levels of Bax were upregulated and the mRNA and protein levels of Bcl-2 were downregulated in the H22 cells treated with Tan ME in a dose-dependent manner.	methionylglutamic acid	183-185	BCL2-associated X protein	Mus musculus	68-71
23117934-6	2013	On histological observation of the small intestine, PG inhibited the immunoreactivity of p53, Bax, and Bak and increased that of Bcl-2 and Bcl-X(S/L).	Phloroglucinol	52-54	BCL2-associated X protein	Mus musculus	94-97
23140172-9	2013	In platelets from mice dosed with ABT-263 in vivo, clopidogrel or deficiency of P2Y(12) receptor enhanced apoptosis along with increased Bak/Bax activation.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	34-37	BCL2-associated X protein	Mus musculus	141-144
23140172-9	2013	In platelets from mice dosed with ABT-263 in vivo, clopidogrel or deficiency of P2Y(12) receptor enhanced apoptosis along with increased Bak/Bax activation.	Clopidogrel	51-62	BCL2-associated X protein	Mus musculus	141-144
24453420-8	2013	The expression of Bcl-2, Bax, Beclin-1, and LC3, which play an important role in the regulation of intrinsic pathway of apoptosis and autophagy, was also obviously decreased by ethyl pyruvate (80 mg/kg).	ethyl pyruvate	177-191	BCL2-associated X protein	Mus musculus	25-28
23064251-6	2013	The mRNA and protein levels of Bax were upregulated and the Bcl-2 levels were downregulated in the H22 tumors of animals treated with Tan ME in a dose-dependent manner.	tan me	134-140	BCL2-associated X protein	Mus musculus	31-34
23255902-0	2013	Role of Ku70 and Bax in epigallocatechin-3-gallate-induced apoptosis of A549 cells in vivo.	epigallocatechin gallate	24-50	BCL2-associated X protein	Mus musculus	17-20
23255902-13	2013	This is the first study demonstrating that the induction of apoptosis by EGCG may be caused by the downregulation of Ku70 and that EGCG disrupts the interaction between Ku70 and Bax in lung cancer.	epigallocatechin gallate	131-135	BCL2-associated X protein	Mus musculus	178-181
23255902-11	2013	In addition, EGCG downregulated the expression of Bcl-xl and upregulated the expression of Bax mRNA and protein.	epigallocatechin gallate	13-17	BCL2-associated X protein	Mus musculus	91-94
23255902-12	2013	Further experiments indicated that EGCG downregulated the protein expression of Ku70 and interrupted the binding of Ku70 and Bax.	epigallocatechin gallate	35-39	BCL2-associated X protein	Mus musculus	125-128
23065091-6	2012	Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF.	ros	12-15	BCL2-associated X protein	Mus musculus	224-227
23418539-6	2013	LMWF also inhibited the activation of MAPK pathways, which consequently resulted in a significant decrease in the release of cytochrome c from mitochondria, ratios of Bax/Bcl-2 and cleaved caspase-3/caspase-3, and phosphorylation of p53.	lmwf	0-4	BCL2-associated X protein	Mus musculus	167-170
23383327-8	2013	We further observed in staurosporine-treated photoreceptor-like 661W cells stably overexpressing alphaA- or alphaB-crystallin that Bax-dependent apoptosis and caspase activation were inhibited.	Staurosporine	23-36	BCL2-associated X protein	Mus musculus	131-134
23127846-8	2012	Furthermore, edaravone treatment inhibited mitochondria-dependent apoptosis pathways in N2a/Swe.Delta9 cells through decreasing the Bax/Bcl-2 ratio, attenuating cytochrome c release and suppressing the activation of caspase-3.	Edaravone	13-22	BCL2-associated X protein	Mus musculus	132-135
23065091-6	2012	Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF.	ros	34-37	BCL2-associated X protein	Mus musculus	224-227
23065091-6	2012	Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF.	celastrol	75-84	BCL2-associated X protein	Mus musculus	224-227
23065091-6	2012	Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF.	celastrol	142-151	BCL2-associated X protein	Mus musculus	224-227
23065091-6	2012	Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF.	ros	34-37	BCL2-associated X protein	Mus musculus	224-227
22763982-7	2012	Moreover, DOX injection attenuated HO-1 expression and enzymatic activity as well as increased P53 expression, modulated Bcl-2/Bax expression and enhanced caspase 3 activity.	Doxorubicin	10-13	BCL2-associated X protein	Mus musculus	127-130
22982332-8	2012	Compounds also inhibited the cleavage of PARP and bax and restored Bcl2, induced on exposure to ethanol.	Ethanol	96-103	BCL2-associated X protein	Mus musculus	50-53
22948180-11	2012	However, amarogentin treatment could significantly induce apoptosis through upregulation of the Bax-Bcl2 ratio, activation of caspase-3 and poly ADP ribose polymerase cleavage.	amarogentin	9-20	BCL2-associated X protein	Mus musculus	96-99
22982332-9	2012	In summary, both ellagitannins effectively protected mouse liver slices against ethanol induced cytotoxicity and apoptosis by reducing oxidative damage to biological molecules and modulating Bax/Bcl-2 ratio respectively, thus minimizing liver injury.	Hydrolyzable Tannins	17-30	BCL2-associated X protein	Mus musculus	191-194
22901235-6	2012	In addition, rapamycin preconditioning decreased the production of NF-kappaB, TNF-alpha, and Bax, but not Bcl-2, an antiapoptotic protein in the ischemic area.	Sirolimus	13-22	BCL2-associated X protein	Mus musculus	93-96
22531968-4	2012	On the other hand, a significant decrease was observed in the number of apoptotic cells and protein expression of bax in the lungs of BP-treated mice.	Benzo(a)pyrene	134-136	BCL2-associated X protein	Mus musculus	114-117
22999860-13	2012	Rapamycin triggered unique cardioprotective signaling including phosphorylation of ERK, STAT3, eNOS and glycogen synthase kinase-3ss in concert with increased prosurvival Bcl-2 to Bax ratio.	Sirolimus	0-9	BCL2-associated X protein	Mus musculus	180-183
23151791-6	2012	Moreover, swainsonine treatment inhibited Bcl-2 expression, promoted Bax translocation, cytochrome c release and caspase-3 activation in xenograft tumour cells, resulting in a significant decrease of tumour volume and tumour weight in the swainsoninetreated xenograft mice groups compared with that in the control group.	Swainsonine	10-21	BCL2-associated X protein	Mus musculus	69-72
23000595-4	2012	The current work tested the hypothesis that MXC induces morphological atresia at early time points (24 and 48 h) by altering pro-apoptotic (Bax, Bok, Casp3, and caspase activity) and anti-apoptotic (Bcl2 and Bcl-xL) factors in the follicles.	Methoxychlor	44-47	BCL2-associated X protein	Mus musculus	140-143
22850444-13	2012	We also demonstrated that GB reduced Bax protein levels and increased Bcl-2 protein levels in the post-ischemic brains.	ginkgolide B	26-28	BCL2-associated X protein	Mus musculus	37-40
23068102-0	2012	Carnitine sensitizes TRAIL-resistant cancer cells to TRAIL-induced apoptotic cell death through the up-regulation of Bax.	Carnitine	0-9	BCL2-associated X protein	Mus musculus	117-120
23123091-6	2012	Knocking down PTEN expression via siRNA inhibited TPA-induced Bax expression.	Tetradecanoylphorbol Acetate	50-53	BCL2-associated X protein	Mus musculus	62-65
23068102-7	2012	We further demonstrate that carnitine, either alone or in combination with TRAIL, enhances the expression of the pro-apoptotic Bcl-2 family protein, Bcl-2-associated X protein (Bax).	Carnitine	28-37	BCL2-associated X protein	Mus musculus	149-175
23068102-7	2012	We further demonstrate that carnitine, either alone or in combination with TRAIL, enhances the expression of the pro-apoptotic Bcl-2 family protein, Bcl-2-associated X protein (Bax).	Carnitine	28-37	BCL2-associated X protein	Mus musculus	177-180
23068102-9	2012	Taken together, our current results suggest that carnitine can reverse the resistance of cancer cells to TRAIL by up-regulating Bax expression.	Carnitine	49-58	BCL2-associated X protein	Mus musculus	128-131
22775755-5	2012	Generation of excess intracellular ROS, nuclear localization of Bax and caspase 3 activation along with decrease of cellular viability, confirmed apoptosis induction in RGC-5 by 72 h serum starvation and 500 M H2O2 exposure for 1 h. Nuclear swelling as supported by nuclear cytoplasmic ratio and conspicuous black spots with nuclear remodelling were observed only upon SFM, but not with H2O2 treatment.	Hydrogen Peroxide	210-214	BCL2-associated X protein	Mus musculus	64-67
22805317-6	2012	Regarding Y(2) receptors, its activation (300 nm NPY13-36) completely prevented METH-induced toxicity in all subregions analysed, which involved changes in levels of pro- and anti-apoptotic proteins Bcl-2 and Bax, respectively.	Methamphetamine	80-84	BCL2-associated X protein	Mus musculus	209-212
23117066-4	2012	We observed an increased level of reactive oxygen species, cellular damage in testes of SA-intoxicated mice and further analysed expressions of apoptotic signal proteins and mRNA like Bax, Bcl2 and caspase3.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	88-90	BCL2-associated X protein	Mus musculus	184-187
22507688-10	2012	Renal cell apoptosis induced by IRI was abrogated in kidneys of mice pretreated by pioglitazone, with an increase in Bcl-2 expression and a decrease in Bax expression.	Pioglitazone	83-95	BCL2-associated X protein	Mus musculus	152-155
22968190-6	2012	This was also supported by the fact that melanin could prevent apoptosis in splenic tissue by decreasing BAX/Bcl-XL ratio, and increasing the expressions of the proliferation markers (PCNA and Cyclin D1), compared to the radiation control group.	Melanins	41-48	BCL2-associated X protein	Mus musculus	105-108
23185674-10	2012	The zinc-citrate compound increased the expression of p21(waf1) and p53 and reduced the expression of Bcl-2 and Bcl-xL proteins but induced expression of Bax protein.	Zinc citrate	4-16	BCL2-associated X protein	Mus musculus	154-157
22457201-7	2012	The combinations enhanced calcitriol activity in regulating target gene expression, including greater up-regulation of anti-proliferative (p21, IGFBP-3) and pro-apoptotic (Bax) genes, increased inhibition of anti-apoptotic (Bcl-2) and cell cycle promoting (cyclin D1) genes, and suppression of prostaglandin (PG) synthesis and signaling (COX-2, 15-PGDH, PG receptors).	Calcitriol	26-36	BCL2-associated X protein	Mus musculus	172-175
22221674-5	2012	Using the thioacetamide (TAA)-induced hepatic fibrosis animal model, we found that curcumin treatment up-regulated P53 protein expression and Bax messenger RNA (mRNA) expression and down-regulated Bcl-2 mRNA expression.	Curcumin	83-91	BCL2-associated X protein	Mus musculus	142-145
22847295-4	2012	Annexin V staining and flow cytometry showed that GA-DM treatment induced apoptosis of melanoma cells, which was supported by a detection of increased Bax proteins, co-localization and elevation of Apaf-1 and cytochrome c, and a subsequent cleavage of caspases 9 and 3.	3,7-dioxolanosta-8,24-dien-26-oic acid	50-55	BCL2-associated X protein	Mus musculus	151-154
22925047-9	2012	Flavins markedly decreased infarct area in MCAO mice, inhibited apoptosis and death in OGD-treated neurons, and decreased Bax protein expression.	Flavins	0-7	BCL2-associated X protein	Mus musculus	122-125
23226790-6	2012	Deguelin-induced apoptosis was characterized by the upregulation of Bax, downregulation of Bcl-2 and activation of caspase-3.	deguelin	0-8	BCL2-associated X protein	Mus musculus	68-71
22828802-11	2012	With longer NMDA exposure (72 h), we observed loss of cells associated with nuclear fragmentation and increased expression of caspase-3, caspase-6, and Bax, suggesting an apoptotic process.	N-Methylaspartate	12-16	BCL2-associated X protein	Mus musculus	152-155
22796215-4	2012	The protective effect of glycine was associated with reduction of terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) positive cells, deactivation of phosphor-JNK, inhibition of caspase-3 cleavage, down-regulation of FasL/Fas, and up-regulation of bcl-2 and bcl-2/bax in the mouse I/R penumbra.	Glycine	25-32	BCL2-associated X protein	Mus musculus	288-291
22889882-11	2012	TCDD, however, decreased levels of the proapoptotic factor Bax.	Polychlorinated Dibenzodioxins	0-4	BCL2-associated X protein	Mus musculus	59-62
22742899-7	2012	Carbenoxolone also prevented hepatic injury through anti-apoptotic action in the livers of C57BL/6-Lep(ob/ob) mice, accompanied by increased Bcl-2 expression and suppressed Bax and cytochrome c expression.	Carbenoxolone	0-13	BCL2-associated X protein	Mus musculus	173-176
22434380-5	2012	Western blot data showed that in zinc+H(2)O(2)-treated cells, zinc decreased the levels of AIF, Bax and active caspase-9 and -3, which are pro-apoptotic factors.	Hydrogen Peroxide	38-46	BCL2-associated X protein	Mus musculus	96-99
22732633-7	2012	TQ triggered the apoptotic pathway, which was characterized by increased Bax/Bcl-2 ratio.	thymoquinone	0-2	BCL2-associated X protein	Mus musculus	73-76
22925072-5	2012	SUL, PEITC, and BITC significantly inhibited apoptosis in the left ventricle by increasing the Bcl-2/Bax ratio compared with LP-BM5-infected mice.	sulforaphane	0-3	BCL2-associated X protein	Mus musculus	101-104
22497970-7	2012	Resveratrol, as well, also had a beneficial effect on the ratios of expressions of Bcl-2/Bax and levels of malondialdehyde/glutathione peroxidase.	Resveratrol	0-11	BCL2-associated X protein	Mus musculus	89-92
22516057-5	2012	Furthermore, dioscin decreased the protein expressions of Fas/FasL, increased Bcl-2/Bax ratio, inhibited the release of cytochrome c from mitochondrion to cytosol and attenuated CCl(4)-induced caspase-3 and -8 activities.	dioscin	13-20	BCL2-associated X protein	Mus musculus	84-87
22837216-5	2012	The alantolactone-induced apoptosis was found to be associated with glutathione (GSH) depletion, reactive oxygen species (ROS) generation, mitochondrial transmembrane potential dissipation, cardiolipin oxidation, upregulation of p53 and Bax, downregulation of Bcl-2, cytochrome c release, activation of caspases (caspase 9 and 3), and cleavage of poly (ADP-ribose) polymerase.	alantolactone	4-17	BCL2-associated X protein	Mus musculus	237-240
22925072-5	2012	SUL, PEITC, and BITC significantly inhibited apoptosis in the left ventricle by increasing the Bcl-2/Bax ratio compared with LP-BM5-infected mice.	phenethyl isothiocyanate	5-10	BCL2-associated X protein	Mus musculus	101-104
22925072-5	2012	SUL, PEITC, and BITC significantly inhibited apoptosis in the left ventricle by increasing the Bcl-2/Bax ratio compared with LP-BM5-infected mice.	benzyl isothiocyanate	16-20	BCL2-associated X protein	Mus musculus	101-104
22727809-9	2012	Exenatide protects RGC-5 from high- or low-glucose-induced Bax increased and Bcl-2 decreased.	Exenatide	0-9	BCL2-associated X protein	Mus musculus	59-62
22727809-9	2012	Exenatide protects RGC-5 from high- or low-glucose-induced Bax increased and Bcl-2 decreased.	Glucose	43-50	BCL2-associated X protein	Mus musculus	59-62
22683839-9	2012	D-Galactose treatment up-regulated the activity, mRNA expression and protein production of nuclear factor-kappaB (NF-kappaB) p65, Bax and cleaved caspase-3 (P&lt;0.05), as well as suppressed Bcl-2 production (P&lt;0.05).	Galactose	0-11	BCL2-associated X protein	Mus musculus	130-133
22469516-6	2012	BBR-induced anti-apoptotic function was demonstrated by increasing anti-apoptotic protein Bcl-2 and survival of motor neuron protein (SMN) and by decreasing apoptotic proteins (cytochrome c, Bax and caspase).	Berberine	0-3	BCL2-associated X protein	Mus musculus	191-194
22683839-10	2012	Oleanolic acid intake at 0.1% and 0.2% suppressed NF-kappaB p65, Bax and cleaved caspase-3 production, and retained Bcl-2 expression (P&lt;0.05).	Oleanolic Acid	0-14	BCL2-associated X protein	Mus musculus	65-68
22561420-10	2012	The expression levels of the proapoptotic proteins, namely Bad and Bax, were increased by the CQ treatment in the protein extracts from tumors.	chloroquine diphosphate	94-96	BCL2-associated X protein	Mus musculus	67-70
22613767-13	2012	Invalidation of bax and bak suppressed p53-dependent cell death and zVAD-fmk regulation of this process.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	68-76	BCL2-associated X protein	Mus musculus	16-19
22553933-0	2012	Elucidation of structure-activity relationship of 2-quinolone derivatives and exploration of their antitumor potential through Bax-induced apoptotic pathway.	carbostyril	50-61	BCL2-associated X protein	Mus musculus	127-130
22211272-8	2012	Furthermore, ethanol induced significantly higher ROS generation in EL-4 cells as compared to lymphocytes and caused PARP cleavage and activation of apoptotic proteins like p53 and Bax, in EL-4 cells and not in normal lymphocytes.	Ethanol	13-20	BCL2-associated X protein	Mus musculus	181-184
22211272-10	2012	Taken together, these results suggest that ethanol upto a concentration of 5% caused no significant immunotoxicity towards normal lymphocytes and induced cell death in EL-4 cells via phosphorylation of p38MAPK and regulation of p53 leading to further activation of both extrinsic (Fas) and intrinsic (Bax) apoptotic markers.	Ethanol	43-50	BCL2-associated X protein	Mus musculus	301-304
22422579-3	2012	Cilostazol rescued HT22 cells from the apoptotic cell death induced by Abeta toxicity through the downregulation of phosphorylated p53 (Ser15), Bax, and caspase-3 and the upregulation of Bcl-2 expression, which improved neuronal cell proliferation and viability.	Cilostazol	0-10	BCL2-associated X protein	Mus musculus	144-147
22318307-8	2012	A decrease in the expression of Bcl-2 and an increase in Bax expression were also observed in tumor tissues of mice treated with D-limonene.	Limonene	129-139	BCL2-associated X protein	Mus musculus	57-60
22269103-7	2012	Ginsenosides also inhibited extracellular signal-regulated kinase (ERK1/2) phosphorylation and BPA-induced alterations of Bcl-2 and Bax protein expression in 15P-1 Sertoli cells.	Ginsenosides	0-12	BCL2-associated X protein	Mus musculus	132-135
22269103-7	2012	Ginsenosides also inhibited extracellular signal-regulated kinase (ERK1/2) phosphorylation and BPA-induced alterations of Bcl-2 and Bax protein expression in 15P-1 Sertoli cells.	bisphenol A	95-98	BCL2-associated X protein	Mus musculus	132-135
22654772-9	2012	Finally, our studies showed that LPS induced an increase in the mitochondrial translocation of Bax, caspase 3 activation, and nuclear DNA fragmentation and these parameters were all prevented with GSH-EE.	Glutathione	197-200	BCL2-associated X protein	Mus musculus	95-98
22542771-10	2012	The present study showed that treatment with exenatide significantly inhibited cytochrome c release and decreased the intracellular expression levels of Bax and caspase-3, whereas Bcl-2 was increased (P&lt;0.05).	Exenatide	45-54	BCL2-associated X protein	Mus musculus	153-156
23057331-0	2012	[Effect of acrylonitrile on the expression of Bcl-2 and Bax in spermatogenic cell of mice].	Acrylonitrile	11-24	BCL2-associated X protein	Mus musculus	56-59
23057331-1	2012	OBJECTIVE: To explore the effect of acrylonitrile exposure on the expression of Bcl-2 and Bax in mice spermatogenic cells.	Acrylonitrile	36-49	BCL2-associated X protein	Mus musculus	90-93
23057331-4	2012	Immunohistochemical method (SABC) was used to detect the expression of Bcl-2 and Bax protein in spermatogenic cells.	sabc	28-32	BCL2-associated X protein	Mus musculus	81-84
22560595-12	2012	(-)-OSU6162 increases the intracellular levels of BDNF and Bcl2/Bax and decreases those of p-ERK/ERK and CHIP in Q111 cells.	OSU 6162	4-11	BCL2-associated X protein	Mus musculus	64-67
22820595-7	2012	CG combined with Taxol increased the expression of Bax and reduced the expression of p53 and VEGF in the tumor xenografts.	cg	0-2	BCL2-associated X protein	Mus musculus	51-54
22820595-7	2012	CG combined with Taxol increased the expression of Bax and reduced the expression of p53 and VEGF in the tumor xenografts.	Paclitaxel	17-22	BCL2-associated X protein	Mus musculus	51-54
22820595-8	2012	CONCLUSION: CG can enhance the inhibitory effects of Taxol on the growth of HCC xenografts, and this effect is related to the up-regulation of Bax and down-regulation of p53 and VEGF expression in the tumor.	cg	12-14	BCL2-associated X protein	Mus musculus	143-146
25722672-4	2012	Results indicated that pine pollen suppressed cell apoptosis in the cerebral cortex of arsenic-poisoned mice by reducing Bax, Bcl-2 protein expression and increasing p53 protein expression.	Arsenic	87-94	BCL2-associated X protein	Mus musculus	121-124
22406624-9	2012	After Aroclor 1254 exposure, the expression level of calcium transport related protein TRPV6 was down-regulated, while the expression level of apoptosis related proteins Apaf-1 and Bax up-regulated in a dose dependant manner.	Chlorodiphenyl (54% Chlorine)	6-18	BCL2-associated X protein	Mus musculus	181-184
22406624-12	2012	The ROS production and alteration of intracellular Ca2+ level induced by down-regulation of TRPV6 might involve the toxic effects, and cell apoptosis induced by Aroclor 1254 exposure is associated with the pro-apoptotic Apaf-1 pathway as well as alteration of Bcl-2/Bax ratio.	Chlorodiphenyl (54% Chlorine)	161-173	BCL2-associated X protein	Mus musculus	266-269
22559167-12	2012	The alteration of the mRNA expression of cell cycle inhibitors p53, p27, p21 and apoptosis associated genes Bcl-2, Bax were also involved in the synergistic antitumor effects of rapamycin and bortezomib.	Sirolimus	178-187	BCL2-associated X protein	Mus musculus	115-118
22559167-12	2012	The alteration of the mRNA expression of cell cycle inhibitors p53, p27, p21 and apoptosis associated genes Bcl-2, Bax were also involved in the synergistic antitumor effects of rapamycin and bortezomib.	Bortezomib	192-202	BCL2-associated X protein	Mus musculus	115-118
26434288-0	2012	Berberine, an isoquinoline alkaloid, inhibits streptozotocin-induced apoptosis in mouse pancreatic islets through down-regulating Bax/Bcl-2 gene expression ratio.	Berberine	0-9	BCL2-associated X protein	Mus musculus	130-133
26434288-0	2012	Berberine, an isoquinoline alkaloid, inhibits streptozotocin-induced apoptosis in mouse pancreatic islets through down-regulating Bax/Bcl-2 gene expression ratio.	Streptozocin	46-60	BCL2-associated X protein	Mus musculus	130-133
26434288-7	2012	The results showed that berberine administration at one time or before STZ-stimulation significantly (P&lt;0.05) down-regulated the Bax/Bcl-2 genes expression ratio, compared to those in STZ-treatment alone group.	Berberine	24-33	BCL2-associated X protein	Mus musculus	132-135
26434288-8	2012	Our results suggest that berberine"s anti-apoptotic effect on pancreatic primary islets is through down-regulating the Bax/Bcl-2 genes expression ratio in both concurrent and preventive manners.	Berberine	25-34	BCL2-associated X protein	Mus musculus	119-122
22367737-4	2012	Herein, we demonstrate that exposure to atmospheric oxygen rapidly induced p53, TOP2A, and BCL2-associated X protein (BAX) expression and mitochondrial reactive oxygen species (ROS) generation in primary mouse MSCs resulting in oxidative stress, reduced cell viability, and inhibition of cell proliferation.	Oxygen	52-58	BCL2-associated X protein	Mus musculus	91-116
22367737-4	2012	Herein, we demonstrate that exposure to atmospheric oxygen rapidly induced p53, TOP2A, and BCL2-associated X protein (BAX) expression and mitochondrial reactive oxygen species (ROS) generation in primary mouse MSCs resulting in oxidative stress, reduced cell viability, and inhibition of cell proliferation.	Oxygen	52-58	BCL2-associated X protein	Mus musculus	118-121
22460798-7	2012	Moreover, an engineered ubiquitination-resistant form of Bax retained its apoptotic function, but Bax KO cells complemented with lysine-mutant Bax did not manifest the antiapoptotic effects of parkin that were observed in cells expressing WT Bax.	Lysine	129-135	BCL2-associated X protein	Mus musculus	98-101
22460798-7	2012	Moreover, an engineered ubiquitination-resistant form of Bax retained its apoptotic function, but Bax KO cells complemented with lysine-mutant Bax did not manifest the antiapoptotic effects of parkin that were observed in cells expressing WT Bax.	Lysine	129-135	BCL2-associated X protein	Mus musculus	98-101
22460798-7	2012	Moreover, an engineered ubiquitination-resistant form of Bax retained its apoptotic function, but Bax KO cells complemented with lysine-mutant Bax did not manifest the antiapoptotic effects of parkin that were observed in cells expressing WT Bax.	Lysine	129-135	BCL2-associated X protein	Mus musculus	98-101
23983374-9	2012	Both of XCHT and biphenyl dicarboxylate significantly decreased the serum IL-6 and TNF-alpha levels and FasmRNA, FasLmRNA, Bax protein expression and increased the Bcl-2 mRNA expression of the liver tissues of model mice (P&lt;0.05).	Biphenyl-4,4'-dicarboxylic acid	17-39	BCL2-associated X protein	Mus musculus	123-126
22467373-6	2012	Furthermore, treatment of PNMC increased expression of the pro-apoptotic protein Bax and decreased expression of the anti-apoptotic protein Bcl-XL in germ cells.	pnmc	26-30	BCL2-associated X protein	Mus musculus	81-84
22134971-2	2012	Exposure of cells to taxol induced time-dependent cytotoxicity and cytoplasmic vacuolization without the involvement of Bax, Bak, Mcl-1, Bcl-XL, and caspase-3.	Paclitaxel	21-26	BCL2-associated X protein	Mus musculus	120-123
22239859-8	2012	In addition, the copper treatments altered the expression of selected cell death related genes such as EndoG and Bax in a dose related manner.	Copper	17-23	BCL2-associated X protein	Mus musculus	113-116
22281782-3	2012	DPHC slightly reduced the expression of Bax induced by H(2)O(2) but recovered the expression of Bcl-xL as well as caspase-9 and -3 mediated PARP cleavage by H(2)O(2).	diphlorethohydroxycarmalol	0-4	BCL2-associated X protein	Mus musculus	40-43
24637330-9	2014	In BAX(-/-)/BAK(-/-) murine embryonic fibroblasts, simvastatin-triggered apoptotic and UPR events were abrogated, but autophagy flux was increased leading to cell death via necrosis.	Simvastatin	51-62	BCL2-associated X protein	Mus musculus	3-6
22089535-8	2012	Aliskiren treatment significantly increased klotho expression and reduced the expression of fibrogenic cystokines, caspase-3 and Bax in ischemic kidneys.	aliskiren	0-9	BCL2-associated X protein	Mus musculus	129-132
21665879-8	2012	Nomilin treatment also exhibited a downregulated Bcl-2 and cyclin-D1 expression and upregulated p53, Bax, caspase-9, caspase-3, p21, and p27 gene expression in B16F-10 cells.	nomilin	0-7	BCL2-associated X protein	Mus musculus	101-104
22219300-5	2012	Incubation with testosterone prior to H(2)O(2) induces BAD inactivation, inhibition of poly(ADP-ribose) polymerase cleavage, and a decrease in BAX levels, and impedes the loss of mitochondrial membrane potential, suggesting that the hormone participates in the regulation of the apoptotic intrinsic pathway.	Testosterone	16-28	BCL2-associated X protein	Mus musculus	143-146
22428454-6	2012	We also found an increased tendency of proinflammatory chemokine CCL3 mRNA and a marked increase in the proapoptotic gene Bax mRNA in the diazinon-injected C3H/HeJ mice.	Diazinon	138-146	BCL2-associated X protein	Mus musculus	122-125
22259050-0	2012	Honokiol traverses the blood-brain barrier and induces apoptosis of neuroblastoma cells via an intrinsic bax-mitochondrion-cytochrome c-caspase protease pathway.	honokiol	0-8	BCL2-associated X protein	Mus musculus	105-108
22259050-9	2012	Sequential treatment of neuro-2a cells with honokiol increased the expression of the proapoptotic Bax protein and its translocation from the cytoplasm to mitochondria.	honokiol	44-52	BCL2-associated X protein	Mus musculus	98-101
22259050-13	2012	Taken together, this study showed that honokiol can pass through the BBB and induce apoptotic insults to neuroblastoma cells through a Bax-mitochondrion-cytochrome c-caspase protease pathway.	honokiol	39-47	BCL2-associated X protein	Mus musculus	135-138
22242953-7	2012	The GM080-treated allergy group exhibited significantly lower p-JNK, JNK1/2, phospholate- Ikappa B (p-IkappaB), Bax and Bad protein products than the Kefir I and Kefir II allergy groups.	gm080	4-9	BCL2-associated X protein	Mus musculus	112-115
21738214-11	2012	Once processed, tBID localizes in the mitochondria of MNNG-treated cells, where it can facilitate BAX activation and PCD.	tBID	16-20	BCL2-associated X protein	Mus musculus	98-101
21682651-6	2012	The proapoptotic genes p53, Bax, caspase-9, and caspase-3 were found upregulated in andrographolide-treated cells, whereas the antiapoptotic gene bcl-2 was downregulated.	andrographolide	84-99	BCL2-associated X protein	Mus musculus	28-31
22302823-9	2012	Oxygen/glucose deprivation-induced injury in organotypic hippocampal slice cultures confirmed that calpains were specifically activated during bax-dependent apoptosis and in this setting function as downstream cell-death executioners.	Oxygen	0-6	BCL2-associated X protein	Mus musculus	143-146
22065578-0	2012	Natural diterpenoid compound elevates expression of Bim protein, which interacts with antiapoptotic protein Bcl-2, converting it to proapoptotic Bax-like molecule.	Diterpenes	8-19	BCL2-associated X protein	Mus musculus	145-148
22065578-3	2012	We identified a natural diterpenoid compound that induced apoptosis in bax/bak double knock-out murine embryonic fibroblasts and substantially reduced the tumor growth from these cells implanted in mice.	Diterpenes	24-35	BCL2-associated X protein	Mus musculus	71-74
22065578-6	2012	Therefore, the diterpenoid compound induces a structural and functional conversion of Bcl-2 through Bim to permeabilize the mitochondrial outer membrane, thereby inducing apoptosis independently of Bax and Bak.	Diterpenes	15-26	BCL2-associated X protein	Mus musculus	198-201
22019121-5	2012	The MAPKs (JNK, ERK and p38) as well as the TGF-beta-related signaling pathways were found to be activated in the pristine grapheme-treated cells, which activated Bim and Bax, two pro-apoptotic member of Bcl-2 protein family.	grapheme	123-131	BCL2-associated X protein	Mus musculus	171-174
22759961-13	2012	Furthermore, quercetin promoted the apoptotic signaling pathway including increasing the phosphorylation of p38-MAPK, c-Jun N-terminal kinases/stress-activated protein kinases (JNK/SAPK), and Bax, while inhibited Bcl-2 expression.	Quercetin	13-22	BCL2-associated X protein	Mus musculus	192-195
22856664-2	2012	Mutation of Bax at lysine 128 (BaxK128E) abrogates its inhibitory effects on mtKv1.3 and prevents apoptosis.	Lysine	19-25	BCL2-associated X protein	Mus musculus	12-15
23243434-7	2012	TSAV (200 mg/kg) also significantly decreased Bak, Bax mRNA and Fas, FasL, p53, and NF-kappaB p65 protein expressions and increased Bcl-2 mRNA and protein expressions.	tsav	0-4	BCL2-associated X protein	Mus musculus	51-54
23320028-10	2012	Western blot analysis showed that SN pretreatment inhibited apoptosis provoked by ACR through decreasing Bax/Bcl-2 ratio, cytosolic cytochrome c content, and cleaved caspase-3 level in heart.	Silymarin	34-36	BCL2-associated X protein	Mus musculus	105-108
22848173-6	2012	METHODS AND RESULTS: Intravenous administration of folate-targeted, paclitaxel-loaded micelles was demonstrated to be more efficient in inhibiting subcutaneous xenograft tumors and extending the survival rate of tumor-bearing nude mice than free paclitaxel and plain paclitaxel micelles at an equivalent paclitaxel dose of 20 mg/kg, which was further backed up by flow cytometry, TUNEL, and expression of apoptosis-related proteins, including Bax, Bcl2, and caspase 3 in this study.	Folic Acid	51-57	BCL2-associated X protein	Mus musculus	443-446
22848173-6	2012	METHODS AND RESULTS: Intravenous administration of folate-targeted, paclitaxel-loaded micelles was demonstrated to be more efficient in inhibiting subcutaneous xenograft tumors and extending the survival rate of tumor-bearing nude mice than free paclitaxel and plain paclitaxel micelles at an equivalent paclitaxel dose of 20 mg/kg, which was further backed up by flow cytometry, TUNEL, and expression of apoptosis-related proteins, including Bax, Bcl2, and caspase 3 in this study.	Paclitaxel	68-78	BCL2-associated X protein	Mus musculus	443-446
21882229-11	2012	When immature mice were treated with 17beta-estradiol (E2) or progesterone (P4) for 3 days, we found that the expressions of Bax and caspase 3 protein were increased by E2 treatment in WT and CaBP-9k KO mice, and by P4 treatment in CaBP-28k KO mice.	Estradiol	37-53	BCL2-associated X protein	Mus musculus	125-128
21882229-11	2012	When immature mice were treated with 17beta-estradiol (E2) or progesterone (P4) for 3 days, we found that the expressions of Bax and caspase 3 protein were increased by E2 treatment in WT and CaBP-9k KO mice, and by P4 treatment in CaBP-28k KO mice.	Progesterone	62-74	BCL2-associated X protein	Mus musculus	125-128
22687777-7	2012	Quantitative real-time PCR analysis demonstrated that the administration of AMC and AAC down-regulated the expression of Bcl-2, Bcl-xL, while on the other hand, up-regulated Bax, Cytochrome c, caspase-9 and caspase-3 mRNA level of the S180 ascites tumor cells.	7-amino-4-methylcoumarin	76-79	BCL2-associated X protein	Mus musculus	174-177
21812816-8	2012	Furthermore, melatonin treatment mitigated apoptotic rate, maintained DeltaPsim, diminished cytochrome c release from mitochondria, down-regulated Bax/Bcl-2 ratio and caspase-3 levels, and consequently inhibited the important steps of irradiation-induced activation of mitochondrial pathway of apoptosis.	Melatonin	13-22	BCL2-associated X protein	Mus musculus	147-150
24716117-7	2012	Tamoxifen could decrease spleen mass and Bcl-2 protein expression, increase the Bax protein expression as well as exert uterotrophic effects by increasing uterus index and inducing the gene expressions in the uterus.	Tamoxifen	0-9	BCL2-associated X protein	Mus musculus	80-83
21902562-0	2012	Allicin induces apoptosis in EL-4 cells in vitro by activation of expression of caspase-3 and -12 and up-regulation of the ratio of Bax/Bcl-2.	allicin	0-7	BCL2-associated X protein	Mus musculus	132-135
21902562-6	2012	Finally, allicin up-regulated the ratio of Bax/Bcl-2 and induced a mitochondrion membrane potential (MMP) decrease.	allicin	9-16	BCL2-associated X protein	Mus musculus	43-46
23300809-6	2012	Instead, the combination treatment of DOX plus PI103 activated Bax, the mitochondrial apoptosis pathway, and caspase 3.	Doxorubicin	38-41	BCL2-associated X protein	Mus musculus	63-66
23251428-7	2012	However, adding cPA led to the suppression of CoCl(2)-induced apoptosis in a cPA dose-dependent manner and attenuated the increase in the Bax/Bcl-2 ratio caused by CoCl(2).	cpa	16-19	BCL2-associated X protein	Mus musculus	138-141
23251428-7	2012	However, adding cPA led to the suppression of CoCl(2)-induced apoptosis in a cPA dose-dependent manner and attenuated the increase in the Bax/Bcl-2 ratio caused by CoCl(2).	cobaltous chloride	164-171	BCL2-associated X protein	Mus musculus	138-141
23272189-9	2012	In addition, melatonin inhibited APAP-induced hepatic c-Jun N-terminal kinase (JNK) phosphorylation and mitochondrial Bax translocation.	Melatonin	13-22	BCL2-associated X protein	Mus musculus	118-121
23272189-9	2012	In addition, melatonin inhibited APAP-induced hepatic c-Jun N-terminal kinase (JNK) phosphorylation and mitochondrial Bax translocation.	Acetaminophen	33-37	BCL2-associated X protein	Mus musculus	118-121
23272189-13	2012	In conclusion, melatonin protects against AIF-dependent cell death during APAP-induced acute liver failure through its direct inhibition of hepatic RIP1 and subsequent JNK phosphorylation and mitochondrial Bax translocation.	Melatonin	15-24	BCL2-associated X protein	Mus musculus	206-209
23272240-6	2012	Treatment of SK-N-SH cells with scFvs I13 and I27 enhanced cell proliferation and migration, neurite outgrowth, and protected against the toxic effects of H(2)O(2) by increasing the ratio of Bcl-2/Bax.	sk-n	13-17	BCL2-associated X protein	Mus musculus	197-200
23056363-7	2012	Modafinil also counteracted the decrease in tyrosine hydroxylase and dopamine transporter levels and prevented methamphetamine-induced increases in the pro-apoptotic BAX and decreases in the anti-apoptotic Bcl-2 protein expression.	Modafinil	0-9	BCL2-associated X protein	Mus musculus	166-169
23056363-7	2012	Modafinil also counteracted the decrease in tyrosine hydroxylase and dopamine transporter levels and prevented methamphetamine-induced increases in the pro-apoptotic BAX and decreases in the anti-apoptotic Bcl-2 protein expression.	Methamphetamine	111-126	BCL2-associated X protein	Mus musculus	166-169
23029230-11	2012	Salidroside increased phosphorylation of Akt on Ser473 and the mitochondrial Bcl-2/Bax ratio at day 1, and enhanced phosphorylation of Akt on Thr308 at day 3.	rhodioloside	0-11	BCL2-associated X protein	Mus musculus	83-86
22880001-6	2012	ABT-737 treatment caused a dose-dependent impairment of maximal O(2) consumption in MCF10A BCL-2 overexpressing cells but not in control-transfected cells or in immortalized mouse embryonic fibroblasts lacking both BAX and BAK.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	0-3	BCL2-associated X protein	Mus musculus	215-218
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	27-44	BCL2-associated X protein	Mus musculus	210-213
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	46-49	BCL2-associated X protein	Mus musculus	210-213
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	jacaranone	105-115	BCL2-associated X protein	Mus musculus	210-213
22511917-8	2012	On the other hand, results showed that carnosine and RU486 (a glucocorticoids receptor antagonist) treatment prevented the reduction in mitochondrion membrane potential and the release of mitochondrial cytochrome c into cytoplasm, increased Bcl-2/Bax mRNA ratio, as well as decreased terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells in spleen lymphocytes of stressed mice.	Mifepristone	53-58	BCL2-associated X protein	Mus musculus	247-250
22442678-5	2012	Furthermore, ablation of Bax in female mice protected against Dexa-induced bone growth impairment.	Dexamethasone	62-66	BCL2-associated X protein	Mus musculus	25-28
22681485-10	2012	The expression of Bax, caspase-9, and caspase-3 in cisplatin-treated cells were also decreased by PC treatment.	Cisplatin	51-60	BCL2-associated X protein	Mus musculus	18-21
22056370-3	2011	In addition, an up-regulation of Bax/Bcl2 ratio with a drop in DeltaPsim and an increase of cleaved caspase 9 and 3 was found, suggesting that the alkylphenol induced osteoblast death via the mitochondrial-dependent apoptotic pathway.	alkylphenol	147-158	BCL2-associated X protein	Mus musculus	33-36
22015602-11	2011	Importantly, hydrogen inhibited the activation of P-JNK, and also reversed changes in Bax, Bcl-xl and caspase-3.	Hydrogen	13-21	BCL2-associated X protein	Mus musculus	86-89
21767629-5	2011	ZEN treatment also results in the loss of mitochondrial membrane potential (MMP), mitochondrial changes in Bcl-2 and Bax proteins, and cytoplasmic release of cytochrome c and apoptosis-inducing factor (AIF).	Zearalenone	0-3	BCL2-associated X protein	Mus musculus	117-120
21739275-4	2011	We found that 6-OHDA treatment triggered translocation and oligomerization of Bax onto the mitochondria in MN9D dopaminergic neuronal cells.	Oxidopamine	14-20	BCL2-associated X protein	Mus musculus	78-81
21739275-6	2011	Cross-linking assay revealed that co-treatment with a ROS scavenger or a pan-caspase inhibitor inhibited 6-OHDA-induced Bax oligomerization.	Reactive Oxygen Species	54-57	BCL2-associated X protein	Mus musculus	120-123
21739275-6	2011	Cross-linking assay revealed that co-treatment with a ROS scavenger or a pan-caspase inhibitor inhibited 6-OHDA-induced Bax oligomerization.	Oxidopamine	105-111	BCL2-associated X protein	Mus musculus	120-123
21739275-7	2011	Among several candidates of ROS-activated MAPKs and caspases, we found that co-treatment with PD169316 or VDVAD specifically inhibited 6-OHDA-induced Bax oligomerization, suggesting critical involvement of p38 MAPK and caspase-2.	Reactive Oxygen Species	28-31	BCL2-associated X protein	Mus musculus	150-153
21739275-7	2011	Among several candidates of ROS-activated MAPKs and caspases, we found that co-treatment with PD169316 or VDVAD specifically inhibited 6-OHDA-induced Bax oligomerization, suggesting critical involvement of p38 MAPK and caspase-2.	2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole	94-102	BCL2-associated X protein	Mus musculus	150-153
21739275-7	2011	Among several candidates of ROS-activated MAPKs and caspases, we found that co-treatment with PD169316 or VDVAD specifically inhibited 6-OHDA-induced Bax oligomerization, suggesting critical involvement of p38 MAPK and caspase-2.	vdvad	106-111	BCL2-associated X protein	Mus musculus	150-153
21739275-7	2011	Among several candidates of ROS-activated MAPKs and caspases, we found that co-treatment with PD169316 or VDVAD specifically inhibited 6-OHDA-induced Bax oligomerization, suggesting critical involvement of p38 MAPK and caspase-2.	Oxidopamine	135-141	BCL2-associated X protein	Mus musculus	150-153
21739275-8	2011	Consequently, overexpression of a dominant negative form of p38 MAPK or a shRNA-mediated knockdown of caspase-2 indeed inhibited 6-OHDA-induced Bax oligomerization.	Oxidopamine	129-135	BCL2-associated X protein	Mus musculus	144-147
21739275-11	2011	Taken together, our data suggest that there is an independent amplification loop of Bax translocation and oligomerization via caspase-2 and p38 MAPK during ROS-mediated dopaminergic neurodegeneration.	Reactive Oxygen Species	156-159	BCL2-associated X protein	Mus musculus	84-87
22002093-11	2011	DMAE-CB may cause apoptosis by disturbing the expression of Bcl-2 and Bax, reducing the mitochondrial potential and inducing release of cytochrome C. Taken together, these findings suggest that the toxicity of the antibacterial monomer DMAE-CB is associated with ROS production, mitochondrial dysfunction, cell cycle disturbance, and cell apoptosis/necrosis.	methacryloxylethyl cetyl dimethyl ammonium	0-7	BCL2-associated X protein	Mus musculus	70-73
21244349-8	2011	The high concentration isoflurane potentiated the Abeta-induced reduction in Bcl-2/Bax ratio and caused a robust elevation of cytosolic calcium levels.	Isoflurane	23-33	BCL2-associated X protein	Mus musculus	83-86
21244349-9	2011	The low concentration isoflurane attenuated the Abeta-induced reduction in Bcl-2/Bax ratio and caused only a mild elevation of cytosolic calcium levels.	Isoflurane	22-32	BCL2-associated X protein	Mus musculus	81-84
20196164-8	2011	The expression levels of Bcl-2, Bax, p53, and GRP 78 in MC-RR-treated groups were altered significantly compared to the control, but no obvious alteration was found in CHOP expression.	Methylcholanthrene	56-58	BCL2-associated X protein	Mus musculus	32-35
22239859-10	2012	In conclusion, these studies show that sublethal exposure to copper (as copper chloride) induces toxicity in the thymus and spleen, and increased Sub G0/G1 population among splenocytes and thymocytes that is mediated, in part, by the EndoG-Bax-ubiquitin pathway.	Copper	61-67	BCL2-associated X protein	Mus musculus	240-243
22239859-10	2012	In conclusion, these studies show that sublethal exposure to copper (as copper chloride) induces toxicity in the thymus and spleen, and increased Sub G0/G1 population among splenocytes and thymocytes that is mediated, in part, by the EndoG-Bax-ubiquitin pathway.	cupric chloride	72-87	BCL2-associated X protein	Mus musculus	240-243
21642840-5	2011	A combined treatment with taxol and pristimerin induced cervical cancer cell death by increasing intracellular reactive oxygen species levels, upregulation of death receptor death receptor 5 (DR5), activation of Bax, and dissipation of mitochondrial membrane potential.	Paclitaxel	26-31	BCL2-associated X protein	Mus musculus	212-215
21756897-5	2011	Furthermore, carrageenan induced the expression of nuclear factor-kappaB (NF-kappaB), inducible nitric oxide synthase (iNOS), nitrotyrosine, the activation of poly-ADP-ribosyl polymerase (PARP), as well as induced apoptosis (FAS-ligand expression, Bax and Bcl-2 expression) in the lung tissues.	Carrageenan	13-24	BCL2-associated X protein	Mus musculus	248-251
21687940-4	2011	Icariin caused a dose-dependent decrease in the viability of MLTC-1 cells, which coincided with an increase in cell apoptosis through regulation of the expression of Bcl-2/Bax and cytochrome c, activation of caspase-9 and -3.	icariin	0-7	BCL2-associated X protein	Mus musculus	172-175
21630270-10	2011	Renal cell apoptosis induced by IR was decreased in kidneys of mice pretreated by clopidogrel, with an increase in Bcl-2 and Bcl-xL expression and a decrease in caspase-3, caspase-8, and Bax expression.	Clopidogrel	82-93	BCL2-associated X protein	Mus musculus	187-190
21642840-9	2011	Furthermore, the reactive oxygen species-dependent activation of the Jun N-terminal kinase/c-Jun pathway is required for the DR5 upregulation and Bax activation.	Reactive Oxygen Species	17-40	BCL2-associated X protein	Mus musculus	146-149
21642840-5	2011	A combined treatment with taxol and pristimerin induced cervical cancer cell death by increasing intracellular reactive oxygen species levels, upregulation of death receptor death receptor 5 (DR5), activation of Bax, and dissipation of mitochondrial membrane potential.	pristimerin	36-47	BCL2-associated X protein	Mus musculus	212-215
21642840-6	2011	Treatment with N-acetyl-L-cysteine, a thiol-containing antioxidant completely blocked combined treatment-induced Bax translocation as well as DR5 upregulation.	Acetylcysteine	15-34	BCL2-associated X protein	Mus musculus	113-116
21642840-6	2011	Treatment with N-acetyl-L-cysteine, a thiol-containing antioxidant completely blocked combined treatment-induced Bax translocation as well as DR5 upregulation.	Sulfhydryl Compounds	38-43	BCL2-associated X protein	Mus musculus	113-116
21642840-8	2011	These results indicate that the triterpenoid, pristimerin, synergistically enhances taxol response of cervical cancer cells through DR5 expression and Bax activation.	triterpenoid TP-222	32-44	BCL2-associated X protein	Mus musculus	151-154
21642840-8	2011	These results indicate that the triterpenoid, pristimerin, synergistically enhances taxol response of cervical cancer cells through DR5 expression and Bax activation.	pristimerin	46-57	BCL2-associated X protein	Mus musculus	151-154
21513768-10	2011	Microscopic examination of tumors revealed that in BA-treated groups the expression of Bax and caspase 3 increased, suggesting drug induced tumor cell apoptosis through activating the pro-apoptotic bcl-2 family and caspase-3.	boswellic acid	51-53	BCL2-associated X protein	Mus musculus	87-90
21710255-6	2011	When comparing exponentially growing Swiss3T3 cells to those synchronized to enter S-phase simultaneously and treated with the DNA damaging agent camptothecin, we found that with cells in S-phase, p53 protein levels increased earlier, Bax and p21 transcription was activated earlier and to a greater extent and apoptosis occurred earlier and to a greater extent.	Camptothecin	146-158	BCL2-associated X protein	Mus musculus	235-238
21911424-9	2011	Deletion of Bak and Bax rendered megakaryocytes resistant to etoposide and ABT-737.	Etoposide	61-70	BCL2-associated X protein	Mus musculus	20-23
21911424-9	2011	Deletion of Bak and Bax rendered megakaryocytes resistant to etoposide and ABT-737.	ABT-737	75-82	BCL2-associated X protein	Mus musculus	20-23
21911424-10	2011	In vivo, mice with a Bak(-/-) Bax(-/-) hematopoietic system were protected against thrombocytopenia induced by the chemotherapeutic agent carboplatin.	bakuchiol	21-24	BCL2-associated X protein	Mus musculus	30-33
21911424-10	2011	In vivo, mice with a Bak(-/-) Bax(-/-) hematopoietic system were protected against thrombocytopenia induced by the chemotherapeutic agent carboplatin.	Carboplatin	138-149	BCL2-associated X protein	Mus musculus	30-33
21788604-6	2011	Eplerenone (MR antagonist), mifepristone (GR antagonist), and candesartan (AT(1)R antagonist) inhibited ACM-induced effects on extracellular signal-regulated kinase 1/2, p38MAPK, and proliferating cell nuclear antigen, without influencing apoptosis (Bax, Bcl, and caspase 3).	Eplerenone	0-10	BCL2-associated X protein	Mus musculus	250-253
21788604-6	2011	Eplerenone (MR antagonist), mifepristone (GR antagonist), and candesartan (AT(1)R antagonist) inhibited ACM-induced effects on extracellular signal-regulated kinase 1/2, p38MAPK, and proliferating cell nuclear antigen, without influencing apoptosis (Bax, Bcl, and caspase 3).	candesartan	62-73	BCL2-associated X protein	Mus musculus	250-253
22013806-0	2011	[Effects of icariin on Bcl-2 and Bax protein expressions and eosinophils apoptosis in bronchial asthmatic mice].	icariin	12-19	BCL2-associated X protein	Mus musculus	33-36
22013806-10	2011	CONCLUSION: In bronchial asthmatic mice, icariin could enhance the apoptosis of eosinophils and lessen their infiltration by decreasing the expression of Bcl-2 protein and increasing the expression of Bax protein in lung.	icariin	41-48	BCL2-associated X protein	Mus musculus	201-204
21610140-5	2011	We also found that nicotine administration increased the relative expression level of the antiapoptotic protein B cell lymphoma-2 versus that of the proapoptotic protein Bax in the brain.	Nicotine	19-27	BCL2-associated X protein	Mus musculus	170-173
22013806-1	2011	OBJECTIVE: To study the effects of icariin on Bcl-2 and Bax protein expressions and eosinophils apoptosis in bronchial asthmatic mice.	icariin	35-42	BCL2-associated X protein	Mus musculus	56-59
21705974-5	2011	Vanillyl alcohol attenuated the elevation of reactive oxygen species (ROS) levels, decreased in the Bax/Bcl-2 ratio and poly (ADP-ribose) polymerase proteolysis.	vanillyl alcohol	0-16	BCL2-associated X protein	Mus musculus	100-103
22356713-7	2011	The expression levels of bcl-2, bax proteins and the ratio of bcl-2 to bax in Cd exposure groups decreased significantly, as compared with the control group (P &lt; 0.05).	Cadmium	78-80	BCL2-associated X protein	Mus musculus	71-74
21683104-7	2011	Moreover, TBHP treatment was associated with the loss of mitochondrial membrane potential, and it induced cell apoptosis through the mitochondrial-mediated pathway involving the down-regulation of Bcl-2 expression and up-regulation of the Bax/Bcl-2 ratio.	tert-Butylhydroperoxide	10-14	BCL2-associated X protein	Mus musculus	239-242
21185334-12	2011	These findings indicate that mitochondrial ROS during ischemia triggers mPTP activation, mitochondrial depolarization, and cell death during reperfusion through a Bax/Bak-independent cell death pathway.	Reactive Oxygen Species	43-46	BCL2-associated X protein	Mus musculus	163-166
21649480-4	2011	The proapoptotic genes, p53, Bax, caspase-9, and caspase-3, were upregulated in vernolide-A-treated cells, whereas the antiapoptotic gene, Bcl-2, was downregulated.	vernolide-A	80-91	BCL2-associated X protein	Mus musculus	29-32
21649489-6	2011	SFN-induced apoptosis was associated with the activation of caspases 3 and 9, Bax, and p53 and the downregulation of Bcl-2, caspase-8, Bid, and NF-kB.	sulforaphane	0-3	BCL2-associated X protein	Mus musculus	78-81
21457087-7	2011	It was found that the Bax/Bcl-2 ratio and phosphorylation of histone H2A.X was decreased at low doses of VPA but was increased at high doses.	Valproic Acid	105-108	BCL2-associated X protein	Mus musculus	22-25
21756336-8	2011	RESULTS: Cyclopalladated complex interacts with thiol groups on the mitochondrial membrane proteins, causes dissipation of the mitochondrial membrane potential, and induces Bax translocation from the cytosol to mitochondria, colocalizing with a mitochondrial tracker.	Sulfhydryl Compounds	48-53	BCL2-associated X protein	Mus musculus	173-176
21533992-7	2011	PD98059 treatment shows therapeutic effects on pulmonary damage, decreasing many inflammatory and apoptotic parameters, such as (1) cytokine production; (2) IkBalpha degradation and NF-kB nuclear translocation; (3) iNOS expression; (4) nitrotyrosine and PAR localization; and (5) the degree of apoptosis, as evaluated by Bax and Bcl-2 balance, FAS ligand expression, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	0-7	BCL2-associated X protein	Mus musculus	321-324
21398594-6	2011	Western blot analysis showed enchanced Bcl-2-to-Bax ratio with sildenafil treatment (P &lt; 0.05 vs. saline).	Sildenafil Citrate	63-73	BCL2-associated X protein	Mus musculus	48-51
21278141-8	2011	It was found by western blot and electrophoretic mobility shift assay that DOX treatment increased p53 protein acetylation and cytochrome c release from mitochondria, activated p53 binding at the Bax promoter, and up-regulated Bax expression, but supplementation with RES could weaken all these effects.	Doxorubicin	75-78	BCL2-associated X protein	Mus musculus	196-199
21278141-8	2011	It was found by western blot and electrophoretic mobility shift assay that DOX treatment increased p53 protein acetylation and cytochrome c release from mitochondria, activated p53 binding at the Bax promoter, and up-regulated Bax expression, but supplementation with RES could weaken all these effects.	Doxorubicin	75-78	BCL2-associated X protein	Mus musculus	227-230
21530568-7	2011	NN-32 increased proapoptotic protein caspase 3 and 9 activity and Bax-Bcl2 ratio.	nn-32	0-5	BCL2-associated X protein	Mus musculus	66-69
21737642-6	2011	Results from Western blotting indicated that etomidate enhanced the levels of cytochrome c, apoptosis-inducing factor (AIF), endonuclease G (Endo G), caspase-9, caspase-3 active form and Bax proteins, but it inhibited the expression of Bcl-xl, leading to apoptosis.	Etomidate	45-54	BCL2-associated X protein	Mus musculus	187-190
21622206-6	2011	The expression levels of Bcl-2 and Bax, which regulate the mitochondria-initiated apoptotic cascade signaling pathway, were significantly different in response to Dex and hypoxia.	Dexamethasone	163-166	BCL2-associated X protein	Mus musculus	35-38
21473852-7	2011	The early activation of NFkappaB during hydrogen treatment was correlated with elevated levels of the antiapoptotic protein Bcl-2 and decreased levels of Bax.	Hydrogen	40-48	BCL2-associated X protein	Mus musculus	154-157
22146483-10	2011	Exposure of MLEC to carbon monoxide inhibited Jo2-induced cell death, which correlated with the inhibition of DISC formation, cleavage of caspases-8, -9, and -3, and Bax activation.	Carbon Monoxide	20-35	BCL2-associated X protein	Mus musculus	166-169
21614693-7	2011	In comparison with the other two groups, LY294002+SN50 group exhibited more severe apoptosis, with expression of Bcl-2 decreased and that of P53 and Bax increased more significantly(P&lt;0.05).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	41-49	BCL2-associated X protein	Mus musculus	149-152
22146483-10	2011	Exposure of MLEC to carbon monoxide inhibited Jo2-induced cell death, which correlated with the inhibition of DISC formation, cleavage of caspases-8, -9, and -3, and Bax activation.	2-[[(3~{S})-2,5-bis(oxidanylidene)pyrrolidin-3-yl]carbamoyl]-4-nitro-benzoic acid	46-49	BCL2-associated X protein	Mus musculus	166-169
22146483-14	2011	In vitro, carbon monoxide may inhibit both Fas/caspase-8 and Bax-dependent apoptotic signaling pathways induced by Fas-activating antibody in endothelial cells.	Carbon Monoxide	10-25	BCL2-associated X protein	Mus musculus	61-64
21349270-11	2011	So, by immunohistochemical analysis and in vitro assays, we have clearly showed that glutamine reduces: 1) the histological damage in pancreas and gut; 2) the inducible nitric oxide synthase expression; 3) nitrotyrosine and poly (ADP-ribose) formation; 4) TNF-alpha and IL-1beta tissue and plasma levels; 5) FasL localization; and 6) alteration of the balance between Bax and Bcl-2.	Glutamine	85-94	BCL2-associated X protein	Mus musculus	368-371
21031634-12	2011	Further analysis showed that these three glycosides were able to decrease DNA damage and the increment in the Bax/Bcl-2 ratio induced by radiation.	Glycosides	41-51	BCL2-associated X protein	Mus musculus	110-113
21031634-13	2011	In summary, the three glycosides showed radioprotective effects on the hematopoietic system in mice, which was associated with changes in the cell cycle, a reduction in DNA damage, and down-regulation of the ratio of Bax/Bcl-2 in bone marrow cells exposed to radiation.	Glycosides	22-32	BCL2-associated X protein	Mus musculus	217-220
21349252-5	2011	Melatonin treatment also increased Bcl-2 expression and suppressed Bax expression and decreased phosphorylation of GSK alpha/beta.	Melatonin	0-9	BCL2-associated X protein	Mus musculus	67-70
21541347-10	2011	Nicorandil treatment also inhibited the increase in BAX, the decrease in BCL2, activation of caspase-3 and apoptotic cell death by mutant HSPB5.	Nicorandil	0-10	BCL2-associated X protein	Mus musculus	52-55
21138475-6	2011	Compared with NO treatment, Bcl-2 expression increased with melatonin treatment, while Bax expression was inhibited by melatonin treatment.	Melatonin	119-128	BCL2-associated X protein	Mus musculus	87-90
21193837-9	2011	In addition, we have demonstrated that rapamycin treatment in the ALS mice causes more severe mitochondrial impairment, higher Bax levels and greater caspase-3 activation.	Sirolimus	39-48	BCL2-associated X protein	Mus musculus	127-130
21496122-6	2011	In this study we clearly demonstrated that pre-treatment with LY294002 reversed the increased activation of eNOS and Akt observed following SCI, and developed a severe trauma characterized by oedema, tissue damage and apoptosis (measured by TUNEL staining, Bax, Bcl-2 and Fas-L expression).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	62-70	BCL2-associated X protein	Mus musculus	257-260
21195450-6	2011	Furthermore, CeCl(3) could effectively activate caspase-3 and -9, decrease the Bcl-2 the levels of gene and protein, and increase the levels of Bax, and cytochrome c genes and their protein expressions, and promote reactive oxygen species production.	cerous chloride	13-20	BCL2-associated X protein	Mus musculus	144-147
20503275-0	2011	A novel BH3 mimetic S1 potently induces Bax/Bak-dependent apoptosis by targeting both Bcl-2 and Mcl-1.	BH 3	8-11	BCL2-associated X protein	Mus musculus	40-43
21138475-11	2011	Together, these results suggest that melatonin protects against apoptotic and autophagic cell death through the common pathway resulted in the increment of Bcl-2 expression and the reduction of Bax expression in C2C12 murine myoblast cells.	Melatonin	37-46	BCL2-associated X protein	Mus musculus	194-197
21216964-7	2011	The loss of caspase-2 significantly inhibited rotenone-induced activation of Bid and Bax and the release of cytochrome c and apoptosis inducing factor from mitochondria.	Rotenone	46-54	BCL2-associated X protein	Mus musculus	85-88
21270764-8	2011	ATP depletion in vitro caused greater mitochondrial Bax accumulation and death in primary proximal tubule cells harvested from knockout compared with wild-type mice and altered serine phosphorylation of a Bax peptide at the Akt-specific target site.	Adenosine Triphosphate	0-3	BCL2-associated X protein	Mus musculus	52-55
21270764-8	2011	ATP depletion in vitro caused greater mitochondrial Bax accumulation and death in primary proximal tubule cells harvested from knockout compared with wild-type mice and altered serine phosphorylation of a Bax peptide at the Akt-specific target site.	Adenosine Triphosphate	0-3	BCL2-associated X protein	Mus musculus	205-208
21270764-8	2011	ATP depletion in vitro caused greater mitochondrial Bax accumulation and death in primary proximal tubule cells harvested from knockout compared with wild-type mice and altered serine phosphorylation of a Bax peptide at the Akt-specific target site.	Serine	177-183	BCL2-associated X protein	Mus musculus	205-208
21429205-8	2011	Furthermore, RT-PCR analysis showed that harmine induced apoptosis in B16F-10 melanoma cells by up-regulating Bax and activating Caspase-3, 9 and p53 and down-regulating Bcl-2.	Harmine	41-48	BCL2-associated X protein	Mus musculus	110-113
21199865-5	2011	In both structures, Met-74 from the Bax peptide engages with the BH3-binding groove in a fifth hydrophobic interaction.	BH 3	65-68	BCL2-associated X protein	Mus musculus	36-39
21199865-7	2011	Bax/Bak-deficient mouse embryonic fibroblast cells reconstituted with several Bax Met-74 mutants are more sensitive to the BH3 mimetic compound ABT-737 as compared with cells expressing wild-type Bax.	BH 3	123-126	BCL2-associated X protein	Mus musculus	0-3
21199865-7	2011	Bax/Bak-deficient mouse embryonic fibroblast cells reconstituted with several Bax Met-74 mutants are more sensitive to the BH3 mimetic compound ABT-737 as compared with cells expressing wild-type Bax.	BH 3	123-126	BCL2-associated X protein	Mus musculus	78-81
21199865-7	2011	Bax/Bak-deficient mouse embryonic fibroblast cells reconstituted with several Bax Met-74 mutants are more sensitive to the BH3 mimetic compound ABT-737 as compared with cells expressing wild-type Bax.	BH 3	123-126	BCL2-associated X protein	Mus musculus	78-81
21199865-7	2011	Bax/Bak-deficient mouse embryonic fibroblast cells reconstituted with several Bax Met-74 mutants are more sensitive to the BH3 mimetic compound ABT-737 as compared with cells expressing wild-type Bax.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	144-147	BCL2-associated X protein	Mus musculus	0-3
21199865-7	2011	Bax/Bak-deficient mouse embryonic fibroblast cells reconstituted with several Bax Met-74 mutants are more sensitive to the BH3 mimetic compound ABT-737 as compared with cells expressing wild-type Bax.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	144-147	BCL2-associated X protein	Mus musculus	78-81
21199865-7	2011	Bax/Bak-deficient mouse embryonic fibroblast cells reconstituted with several Bax Met-74 mutants are more sensitive to the BH3 mimetic compound ABT-737 as compared with cells expressing wild-type Bax.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	144-147	BCL2-associated X protein	Mus musculus	78-81
21498692-5	2011	Administration of nutlin-3, an MDM2 antagonist, induced cellular senescence and increased the expression of BAX.	nutlin 3	18-26	BCL2-associated X protein	Mus musculus	108-111
21337715-7	2011	In addition, cadmium provoked germ cell apoptosis by upregulating expression of the proapoptotic proteins Bax and caspase-3 and downregulating expression of the antiapoptotic protein Bcl-XL.	Cadmium	13-20	BCL2-associated X protein	Mus musculus	106-109
21337715-10	2011	Additionally, quercetin protected germ cells from cadmium-induced apoptosis by downregulating the expression of Bax and caspase-3 and upregulating Bcl-XL expression.	Quercetin	14-23	BCL2-associated X protein	Mus musculus	112-115
21337715-10	2011	Additionally, quercetin protected germ cells from cadmium-induced apoptosis by downregulating the expression of Bax and caspase-3 and upregulating Bcl-XL expression.	Cadmium	50-57	BCL2-associated X protein	Mus musculus	112-115
21147071-4	2011	Furthermore, carrageenan induced the expression of nuclear factor-kappaB (NF-kappaB) inducible nitric oxide synthase (iNOS), nitrotyrosine, poly-ADP-ribosyl polymerase (PARP) as well as induced apoptosis (TUNEL staining, FAS-ligand expression, Bax and Bcl-2 expression) and mitogen-activated protein kinase (MAPK) activation in the lung tissues.	Carrageenan	13-24	BCL2-associated X protein	Mus musculus	244-247
20885444-0	2011	Single-point mutations of a lysine residue change function of Bax and Bcl-xL expressed in Bax- and Bak-less mouse embryonic fibroblasts: novel insights into the molecular mechanisms of Bax-induced apoptosis.	Lysine	28-34	BCL2-associated X protein	Mus musculus	62-65
20885444-0	2011	Single-point mutations of a lysine residue change function of Bax and Bcl-xL expressed in Bax- and Bak-less mouse embryonic fibroblasts: novel insights into the molecular mechanisms of Bax-induced apoptosis.	Lysine	28-34	BCL2-associated X protein	Mus musculus	90-93
20885444-0	2011	Single-point mutations of a lysine residue change function of Bax and Bcl-xL expressed in Bax- and Bak-less mouse embryonic fibroblasts: novel insights into the molecular mechanisms of Bax-induced apoptosis.	Lysine	28-34	BCL2-associated X protein	Mus musculus	90-93
20885444-4	2011	Mutation of Bax at lysine 128 (BaxK128E) abrogated its effects on Kv1.3 and the induction of apoptotic changes in mitochondria.	Lysine	19-25	BCL2-associated X protein	Mus musculus	12-15
20885444-9	2011	Both wild-type Bax and BaxK128E can form similar ion-conducting pores upon incorporation into planar lipid bilayers.	Lipid Bilayers	101-115	BCL2-associated X protein	Mus musculus	15-18
21185940-6	2011	It lowered levels of cyclin kinase inhibitor p21, affected G1 to S phase cell cycle transition; partially blocked the elevation in p53 transcriptional activity, p21 and Bcl-2-associated X protein (Bax) levels caused by bleomycin, but had no influence on enhancement of Bax in response to staurosporine.	Bleomycin	219-228	BCL2-associated X protein	Mus musculus	169-195
20964710-8	2011	Silymarin/melatonin attenuated the increases in lipid peroxidation, number of degenerating neurons, nitrite content, mRNA expressions of cytochrome P-450 2E1 (CYP2E1) and GSTA4-4, catalytic activities of CYP2E1 and GST and P-p53, Bax and caspase 9 protein expressions.	Silymarin	0-9	BCL2-associated X protein	Mus musculus	230-233
20964710-8	2011	Silymarin/melatonin attenuated the increases in lipid peroxidation, number of degenerating neurons, nitrite content, mRNA expressions of cytochrome P-450 2E1 (CYP2E1) and GSTA4-4, catalytic activities of CYP2E1 and GST and P-p53, Bax and caspase 9 protein expressions.	Melatonin	10-19	BCL2-associated X protein	Mus musculus	230-233
21185940-6	2011	It lowered levels of cyclin kinase inhibitor p21, affected G1 to S phase cell cycle transition; partially blocked the elevation in p53 transcriptional activity, p21 and Bcl-2-associated X protein (Bax) levels caused by bleomycin, but had no influence on enhancement of Bax in response to staurosporine.	Bleomycin	219-228	BCL2-associated X protein	Mus musculus	197-200
21074598-7	2011	The levels of the pro-apoptotic proteins p53 and Bax and the anti-apoptotic protein Bcl-xL were significantly increased in Dox-treated mice compared with the control group.	Doxorubicin	123-126	BCL2-associated X protein	Mus musculus	49-52
21115635-7	2011	SV40 immortalized mouse embryonic fibroblasts derived from Bax-Bak double-knockout mice were significantly more resistant to GL-induced cell killing compared with wild-type cells.	guggulu extract	125-127	BCL2-associated X protein	Mus musculus	59-62
20671748-8	2011	Therefore, we propose that Bcl-xL/Bax H5 disturbs mitochondrial morphology by binding and inhibiting Mfn1 and Mfn2 activity, supporting the hypothesis that Bcl-2 family members have the capacity to regulate mitochondrial morphology through binding to the mitofusins in healthy cells.	mitofusins	255-265	BCL2-associated X protein	Mus musculus	34-37
21245196-7	2011	Moreover, this Bax-derived "poropeptide" produced effective tumor regression after peritumoral injection in a nude mouse xenograft model.	peritumoral	83-94	BCL2-associated X protein	Mus musculus	15-18
19851711-8	2011	Furthermore, TA treatment significantly increased the number of apoptotic cells and pro-apoptotic markers c-PARP and Bax confirming the activation of apoptotic pathways.	tolfenamic acid	13-15	BCL2-associated X protein	Mus musculus	117-120
21092747-10	2011	Our results suggest that polyglutamine-expanded ataxin-3 upregulates mRNA expression of Bax and PUMA and causes apoptotic death of affected neurons by enhancing phosphorylation and transcriptional activity of p53.	polyglutamine	25-38	BCL2-associated X protein	Mus musculus	88-91
21428210-7	2011	The results suggested that p38MAPK mediates high glucose induced osteoblast apoptosis, partly through modulating the expressions of caspase-3, bax and bcl-2.	Glucose	49-56	BCL2-associated X protein	Mus musculus	143-146
21609313-0	2011	Oleanolic acid induces apoptosis by modulating p53, Bax, Bcl-2 and caspase-3 gene expression and regulates the activation of transcription factors and cytokine profile in B16F.	Oleanolic Acid	0-14	BCL2-associated X protein	Mus musculus	52-55
21092747-0	2011	p53 activation mediates polyglutamine-expanded ataxin-3 upregulation of Bax expression in cerebellar and pontine nuclei neurons.	polyglutamine	24-37	BCL2-associated X protein	Mus musculus	72-75
21092747-3	2011	Polyglutamine-expanded ataxin-3-Q79 caused apoptotic death of cerebellar and pontine nuclei neurons by upregulating mRNA expression of pro-apoptotic Bax and activating mitochondria-mediated apoptotic cascade.	polyglutamine	0-13	BCL2-associated X protein	Mus musculus	149-152
21247434-6	2011	The present study analyzed the interaction of calmodulin with the BH3 sequence of Bax, and the calmodulin-binding sequence of myristoylated alanine-rich C-kinase substrate in the presence of xanthurenic acid in primary retinal epithelium cell cultures and murine epithelial fibroblast cell lines transformed with SV40 (wild type [WT], Bid knockout [Bid-/-], and Bax-/-/Bak-/- double knockout [DKO]).	BH 3	66-69	BCL2-associated X protein	Mus musculus	82-85
21471712-5	2011	The deltonin treatment caused a noticeable apoptosis in tumor tissue, which associated with increased levels of Bax, activated caspase-3, caspase-9, and cleaved poly (ADPribose) polymerase, decreased pro-caspase-8, pro-caspase-9, Bcl-2 expression levels and extracellular signal-regulated kinase-1/2 activity; and dose-dependently inhibit angiogenesis.	deltonin	4-12	BCL2-associated X protein	Mus musculus	112-115
21957577-7	2011	More significant antiapoptotic action of alpha-tocoferoli acetate in stress condition in young mice is obviously connected with quick reaction of compensatory mechanisms (low expression of proapoptotic proteins p53, Bax and high expression of antiapoptotic protein Bcl-2).	alpha-tocoferoli acetate	41-65	BCL2-associated X protein	Mus musculus	216-219
21963495-6	2011	Moreover, the augmented expressions of apoptosis-related proteins, Bax and cytochrome c, were down-regulated by morroniside administration.	morroniside	112-123	BCL2-associated X protein	Mus musculus	67-70
21846192-8	2011	CONCLUSIONS: MIH not only promotes the tumour-cell killing effect of radiotherapy through Bax-mediated cell death, but also improves cellular immunity in mice under radiotherapy and decreases the potential of radiotherapy to enhance MMP-9 expression, which leads to significant improvement in lung metastasis and overall survival of mice under combined treatment of MIH and R. This study is the first to have explored the effect of combined hyperthermia and radiotherapy on tumour metastasis and the underlying mechanisms.	Procarbazine	13-16	BCL2-associated X protein	Mus musculus	90-93
21609313-4	2011	The apoptotic genes p53, BAX, caspase-9, and caspase-3 were found upregulated in oleanolic acid-treated cells, whereas the antiapoptotic gene Bcl-2 was downregulated.	Oleanolic Acid	81-95	BCL2-associated X protein	Mus musculus	25-28
21282935-11	2011	In contrast, Bax expression was decreased in the MS-IPA1-treated cell as compared to that in the vehicle-treated cells.	ipa1	52-56	BCL2-associated X protein	Mus musculus	13-16
21850191-8	2011	RESULTS: WB experiments and luciferase reporter assays showed that NF-kappaB-inducible BCL2-associated X protein (Bax) and a pro-apoptotic factor, activated caspase 3 were expressed in the retina of p50-deficient mice as well as NMDA-treated RGC-5 cells.	N-Methylaspartate	229-233	BCL2-associated X protein	Mus musculus	87-112
21799245-10	2011	4-O-methylhonokiol treatment also prevented neuronal cell death in the AbetaPPsw mousee brain through inactivation of caspase-3 and BAX.	4-O-methylhonokiol	0-18	BCL2-associated X protein	Mus musculus	132-135
21850191-8	2011	RESULTS: WB experiments and luciferase reporter assays showed that NF-kappaB-inducible BCL2-associated X protein (Bax) and a pro-apoptotic factor, activated caspase 3 were expressed in the retina of p50-deficient mice as well as NMDA-treated RGC-5 cells.	N-Methylaspartate	229-233	BCL2-associated X protein	Mus musculus	114-117
21346313-6	2011	Moreover, we demonstrated that both iron chelators were able to decrease TDP-43 protein aggregation and the proapoptotic molecule Bax, and to enhance antiapoptotic protein Bcl-2 expression, in the ALS mice.	Iron	36-40	BCL2-associated X protein	Mus musculus	130-133
22205977-6	2011	While Idebenone acts by downregulating the integrated stress response, Resveratrol acts by attenuating apoptosis at the level of Bax.	Resveratrol	71-82	BCL2-associated X protein	Mus musculus	129-132
21799745-5	2011	While 14-3-3s can inhibit many pro-apoptotic factors, we demonstrate that inhibition of one factor in particular, Bax, is important to 14-3-3s" protection against rotenone toxicity in dopaminergic cells.	Rotenone	163-171	BCL2-associated X protein	Mus musculus	114-117
21799745-7	2011	Pharmacological inhibition or shRNA knockdown of Bax provided protection against rotenone, comparable to 14-3-3theta"s neuroprotective effects.	Rotenone	81-89	BCL2-associated X protein	Mus musculus	49-52
21434306-7	2011	CONCLUSION: GPC could suppressing the expression of Caspase-3 and Bax in the liver of mice with ethanol-induced liver injury.	Ethanol	96-103	BCL2-associated X protein	Mus musculus	66-69
21084837-7	2011	Using the dopamine neuron specific promoter Pdat-1, we also show that expression of the murine BAX, a pro-apoptotic member of the Bcl-2 family, causes dopamine neuron destruction in the nematode.	Dopamine	10-18	BCL2-associated X protein	Mus musculus	95-98
21084837-7	2011	Using the dopamine neuron specific promoter Pdat-1, we also show that expression of the murine BAX, a pro-apoptotic member of the Bcl-2 family, causes dopamine neuron destruction in the nematode.	Dopamine	151-159	BCL2-associated X protein	Mus musculus	95-98
21084837-8	2011	However, co-expression of PrP inhibits BAX-mediated dopamine neuron degeneration, demonstrating for the first time that PrP has anti-BAX activity in living animals.	Dopamine	52-60	BCL2-associated X protein	Mus musculus	39-42
21434306-0	2011	[Effect of grape procyanidins on expressions of Caspase-3 and Bax in ethanol-induced liver injury in mice].	Proanthocyanidins	17-29	BCL2-associated X protein	Mus musculus	62-65
21434306-0	2011	[Effect of grape procyanidins on expressions of Caspase-3 and Bax in ethanol-induced liver injury in mice].	Ethanol	69-76	BCL2-associated X protein	Mus musculus	62-65
21209944-6	2010	In xenografted tumors, resveratrol upregulated the expressions of TRAIL-R1/DR4, TRAIL-R2/DR5, Bax and p27(/KIP1), and inhibited the expression of Bcl-2 and cyclin D1.	Resveratrol	23-34	BCL2-associated X protein	Mus musculus	94-97
21434306-1	2011	OBJECTIVE: To study the effect of grape procyanidins (GPC) on the expressions of Caspase-3 and Bax in the liver of mice with ethanol-induced liver injury.	Proanthocyanidins	40-52	BCL2-associated X protein	Mus musculus	95-98
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Oxidopamine	106-112	BCL2-associated X protein	Mus musculus	61-64
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Oxidopamine	106-112	BCL2-associated X protein	Mus musculus	66-69
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Oxidopamine	106-112	BCL2-associated X protein	Mus musculus	66-69
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Dopamine	110-112	BCL2-associated X protein	Mus musculus	61-64
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Dopamine	110-112	BCL2-associated X protein	Mus musculus	66-69
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Dopamine	110-112	BCL2-associated X protein	Mus musculus	66-69
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Oxidopamine	187-193	BCL2-associated X protein	Mus musculus	61-64
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Oxidopamine	187-193	BCL2-associated X protein	Mus musculus	66-69
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Oxidopamine	187-193	BCL2-associated X protein	Mus musculus	66-69
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Dopamine	121-123	BCL2-associated X protein	Mus musculus	61-64
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Dopamine	121-123	BCL2-associated X protein	Mus musculus	66-69
22043283-5	2011	However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation.	Dopamine	121-123	BCL2-associated X protein	Mus musculus	66-69
22043283-6	2011	On the other hand, DA neurons that survived in Bax-KO mice exhibited marked neuronal atrophy, without significant improvement of PD-related behavioral deficits.	Dopamine	19-21	BCL2-associated X protein	Mus musculus	47-50
20868657-3	2010	Furthermore, we investigated whether feeding a diet of n-3 PUFA ethyl-eicosapentaenoate (E-EPA) to these mice can attenuate the MPP(+) induced changes in brain PUFA content and expression of cPLA2 and COX-2, and attenuate MPP(+) induced changes in neurotransmitters and metabolites and apoptotic markers, bax, bcl-2 and caspase-3.	Nitrogen	17-18	BCL2-associated X protein	Mus musculus	305-308
20850421-5	2010	The molecular mechanisms involved in baicalein-induced inhibition of d-GalN/LPS-caused apoptosis were associated with the protection of mitochondria, increasing the Bcl-2/Bax ratio, blocking the release of cytochrome c, and suppressing the phosphorylation of IkappaBalpha, ERK and JNK.	baicalein	37-46	BCL2-associated X protein	Mus musculus	171-174
20868657-8	2010	More importantly, E-EPA attenuated the MPP(+) induced increase in n-6 fatty acids content, partially attenuated the striatal dopaminergic turnover, and prevented the increases of pro-apoptotic bax and caspase-3 mRNAs.	eicosapentaenoic acid ethyl ester	18-23	BCL2-associated X protein	Mus musculus	193-196
21127253-4	2010	Genetic deletion of Bid, Bim, and Puma prevented the homo-oligomerization of BAX and BAK, and thereby cytochrome c-mediated activation of caspases in response to diverse death signals in neurons and T lymphocytes, despite the presence of other BH3-only molecules.	BH 3	244-247	BCL2-associated X protein	Mus musculus	77-80
20937379-7	2010	Paraquat promoted overt apoptosis and ER stress as evidenced by increased caspase-3 activity, apoptosis, and ER stress markers including Bax, Bcl-2, GADD153, calregulin, and phosphorylated JNK, IRE1alpha, and eIF2alpha; all were ablated by the catalase transgene.	Paraquat	0-8	BCL2-associated X protein	Mus musculus	137-140
20889222-8	2010	Exendin-4 down-regulated caspase 3 activity, reduced cytochrome c levels in cytoplasm, and increased Bcl-2 protein levels and the Bcl-2 to Bax ratio in dexamethasone-treated beta-cells.	Dexamethasone	152-165	BCL2-associated X protein	Mus musculus	139-142
26760337-3	2010	Antiapoptotic members of the Bcl-2 family (B cell CLL/lymphoma 2), that belong to the intrinsic route of the activation of caspases, such as Bcl-xL (extra-large B-cell lymphoma) and Bcl-w (Bcl-2-like 2), act predominantly to prevent that pro-apoptotic members, such as Bax (Bcl-2-associated X protein) and Bak (Bcl-2 relative bak) lead to cell death.	bakuchiol	326-329	BCL2-associated X protein	Mus musculus	269-272
26760337-3	2010	Antiapoptotic members of the Bcl-2 family (B cell CLL/lymphoma 2), that belong to the intrinsic route of the activation of caspases, such as Bcl-xL (extra-large B-cell lymphoma) and Bcl-w (Bcl-2-like 2), act predominantly to prevent that pro-apoptotic members, such as Bax (Bcl-2-associated X protein) and Bak (Bcl-2 relative bak) lead to cell death.	bakuchiol	326-329	BCL2-associated X protein	Mus musculus	274-309
20980646-11	2010	The oxLDL-induced alterations in levels of Bcl-2, Bax, and cytochrome c were completely normalized by resveratrol.	Resveratrol	102-113	BCL2-associated X protein	Mus musculus	50-53
21123558-0	2010	Bax regulates production of superoxide in both apoptotic and nonapoptotic neurons: role of caspases.	Superoxides	28-38	BCL2-associated X protein	Mus musculus	0-3
21123558-1	2010	A Bax- and, apparently, mitochondria-dependent increase in superoxide (O(2)( -)) and other reactive oxygen species (ROS) occurs in apoptotic superior cervical ganglion (SCG) and cerebellar granule (CG) neurons.	Superoxides	59-69	BCL2-associated X protein	Mus musculus	2-5
21123558-1	2010	A Bax- and, apparently, mitochondria-dependent increase in superoxide (O(2)( -)) and other reactive oxygen species (ROS) occurs in apoptotic superior cervical ganglion (SCG) and cerebellar granule (CG) neurons.	Superoxides	71-75	BCL2-associated X protein	Mus musculus	2-5
21123558-1	2010	A Bax- and, apparently, mitochondria-dependent increase in superoxide (O(2)( -)) and other reactive oxygen species (ROS) occurs in apoptotic superior cervical ganglion (SCG) and cerebellar granule (CG) neurons.	Reactive Oxygen Species	91-114	BCL2-associated X protein	Mus musculus	2-5
21123558-1	2010	A Bax- and, apparently, mitochondria-dependent increase in superoxide (O(2)( -)) and other reactive oxygen species (ROS) occurs in apoptotic superior cervical ganglion (SCG) and cerebellar granule (CG) neurons.	Reactive Oxygen Species	116-119	BCL2-associated X protein	Mus musculus	2-5
21123558-2	2010	Here we show that Bax also lies upstream of ROS produced in nonapoptotic neurons and present evidence that caspases partially mediate the pro-oxidant effect of Bax.	Reactive Oxygen Species	44-47	BCL2-associated X protein	Mus musculus	18-21
21123558-3	2010	We used the O(2)( -)-sensitive dye MitoSOX to monitor O(2)( -) in neurons expressing different levels of Bax and mitochondrial superoxide dismutase (SOD2).	Superoxides	12-16	BCL2-associated X protein	Mus musculus	105-108
21123558-10	2010	These data indicate that Bax lies upstream of most O(2)( -) produced in neurons, that caspase 3 is required for increased O(2)( -) production during neuronal apoptosis, that caspase 3 is partially involved in O(2)( -) production in nonapoptotic neurons, and that other caspases may also be involved in Bax-dependent O(2)( -) production in nonapoptotic cells.	Superoxides	51-55	BCL2-associated X protein	Mus musculus	25-28
21123558-10	2010	These data indicate that Bax lies upstream of most O(2)( -) produced in neurons, that caspase 3 is required for increased O(2)( -) production during neuronal apoptosis, that caspase 3 is partially involved in O(2)( -) production in nonapoptotic neurons, and that other caspases may also be involved in Bax-dependent O(2)( -) production in nonapoptotic cells.	Superoxides	51-59	BCL2-associated X protein	Mus musculus	25-28
20718735-4	2010	KEY RESULTS: We demonstrated that carboplatin initiated an intrinsic apoptotic pathway of activating caspase-3 and -9, accompanied by a decrease in the ratio of Bcl-XL/Bax and a significant increase in Bcl-XS.	Carboplatin	34-45	BCL2-associated X protein	Mus musculus	168-171
20655905-7	2010	Both mitochondrion-dependent and endoplasmic reticulum stress-induced apoptotic pathways were also activated in the hearts of doxorubicin-treated mice as reflected by decreased Bcl-2/Bcl-(XL) and elevated Bax/Bad, p53/Apaf-1, endoplasmic reticulum glucose-related protein 78, C/EBP homologous protein, cytochrome c release from mitochondria, caspases-9/-3 cleavage, and cardiomyocyte apoptosis.	Doxorubicin	126-137	BCL2-associated X protein	Mus musculus	205-208
20813173-11	2010	In addition, pubertal BPA exposure upregulated the level of Bax and active caspase-9 in testes.	bisphenol A	22-25	BCL2-associated X protein	Mus musculus	60-63
20494511-4	2010	Mechanistic studies showed that ATA could induce significant reactive oxygen species (ROS) generation, Bax translocation to mitochondria, resulting in mitochondria damage, cytochrome c release, caspase-3 activation and apoptotic cell death.	acetyltanshinone IIA	32-35	BCL2-associated X protein	Mus musculus	103-106
20494511-8	2010	ROS-mediated Bax activation should be the mechanism by which ATA induces apoptosis and inhibits tumor growth.	Reactive Oxygen Species	0-3	BCL2-associated X protein	Mus musculus	13-16
20708296-7	2010	Furthermore, overexpression of TIP47 facilitated Bcl-2 expression and suppressed Bax expression in taxol-treated cells.	Paclitaxel	99-104	BCL2-associated X protein	Mus musculus	81-84
20845518-6	2010	Cell cycle analysis revealed a decreased proportion of cells in G0/G1 phase, with arrest at S. Paeonol treatment in gastric cancer cell line MFC and SGC-790 cells significantly reduced the expression of Bcl-2 and increased the expression of Bax in a concentration-related manner.	paeonol	95-102	BCL2-associated X protein	Mus musculus	241-244
20651282-8	2010	By using primary cultured macrophages, we further showed that unesterified free cholesterol derived from incorporated denatured low-density lipoprotein was accumulated in the ER and induced ER stress-mediated apoptosis in a CHOP-Bcl2-associated X protein (Bax) pathway-dependent manner.	Cholesterol	80-91	BCL2-associated X protein	Mus musculus	224-254
20651282-8	2010	By using primary cultured macrophages, we further showed that unesterified free cholesterol derived from incorporated denatured low-density lipoprotein was accumulated in the ER and induced ER stress-mediated apoptosis in a CHOP-Bcl2-associated X protein (Bax) pathway-dependent manner.	Cholesterol	80-91	BCL2-associated X protein	Mus musculus	256-259
20876793-7	2010	Mechanistically, gamitrinibs, but not 17-AAG, induced acute mitochondrial dysfunction in prostate cancer cells with loss of organelle membrane potential, release of cytochrome c, and caspase activity, independently of proapoptotic Bcl-2 proteins Bax and Bak.	gamitrinibs	17-28	BCL2-associated X protein	Mus musculus	246-249
20738751-9	2010	Caspase 8, caspase 3, Bax, Bid increase expression and more TUNEL positive cells in both experimental groups than control, suggest that apoptosis induced by fluoride is related to oxidative stress due to reduction of the enzymatic antioxidant.	Fluorides	157-165	BCL2-associated X protein	Mus musculus	22-25
20558151-9	2010	Also, the increased ratio of Bax and Bcl-2 protein was significantly attenuated by gentiopicroside.	gentiopicroside	83-98	BCL2-associated X protein	Mus musculus	29-32
20121342-7	2010	Importantly, MtFt strongly inhibited mitochondrial damage, decreased production of the reactive oxygen species and lipid peroxidation, and dramatically rescued apoptosis by regulating Bcl-2, Bax and caspase-3 pathways.	mtft	13-17	BCL2-associated X protein	Mus musculus	191-194
20566416-1	2010	The ability of cisplatin (cis-diaminedichloroplatinum-II) to induce DNA double-strand breaks and expression of p53, Bax and Bcl-2 and possible protective effects of L-ascorbic acid was investigated in epididymis.	Cisplatin	26-56	BCL2-associated X protein	Mus musculus	116-119
20566416-9	2010	p53 expression was reduced in groups III and V. Bcl-2 staining was weakly positive in all groups except groups III and V. In conclusion, cisplatin induces structural changes, oxidative stress, irreparable DNA double-strand breaks bearing duplex 3" dT overhangs and 5" P-blunt ends in a Bax-dependent manner, but L-ascorbic acid has little, if any, preventive effects on cisplatin-induced epididymal damage.	Cisplatin	137-146	BCL2-associated X protein	Mus musculus	286-289
20566416-0	2010	Cisplatin induces duplex 3" overhangs and 5" blunt ends in epididymal epithelium in a Bax-dependent manner without any protection from L-ascorbic acid.	Cisplatin	0-9	BCL2-associated X protein	Mus musculus	86-89
20796191-11	2010	Our results also demonstrated that chalcone 8 promoted a modification in Bax:Bcl-2 ratio and increased p53 expression and caspase-3 activation.	Chalcone	35-43	BCL2-associated X protein	Mus musculus	73-76
20566416-1	2010	The ability of cisplatin (cis-diaminedichloroplatinum-II) to induce DNA double-strand breaks and expression of p53, Bax and Bcl-2 and possible protective effects of L-ascorbic acid was investigated in epididymis.	Cisplatin	15-24	BCL2-associated X protein	Mus musculus	116-119
20796191-12	2010	CONCLUSIONS: The studied chalcone 8 has cytotoxic effect against L-1210 lymphoblastic leukaemic cells, and this effect is associated with increase of p-53 and Bax expression.	Chalcone	25-33	BCL2-associated X protein	Mus musculus	159-162
20803734-5	2010	Western blot analysis revealed that repeated ethanol treatment decreased the expression of steroidogenic acute regulatory protein (StAR), 3 beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17beta-HSD); increased the expression of active caspase-3, p53, Fas and Fas-L; and led to up-regulation of Bax/Bcl-2 ratio and translocation of cytochrome c from mitochondria to cytosol in testis.	Ethanol	45-52	BCL2-associated X protein	Mus musculus	335-338
20673169-9	2010	On the other hand, the administration of SCLM (100 mg/kg) and fluoxetine (20 mg/kg) reversed these effects induced by CMS, showing a significant increase of sucrose intake and a dramatic reduction of TUNEL-positive neurons and decreased expression of Bax and caspase-3 proteins.	sclm	41-45	BCL2-associated X protein	Mus musculus	251-254
21141502-6	2010	RESULT: Average optical density analysis indicated that, compared to the normal group, 0.03 mmol x L(-1) gentamycin could significantly activate Caspase-9 and Caspase-3, downregulate the ratio of Bcl-2 and Bax protein expression.	Gentamicins	105-115	BCL2-associated X protein	Mus musculus	206-209
20546728-0	2010	Polyglutamine-expanded ataxin-7 upregulates Bax expression by activating p53 in cerebellar and inferior olivary neurons.	polyglutamine	0-13	BCL2-associated X protein	Mus musculus	44-47
20546728-3	2010	Mutant polyglutamine ataxin-7 activated mitochondrial apoptotic pathway and induced apoptotic death of cerebellar and inferior olivary neurons by upregulating mRNA expression of proapoptotic Bax.	polyglutamine	7-20	BCL2-associated X protein	Mus musculus	191-194
20546728-5	2010	Cellular and animal models of SCA7 were used to test the hypothesis that polyglutamine-expanded ataxin-7-Q52 upregulates Bax expression of cerebellar and inferior olivary neurons by enhancing transcriptional activity of p53.	polyglutamine	73-86	BCL2-associated X protein	Mus musculus	121-124
20546728-9	2010	Our study provides the evidence that polyglutamine-expanded ataxin-7 upregulates the expression of Bax and Puma and causes apoptotic neuronal death by enhancing phosphorylation and transcriptional activity of p53.	polyglutamine	37-50	BCL2-associated X protein	Mus musculus	99-102
20803734-7	2010	The present study has indicated that the ethanol treatment induced apoptosis in the mouse testis through the increased expression of Fas/Fas-L and p53, up-regulation of Bax/Bcl-2 ratio, cytosolic translocation of cytochrome c along with caspase-3 activation and glutathione depletion.	Ethanol	41-48	BCL2-associated X protein	Mus musculus	169-172
20550194-11	2010	More importantly, the similar disruption of Bcl-2/Bax was found in S1-gamma-CD treated mice and free S1 treated ones.	gamma-cyclodextrin	70-78	BCL2-associated X protein	Mus musculus	50-53
20354138-6	2010	Moreover, the exposure to pyrimidine derivatives induces apoptosis, assayed by the supravital propidium iodide assay, through modulation of the apoptotic proteins Bax and Bcl2, and inhibits tumor growth in vivo in a mouse model.	pyrimidine	26-36	BCL2-associated X protein	Mus musculus	163-166
20354138-6	2010	Moreover, the exposure to pyrimidine derivatives induces apoptosis, assayed by the supravital propidium iodide assay, through modulation of the apoptotic proteins Bax and Bcl2, and inhibits tumor growth in vivo in a mouse model.	supravital propidium iodide	83-110	BCL2-associated X protein	Mus musculus	163-166
20431251-5	2010	Progesterone (10(-6) M) in the presence or absence of TGF-beta1 diminished the ratio Bax/Bcl-2.	Progesterone	0-12	BCL2-associated X protein	Mus musculus	85-88
20673169-9	2010	On the other hand, the administration of SCLM (100 mg/kg) and fluoxetine (20 mg/kg) reversed these effects induced by CMS, showing a significant increase of sucrose intake and a dramatic reduction of TUNEL-positive neurons and decreased expression of Bax and caspase-3 proteins.	Fluoxetine	62-72	BCL2-associated X protein	Mus musculus	251-254
20495354-6	2010	Bortezomib caused a decrease in the expression of the antiapoptotic protein Bcl-2, and an increase in the proapoptotic protein Bax and in p53.	Bortezomib	0-10	BCL2-associated X protein	Mus musculus	127-130
20431057-12	2010	Lactacystin (lac) pretreatment of preconditioned hearts increased Bax by 140% (P&lt;0.05) and also increased ubiquitinated proteins.	lactacystin	0-11	BCL2-associated X protein	Mus musculus	66-69
20537511-13	2010	Eugenol treatment led to the downregulation of c-Myc, H-ras and Bcl2 expression along with upregulation of P53, Bax and active Caspase-3 expression in the skin lesions.	Eugenol	0-7	BCL2-associated X protein	Mus musculus	112-115
20395372-6	2010	Rottlerin, a pharmacologic inhibitor of PKC-delta, suppressed albumin-induced Bax translocation, cytochrome c release, and apoptosis.	rottlerin	0-9	BCL2-associated X protein	Mus musculus	78-81
20353770-4	2010	Results showed a massive impairment of erythropoiesis early post paclitaxel administration (1-2 days), which involved induction of high Bax/Bcl-x(L) ratio, caspase-3 activation, disruptions of the medullar niche and cell death by both apoptosis and necrosis.	Paclitaxel	65-75	BCL2-associated X protein	Mus musculus	136-139
20431057-12	2010	Lactacystin (lac) pretreatment of preconditioned hearts increased Bax by 140% (P&lt;0.05) and also increased ubiquitinated proteins.	lactacystin	13-16	BCL2-associated X protein	Mus musculus	66-69
20363884-9	2010	Further studies indicated that the Dox-induced higher levels of Hsp25 transactivated p53 leading to higher levels of the pro-apoptotic protein Bax, but other p53-related proteins remained unaltered.	Doxorubicin	35-38	BCL2-associated X protein	Mus musculus	143-146
20363884-11	2010	From these results we propose a novel mechanism for Dox-induced heart failure: increased expression of Hsp25 because of oxidant-induced activation of HSF-1 transactivates p53 to increase Bax levels, which leads to heart failure.	Doxorubicin	52-55	BCL2-associated X protein	Mus musculus	187-190
19951366-5	2010	These data were further supported by transfection of a mouse Bax (mBax) mutant, whose BH3 was replaced by the mBNIP-21 BH3-like domain.	BH 3	86-89	BCL2-associated X protein	Mus musculus	61-64
20370565-4	2010	Deferoxamine treatment 30 min before and 1 and 6 h after the SCI significantly reduced: (1) GFAP immunoreactivity, (2) neutrophil infiltration, (3) NF-kappaB activation, (4) iNOS expression, (5) nitrotyrosine and MDA formation, (6) DNA damage (methyl green pyronin staining and PAR formation and (7) apoptosis (TUNEL staining, FasL, Bax and Bcl-2 expression, S-100 expression).	Deferoxamine	0-12	BCL2-associated X protein	Mus musculus	333-336
20153410-12	2010	The mRNA levels of proteins in apoptotic signaling, including p53, mdm-2, Bax, Bad, and caspase-3 were increased in mice after exposure to MeHgCl.	methylmercuric chloride	139-145	BCL2-associated X protein	Mus musculus	74-77
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	125-128	BCL2-associated X protein	Mus musculus	335-338
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	223-226	BCL2-associated X protein	Mus musculus	335-338
20512926-7	2010	Further investigation revealed that cystamine significantly decreased the levels of apoptotic Bax and Apaf-1 and the activity of caspase-3, and increased the levels of anti-apoptotic Bcl-2 in APM.	Cystamine	36-45	BCL2-associated X protein	Mus musculus	94-97
20070537-5	2010	RESULTS: Intracellular Bax detection was significantly decreased in animals fed with modified diets, particularly in those treated with copper-depleted diets.	Copper	136-142	BCL2-associated X protein	Mus musculus	23-26
20074638-2	2010	Here we show that in adult mouse cardiomyocytes, DOX activates (i) the pro-apoptotic p53, (ii) p38MAPK and JNK, (iii) Bax translocation, (iv) cytochrome c release, and (v) caspase 3.	Doxorubicin	49-52	BCL2-associated X protein	Mus musculus	118-121
19951366-5	2010	These data were further supported by transfection of a mouse Bax (mBax) mutant, whose BH3 was replaced by the mBNIP-21 BH3-like domain.	BH 3	86-89	BCL2-associated X protein	Mus musculus	66-70
19759125-7	2010	The apoptotic effect of MK801-induced BAX expression, mitochondrial potential collapse and caspase-9 activation.	Dizocilpine Maleate	24-29	BCL2-associated X protein	Mus musculus	38-41
20172858-12	2010	By establishing a unique role for BAK in long-chain ceramide metabolism, these studies further demonstrate that the seemingly redundant proteins BAK and BAX have distinct mechanisms of action during apoptosis induction.	Ceramides	52-60	BCL2-associated X protein	Mus musculus	153-156
19759125-8	2010	In vivo Bax small interfering ribonucleic acid and a caspase-9 inhibitor abrogated MK801-induced apoptosis and pyknotic nucleus formation.	Dizocilpine Maleate	83-88	BCL2-associated X protein	Mus musculus	8-11
20116082-10	2010	In comparison with the control cells, the SDT-treated cells showed obvious cytochrome-c and Bax translocations, caspase activation, Bax expression, and PARP cleavage at 1h after SDT-treatment.	3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione	42-45	BCL2-associated X protein	Mus musculus	92-95
20116082-10	2010	In comparison with the control cells, the SDT-treated cells showed obvious cytochrome-c and Bax translocations, caspase activation, Bax expression, and PARP cleavage at 1h after SDT-treatment.	3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione	42-45	BCL2-associated X protein	Mus musculus	132-135
20069556-6	2010	Exposure of capsaicin also causes increased accumulation of ubiquitinated proteins as wells as various target substrates of proteasome like p53 and Bax and p27.	Capsaicin	12-21	BCL2-associated X protein	Mus musculus	148-151
20154710-8	2010	Moreover, FLZ showed neuroprotective effects on neuronal apoptosis by increasing the Bcl-2/Bax ratio and decreasing the active caspase-3 fragment/caspase-3 ratio in the hippocampus of APP/PS1 mice.	flz	10-13	BCL2-associated X protein	Mus musculus	91-94
19629484-8	2010	Western blot analysis also showed the same pattern of chemoprevention with [6]-gingerol treatment increasing the B[a]P suppressed p53 levels, also evident by immunohistochemistry, and Bax while decreasing the expression of Bcl-2 and Survivin.	gingerol	75-87	BCL2-associated X protein	Mus musculus	184-187
20179769-3	2010	Accumulating evidence now indicate that the binding of tBid initiates an ordered sequences of events that prime mitochondria from the action of Bax and Bak: (1) tBid interacts with mitochondria via a specific binding to cardiolipin (CL) and immediately disturbs mitochondrial structure and function idependently of its BH3 domain; (2) Then, tBid activates through its BH3 domain Bax and/or Bak and induces their subsequent oligomerization in mitochondrial membranes.	tBID	55-59	BCL2-associated X protein	Mus musculus	144-147
20163293-0	2010	Gynostemma pentaphyllum protects mouse male germ cells against apoptosis caused by zearalenone via Bax and Bcl-2 regulation.	Zearalenone	83-94	BCL2-associated X protein	Mus musculus	99-102
20163293-5	2010	Taken together, these results suggest that Gynostemma pentaphyllum protects against toxicity caused by Zearalenone through anti-oxidation and anti-apoptosis via the regulation of Bax and Bcl-2 expression.	Zearalenone	103-114	BCL2-associated X protein	Mus musculus	179-182
20175894-5	2010	Furthermore, carrageenan induced the expression of iNOS, nitrotyrosine and PARP, as well as induced apoptosis (TUNEL staining and Bax and Bcl-2 expression) in the lung tissues.	Carrageenan	13-24	BCL2-associated X protein	Mus musculus	130-133
19901272-2	2010	We previously reported that staurosporine (STS), a broad-spectrum kinase inhibitor and prototypical apoptosis-inducing agent, produced p53-dependent, Bax-dependent, neural precursor cell (NPC) apoptosis, but that this effect occurred independently of new gene transcription and PUMA expression.	Staurosporine	28-41	BCL2-associated X protein	Mus musculus	150-153
19901272-2	2010	We previously reported that staurosporine (STS), a broad-spectrum kinase inhibitor and prototypical apoptosis-inducing agent, produced p53-dependent, Bax-dependent, neural precursor cell (NPC) apoptosis, but that this effect occurred independently of new gene transcription and PUMA expression.	Staurosporine	43-46	BCL2-associated X protein	Mus musculus	150-153
19901272-5	2010	Confocal microscopy analysis of STS-treated cells revealed partial colocalization of p53 with the mitochondrial marker pyruvate dehydrogenase as well as with conformationally altered "activated" Bax, suggesting an interaction between these proapoptotic molecules in triggering apoptotic death.	Staurosporine	32-35	BCL2-associated X protein	Mus musculus	195-198
20195368-11	2010	Bax was higher in CR vs. AL mice (41%) and CR vs. AL females (52%).	Aluminum	25-27	BCL2-associated X protein	Mus musculus	0-3
20179769-3	2010	Accumulating evidence now indicate that the binding of tBid initiates an ordered sequences of events that prime mitochondria from the action of Bax and Bak: (1) tBid interacts with mitochondria via a specific binding to cardiolipin (CL) and immediately disturbs mitochondrial structure and function idependently of its BH3 domain; (2) Then, tBid activates through its BH3 domain Bax and/or Bak and induces their subsequent oligomerization in mitochondrial membranes.	tBID	55-59	BCL2-associated X protein	Mus musculus	379-382
20179769-3	2010	Accumulating evidence now indicate that the binding of tBid initiates an ordered sequences of events that prime mitochondria from the action of Bax and Bak: (1) tBid interacts with mitochondria via a specific binding to cardiolipin (CL) and immediately disturbs mitochondrial structure and function idependently of its BH3 domain; (2) Then, tBid activates through its BH3 domain Bax and/or Bak and induces their subsequent oligomerization in mitochondrial membranes.	tBID	161-165	BCL2-associated X protein	Mus musculus	144-147
20179769-3	2010	Accumulating evidence now indicate that the binding of tBid initiates an ordered sequences of events that prime mitochondria from the action of Bax and Bak: (1) tBid interacts with mitochondria via a specific binding to cardiolipin (CL) and immediately disturbs mitochondrial structure and function idependently of its BH3 domain; (2) Then, tBid activates through its BH3 domain Bax and/or Bak and induces their subsequent oligomerization in mitochondrial membranes.	tBID	161-165	BCL2-associated X protein	Mus musculus	144-147
19816507-6	2010	Furthermore, the BH3 mimetic ABT-737, which acts through Bax/Bak, also stimulates nuclear protein redistribution in a Bax/Bak-dependent manner.	BH 3	17-20	BCL2-associated X protein	Mus musculus	57-60
20179769-11	2010	These support the notion that tBid acts as a bifunctional molecule: first, it binds to mitochondrial CL via its helix alphaH6 and destabilizes mitochondrial structure and function, and then it promotes through its BH3 domain the activation and oligomerization of Bax and/or Bak, leading to cytochrome c release and execution of apoptosis.	tBID	30-34	BCL2-associated X protein	Mus musculus	263-266
20007710-5	2010	Here we show for the first time that treatment with 2% isoflurane for 6 h can increase pro-apoptotic factor Bax levels, decrease anti-apoptotic factor Bcl-2 levels, increase ROS accumulation, facilitate cytochrome c release from the mitochondria to the cytosol, induce activation of caspase-9 and caspase-3, and finally cause apoptosis as compared with the control condition.	Isoflurane	55-65	BCL2-associated X protein	Mus musculus	108-111
20007710-6	2010	We have further found that isoflurane can increase the mRNA levels of Bax and reduce the mRNA levels of Bcl-2.	Isoflurane	27-37	BCL2-associated X protein	Mus musculus	70-73
19085997-13	2010	The expression of p53 and Bax were also upregulated by TCDD and did not return to normal levels by PND 60.	Polychlorinated Dibenzodioxins	55-59	BCL2-associated X protein	Mus musculus	26-29
19219935-2	2010	This study was undertaken to determine effects of single oral 0, 25, 50, and 100 mg/kg body weight doses of potassium dichromate on the expression level of p53, Bcl-2, Bax, cytochrome c, and caspase-3, which are vital regulators of apoptosis, in mice liver.	Potassium Dichromate	108-128	BCL2-associated X protein	Mus musculus	168-171
19219935-3	2010	The results showed that Cr(VI) could upregulate the protein expression of p53, Bax, cytochrome c, and caspase-3 and downregulate the expression of Bcl-2 in mice liver.	Chromium	24-26	BCL2-associated X protein	Mus musculus	79-82
19816507-6	2010	Furthermore, the BH3 mimetic ABT-737, which acts through Bax/Bak, also stimulates nuclear protein redistribution in a Bax/Bak-dependent manner.	BH 3	17-20	BCL2-associated X protein	Mus musculus	118-121
19816507-6	2010	Furthermore, the BH3 mimetic ABT-737, which acts through Bax/Bak, also stimulates nuclear protein redistribution in a Bax/Bak-dependent manner.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	29-32	BCL2-associated X protein	Mus musculus	57-60
19816507-6	2010	Furthermore, the BH3 mimetic ABT-737, which acts through Bax/Bak, also stimulates nuclear protein redistribution in a Bax/Bak-dependent manner.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	29-32	BCL2-associated X protein	Mus musculus	118-121
20090911-8	2010	Myocardium from ethanol-treated mice displayed enhanced Bax, Caspase-3 and decreased Bcl-2 expression, the effect of which with the exception of Caspase-3 was augmented by ADH.	Ethanol	16-23	BCL2-associated X protein	Mus musculus	56-59
20423011-8	2010	The result showed that SP could down-regulate the expression of Ki-67, CyclinD1 and Bcl-2 protein, and up-regulate the expression of Bax protein.	sp	23-25	BCL2-associated X protein	Mus musculus	133-136
19819333-10	2010	The degree of staining for nitrotyrosine, iNOS, PAR, ICAM-1, P-selectin, Bax, Bcl-2 and FAS-ligand were markedly reduced in tissue sections obtained from zymosan-injected mice, which had received PD98059.	Zymosan	154-161	BCL2-associated X protein	Mus musculus	73-76
19699182-8	2010	Downregulation of Mcl-1 by small interfering RNA promoted Bax activation and cytochrome c and AIF release, suggesting that cisplatin-induced Mcl-1 depletion and associated Bax activation are involved in the release of AIF.	Cisplatin	123-132	BCL2-associated X protein	Mus musculus	58-61
19739150-7	2010	In addition, the free radical scavenger N-acetylcysteine dramatically attenuated arsenic-mediated ROS production and apoptosis, and exposure to arsenate increased Bax and decreased Bcl protein levels in MEMM cells.	arsenic acid	144-152	BCL2-associated X protein	Mus musculus	163-166
19699182-8	2010	Downregulation of Mcl-1 by small interfering RNA promoted Bax activation and cytochrome c and AIF release, suggesting that cisplatin-induced Mcl-1 depletion and associated Bax activation are involved in the release of AIF.	Cisplatin	123-132	BCL2-associated X protein	Mus musculus	172-175
19739150-8	2010	CONCLUSIONS: Taken together, these findings suggest that in MEMM cells arsenate-mediated oxidative injury acts as an early and upstream initiator of the cell death cascade, triggering cytotoxicity, mitochondrial dysfunction, altered Bcl/Bax protein ratios, and activation of caspase-9.	arsenic acid	71-79	BCL2-associated X protein	Mus musculus	237-240
20921820-7	2010	The expressions of Cdkn1a, Bax, and Ccng, which are well known as radioresponsive genes, were upregulated in WBI mice and Zn-yeast treated WBI mice.	Zinc	122-124	BCL2-associated X protein	Mus musculus	27-30
19796711-4	2010	Our data indicate that resveratrol contributes to inhibiting growth, inducing apoptosis and cell cycle arrest in the three leukemia cell lines (Jurkat, SUP-B15, and Kasumi-1), and reducing the phosphorylation of STAT3, meanwhile modulating the expression of Bcl-2 and Bax.	Resveratrol	23-34	BCL2-associated X protein	Mus musculus	268-271
20164595-4	2010	Here, we observed that the cells bearing high level of Abeta were more vulnerable than the controls to H2O2-induced apoptosis, and this effect of Abeta was associated with decrease of Bcl-2, elevation of Bax and cytosolic cytochrome-c, as well as activation of caspase-3, suggesting that Abeta could potentiate the oxidant-induced cell apoptosis with involvement of mitochondria-caspase-3 pathway.	Hydrogen Peroxide	103-107	BCL2-associated X protein	Mus musculus	204-207
19841471-0	2010	Cyanide-induced apoptosis of dopaminergic cells is promoted by BNIP3 and Bax modulation of endoplasmic reticulum-mitochondrial Ca2+ levels.	Cyanides	0-7	BCL2-associated X protein	Mus musculus	73-76
19841471-3	2010	Treatment of mice with cyanide up-regulated BNIP3 and Bax expression in tyrosine hydroxylase (TH)-positive cells of the substantia nigra, and progressive loss of TH-positive neurons was observed over a 9-day period.	Cyanides	23-30	BCL2-associated X protein	Mus musculus	54-57
19841471-6	2010	Cyanide also activated Bax to colocalize with BNIP3 in ER and mitochondria.	Cyanides	0-7	BCL2-associated X protein	Mus musculus	23-26
19841471-8	2010	Knockdown of Bax expression by small interfering RNA blocked the BNIP3-mediated changes in ER and mitochondrial Ca(2+) to block cyanide-induced mitochondrial dysfunction and cell death.	Cyanides	128-135	BCL2-associated X protein	Mus musculus	13-16
19841471-9	2010	These findings show that BNIP3-mediates cyanide-induced dopaminergic cell death through a Bax downstream signal that mobilizes ER Ca(2+) stores, followed by mitochondrial Ca(2+) overload.	Cyanides	40-47	BCL2-associated X protein	Mus musculus	90-93
19920074-2	2009	Here, we demonstrate that murine embryonic fibroblasts deficient for both Bak and Bax are, however, efficiently killed by thapsigargin, a specific inhibitor of ER Ca(2+) pumps that induces ER stress by depleting ER Ca(2+) stores.	Thapsigargin	122-134	BCL2-associated X protein	Mus musculus	82-85
19920074-3	2009	In the presence of Bak and Bax, thapsigargin eliminates cells by release of mitochondrial cytochrome c and subsequent caspase activation, which leads to the proteolytic inactivation of the molecular necrosis switch PARP-1 and results in apoptosis.	Thapsigargin	32-44	BCL2-associated X protein	Mus musculus	27-30
19920074-8	2009	Importantly, thapsigargin induces caspase-independent cell death also in colon and prostate carcinoma cells deficient in Bak and Bax expression.	Thapsigargin	13-25	BCL2-associated X protein	Mus musculus	129-132
19920074-6	2009	Moreover, in cells deficient for both Bak and Bax, thapsigargin induces permanent mitochondrial damage by Ca(2+) overload, permeability transition and membrane rupture.	Thapsigargin	51-63	BCL2-associated X protein	Mus musculus	46-49
19920074-9	2009	Therefore, targeted application of ER stressors such as thapsigargin might be a promising approach for the treatment of Bak- and Bax-deficient, drug-resistant tumors.	Thapsigargin	56-68	BCL2-associated X protein	Mus musculus	129-132
19692349-5	2009	In addition, cell permeable pentapeptides designed from Ku70, termed Bax-inhibiting peptides (BIPs), inhibited staurosporine-induced Bax translocation and cell death in mouse myogenic cells.	Staurosporine	111-124	BCL2-associated X protein	Mus musculus	69-72
19820692-1	2009	Truncated BID (tBID), a proapoptotic BCL2 family protein, induces BAK/BAX-dependent release of cytochrome c and other mitochondrial intermembrane proteins to the cytosol to induce apoptosis.	tBID	15-19	BCL2-associated X protein	Mus musculus	70-73
19820692-6	2009	tBID sensitivity of BAK(-/-) MEFs is also reduced, although not to the same extent as V2(-/-) MEFs, which might result from their strong overexpression of BAX.	tBID	0-4	BCL2-associated X protein	Mus musculus	155-158
19820692-7	2009	Indeed, addition of recombinant BAX also sensitized V2(-/-) MEFs to tBID.	tBID	68-72	BCL2-associated X protein	Mus musculus	32-35
20097962-10	2009	Consistent with this observation, CisPt induced a larger decrease of the Bcl-2 content in the Bcl-2:Bax heterooligomer in L1210 cells than in L1210/VCR cells.	Cisplatin	34-39	BCL2-associated X protein	Mus musculus	100-103
19692349-5	2009	In addition, cell permeable pentapeptides designed from Ku70, termed Bax-inhibiting peptides (BIPs), inhibited staurosporine-induced Bax translocation and cell death in mouse myogenic cells.	Staurosporine	111-124	BCL2-associated X protein	Mus musculus	133-136
19839062-7	2009	tBid was capable of binding to Bcl-xL and displacing Bak and Bax from Bcl-xL, leading to release of cytochrome c from wild-type mitochondria.	tBID	0-4	BCL2-associated X protein	Mus musculus	61-64
19890356-6	2009	Further studies showed that THSG inhibited reactive oxygen species (ROS) generation and prevented DOX-induced loss of mitochondrial membrane potential, caspase-3 activation and upregulation of Bax protein expression.	2,3,5,4'-tetrahydroxystilbene 2-O-glucopyranoside	28-32	BCL2-associated X protein	Mus musculus	193-196
19839062-9	2009	Finally, administration of ABT-737, a pharmacological inhibitor of Bcl-2/Bcl-xL, caused Bak/Bax-dependent liver injury, but this was clearly ameliorated with a Bid KO background.	ABT-737	27-34	BCL2-associated X protein	Mus musculus	92-95
19915483-5	2009	Bax/Bak-deficient NPCs were protected from desferrioxamine-induced death and exhibited minimal caspase-3 activation.	Deferoxamine	43-58	BCL2-associated X protein	Mus musculus	0-3
19679388-4	2009	Using western blot analysis 3h after ESWT, an increased expression of Bax was found, indicating a fast pro-apoptotic effect of treatment on some of the osteoblasts.	Tritium	28-30	BCL2-associated X protein	Mus musculus	70-73
19833167-9	2009	Induction levels of proapoptotic Bcl-2 associated X protein (Bax) in renal proximal tubular cells was significantly higher in IL-6(-/-) mice than in WT mice at 24h after CDDP injection.	Cisplatin	170-174	BCL2-associated X protein	Mus musculus	61-64
19833167-11	2009	Bax might contribute to the development of CDDP-induced ARF at 24h; however, high expression levels of Bcl-x(L) and Bcl-2 might overcome the proapoptosis signaling at 72 h in IL-6(-/-) mice.	Cisplatin	43-47	BCL2-associated X protein	Mus musculus	0-3
19890356-6	2009	Further studies showed that THSG inhibited reactive oxygen species (ROS) generation and prevented DOX-induced loss of mitochondrial membrane potential, caspase-3 activation and upregulation of Bax protein expression.	Doxorubicin	98-101	BCL2-associated X protein	Mus musculus	193-196
19666080-8	2009	The bax/bcl-2 mRNA ratio increased 12 and 24 h following R-SO and 120 h following styrene administration.	styrene oxide	57-61	BCL2-associated X protein	Mus musculus	4-7
19664609-2	2009	We compared DNA damage, Ku70-Bax interaction, and Bax-dependent excitotoxic cell death in kainic acid-treated primary cortical neurons derived from both wild-type mice and mice deficient in the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) encoded by the Prkdc gene.	Kainic Acid	90-101	BCL2-associated X protein	Mus musculus	29-32
19664609-2	2009	We compared DNA damage, Ku70-Bax interaction, and Bax-dependent excitotoxic cell death in kainic acid-treated primary cortical neurons derived from both wild-type mice and mice deficient in the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) encoded by the Prkdc gene.	Kainic Acid	90-101	BCL2-associated X protein	Mus musculus	50-53
19664609-5	2009	Cotransfection of DNA-PKcs with Bax shRNA restored Bax shRNA-mediated neuroprotection in Prkdc(-/-) neurons, suggesting that DNA-PKcs is required for kainate-induced activation of the pro-apoptotic Bax pathway.	Kainic Acid	150-157	BCL2-associated X protein	Mus musculus	32-35
19664609-5	2009	Cotransfection of DNA-PKcs with Bax shRNA restored Bax shRNA-mediated neuroprotection in Prkdc(-/-) neurons, suggesting that DNA-PKcs is required for kainate-induced activation of the pro-apoptotic Bax pathway.	Kainic Acid	150-157	BCL2-associated X protein	Mus musculus	51-54
19664609-5	2009	Cotransfection of DNA-PKcs with Bax shRNA restored Bax shRNA-mediated neuroprotection in Prkdc(-/-) neurons, suggesting that DNA-PKcs is required for kainate-induced activation of the pro-apoptotic Bax pathway.	Kainic Acid	150-157	BCL2-associated X protein	Mus musculus	51-54
19664609-7	2009	In support of this, kainic acid induced translocation of a Bax-EGFP fusion protein to the mitochondria in the presence of a cotransfected wild-type, but not mutant Ku70 (S6A/S51A) gene when examined at 4 and 8 h following kainate addition.	Kainic Acid	20-31	BCL2-associated X protein	Mus musculus	59-62
19664609-7	2009	In support of this, kainic acid induced translocation of a Bax-EGFP fusion protein to the mitochondria in the presence of a cotransfected wild-type, but not mutant Ku70 (S6A/S51A) gene when examined at 4 and 8 h following kainate addition.	Kainic Acid	222-229	BCL2-associated X protein	Mus musculus	59-62
19664609-8	2009	We conclude that DNA-PKcs links DNA damage to Bax-dependent excitotoxic cell death, by phosphorylating Ku70 on serines 6 and/or 51, to initiate Bax translocation to the mitochondria and directly activate a pro-apoptotic Bax-dependent death cascade.	Serine	111-118	BCL2-associated X protein	Mus musculus	46-49
19664609-8	2009	We conclude that DNA-PKcs links DNA damage to Bax-dependent excitotoxic cell death, by phosphorylating Ku70 on serines 6 and/or 51, to initiate Bax translocation to the mitochondria and directly activate a pro-apoptotic Bax-dependent death cascade.	Serine	111-118	BCL2-associated X protein	Mus musculus	144-147
19664609-8	2009	We conclude that DNA-PKcs links DNA damage to Bax-dependent excitotoxic cell death, by phosphorylating Ku70 on serines 6 and/or 51, to initiate Bax translocation to the mitochondria and directly activate a pro-apoptotic Bax-dependent death cascade.	Serine	111-118	BCL2-associated X protein	Mus musculus	144-147
19996687-4	2009	In Western blot analysis, astaxanthin-pretreated cells showed the activation of p-Akt, p-MEK, p-ERK, and Bcl-2, and the reduction of p-P38, p-SAPK/JNK, Bax, p-GSK3beta, cytochrome c, caspase-3, and PARP.	astaxanthine	26-37	BCL2-associated X protein	Mus musculus	152-155
19709125-7	2009	Meloxicam therapy inhibited cell proliferation, induced cell apoptosis, reduced expression of proliferating cell nuclear antigen, increased activation of caspase-3, and upregulated Bax.	Meloxicam	0-9	BCL2-associated X protein	Mus musculus	181-184
19765187-7	2009	Treatment with either l-dopa or PPX in MPTP-treated mice led to significantly decreased expressions of JNK phosphorylation, Bax, and cytochrome c and to an increased level of Bcl-2 expression with a similar degree, compared with the levels in MPTP-only treated mice.	Levodopa	22-28	BCL2-associated X protein	Mus musculus	124-127
19765187-7	2009	Treatment with either l-dopa or PPX in MPTP-treated mice led to significantly decreased expressions of JNK phosphorylation, Bax, and cytochrome c and to an increased level of Bcl-2 expression with a similar degree, compared with the levels in MPTP-only treated mice.	Pramipexole	32-35	BCL2-associated X protein	Mus musculus	124-127
19765187-7	2009	Treatment with either l-dopa or PPX in MPTP-treated mice led to significantly decreased expressions of JNK phosphorylation, Bax, and cytochrome c and to an increased level of Bcl-2 expression with a similar degree, compared with the levels in MPTP-only treated mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	39-43	BCL2-associated X protein	Mus musculus	124-127
19548187-4	2009	Moreover, the modulation influence of acteoside on the expression of B cell lymphoma/leukemia-2 (Bcl-2, hepatocyte apoptosis inhibitor) and Bcl-2 associated X protein (Bax, hepatocyte apoptosis promoter) in the mice liver with immunological hepatic injury was studied also.	acteoside	38-47	BCL2-associated X protein	Mus musculus	168-171
19666080-8	2009	The bax/bcl-2 mRNA ratio increased 12 and 24 h following R-SO and 120 h following styrene administration.	Styrene	82-89	BCL2-associated X protein	Mus musculus	4-7
19823063-10	2009	The results also showed that letrozole enhanced the expression of Bax and cytochrome c release and suppressed the expression of estrogen receptor in tumor cells.	Letrozole	29-38	BCL2-associated X protein	Mus musculus	66-69
21158056-5	2009	RESULTS: Chronic PA dose-dependently (1) decreased the availability and increased the apoptosis of MIN6 cells; (2) decreased the phosphorylation of Akt and Bcl-2, but had no significant effects on Akt and Bax.	Palmitic Acid	17-19	BCL2-associated X protein	Mus musculus	205-208
19691447-4	2009	Compounds that blocked the release of fluorescein from liposomes by recombinant Bax were tested for their ability to directly close MAC and suppress apoptosis in FL5.12 cells.	Fluorescein	38-49	BCL2-associated X protein	Mus musculus	80-83
19602847-5	2009	Treatment with actinomycin D also changed the ratio between the mRNA levels of some pro-apoptotic and anti-apoptotic genes: the Bad/Bcl2l2 and the Bax/Bcl2l2 ratios were on average 4.39 and 2.66 times higher in the treated embryos than in the controls, respectively.	Dactinomycin	15-28	BCL2-associated X protein	Mus musculus	147-150
19481066-0	2009	Bz-423 superoxide signals B cell apoptosis via Mcl-1, Bak, and Bax.	Quinuclidinyl Benzilate	0-2	BCL2-associated X protein	Mus musculus	63-66
19481066-0	2009	Bz-423 superoxide signals B cell apoptosis via Mcl-1, Bak, and Bax.	Superoxides	7-17	BCL2-associated X protein	Mus musculus	63-66
19481066-4	2009	Following the generation of superoxide, Bz-423-induced apoptosis requires the activation of Bax and Bak to induce mitochondrial outer membrane permeabilization and cytochrome c release.	Bz-423	40-46	BCL2-associated X protein	Mus musculus	92-95
19481066-6	2009	Treatment with Bz-423 results in superoxide-dependent Mcl-1 degradation, implicating this protein as the link between Bz-423-induced superoxide and Bax and Bak activation.	Quinuclidinyl Benzilate	15-17	BCL2-associated X protein	Mus musculus	148-151
19481066-6	2009	Treatment with Bz-423 results in superoxide-dependent Mcl-1 degradation, implicating this protein as the link between Bz-423-induced superoxide and Bax and Bak activation.	Superoxides	33-43	BCL2-associated X protein	Mus musculus	148-151
19481066-6	2009	Treatment with Bz-423 results in superoxide-dependent Mcl-1 degradation, implicating this protein as the link between Bz-423-induced superoxide and Bax and Bak activation.	Quinuclidinyl Benzilate	118-120	BCL2-associated X protein	Mus musculus	148-151
19550108-3	2009	Quantitative reverse transcriptase (RT) PCR analysis revealed that the expression levels of the pro-apoptotic genes Bax and Casp3 at the blastocyst stage were increased significantly by the addition of either 25 or 55 mM glucose to the culture medium.	Glucose	221-228	BCL2-associated X protein	Mus musculus	116-119
20074457-3	2009	Furthermore, carrageenan induced lung apoptosis (Bax and Bcl-2 expression) as well as nitrotyrosine formation, NF-kB activation, and pJNK expression, as determined by immunohistochemical analysis of lung tissues and the degree of lung inflammation and tissue injury (histological score).	Carrageenan	13-24	BCL2-associated X protein	Mus musculus	49-52
19477251-5	2009	1,3-DNB treatment decreased total transcript and protein levels of the apoptosis inhibitory protein Bcl-2, and increased expression levels of the pro-apoptotic protein Bax.	3-dinitrobenzene	0-7	BCL2-associated X protein	Mus musculus	168-171
19393233-5	2009	Feeding of this synthetic coumarin induced positive modulations in expression of all biomarkers in DMBA administered mice, giving clues on its possible signaling pathway(s) - primarily through down-regulation of Aryl hydrocarbon receptor and PCNA and up-regulation of apoptotic proteins like Bax, Bad, Cytochrome c, Apaf, Caspase-3 and Caspase-9, resulting in an appreciable reduction in growth of papilloma in mice.	coumarin	26-34	BCL2-associated X protein	Mus musculus	292-295
19549073-5	2009	The treatment with epoxomicin increases, in wild type (WT) cultures, the pro-apoptotic Bax/Bcl-2 ratio, the phosphorylation of tau, and the levels of chaperones heat-shock protein 70 and C-terminal Hsc-interacting protein, but none of these effects took place in epoxomicin-treated PK-KO cultures.	epoxomicin	19-29	BCL2-associated X protein	Mus musculus	87-90
19524032-0	2009	Bax-associated mechanisms underlying the response of embryonic cells to methotrexate.	Methotrexate	72-84	BCL2-associated X protein	Mus musculus	0-3
19524032-5	2009	In parallel, WT MEFs demonstrated a MTX-induced increase in the percentage of Bax-positive cells and a significant decrease in the percentage of bcl-2-, p65- or IkappaBalpha-positive cells, which were not detected in Bax(-/-) MEFs.	Methotrexate	36-39	BCL2-associated X protein	Mus musculus	78-81
19524032-5	2009	In parallel, WT MEFs demonstrated a MTX-induced increase in the percentage of Bax-positive cells and a significant decrease in the percentage of bcl-2-, p65- or IkappaBalpha-positive cells, which were not detected in Bax(-/-) MEFs.	Methotrexate	36-39	BCL2-associated X protein	Mus musculus	217-220
19524032-6	2009	Altogether, the differential sensitivity of WT or Bax(-/-) MEFs to MTX suggests a possible involvement of this molecule in the response of embryonic cells to teratogens.	Methotrexate	67-70	BCL2-associated X protein	Mus musculus	50-53
19459852-6	2009	ACS inhibition by Triacsin c markedly potentiated the Bax-induced intrinsic apoptotic pathway by promoting cytochrome c release and subsequent caspase activation.	triacsin C	18-28	BCL2-associated X protein	Mus musculus	54-57
19662359-0	2009	Effects of high concentration glucose on the expression of NF-kappaB, Bax and cytochrome C and apoptosis of islet cells in mice.	Glucose	30-37	BCL2-associated X protein	Mus musculus	70-73
19470390-10	2009	Moreover, farnesol at all doses altered Bax/Bcl-2 ratio which leads to induction of apoptosis as confirmed by DNA fragmentation.	Farnesol	10-18	BCL2-associated X protein	Mus musculus	40-43
19376889-4	2009	In control HUVEC treated with H(2)O(2) or in WT mice exposed to 100% O(2), a marked induction of Bax translocation and dimerization was associated with increased JNK and p38 kinase activity.	Hydrogen Peroxide	30-38	BCL2-associated X protein	Mus musculus	97-100
19376889-4	2009	In control HUVEC treated with H(2)O(2) or in WT mice exposed to 100% O(2), a marked induction of Bax translocation and dimerization was associated with increased JNK and p38 kinase activity.	o(2)	34-38	BCL2-associated X protein	Mus musculus	97-100
19376889-6	2009	IL-6 Tg(+) mice exposed to 100% O(2) exhibited enhanced phosphatidylinositol 3-kinase (PI3K)/Akt kinase and increased serine phosphorylation of Bax at Ser(184) compared with WT mice.	o(2)	32-36	BCL2-associated X protein	Mus musculus	144-147
19376889-6	2009	IL-6 Tg(+) mice exposed to 100% O(2) exhibited enhanced phosphatidylinositol 3-kinase (PI3K)/Akt kinase and increased serine phosphorylation of Bax at Ser(184) compared with WT mice.	Serine	118-124	BCL2-associated X protein	Mus musculus	144-147
19376889-6	2009	IL-6 Tg(+) mice exposed to 100% O(2) exhibited enhanced phosphatidylinositol 3-kinase (PI3K)/Akt kinase and increased serine phosphorylation of Bax at Ser(184) compared with WT mice.	Serine	151-154	BCL2-associated X protein	Mus musculus	144-147
19376889-7	2009	The PI3K-specific inhibitor LY-2940002 blocked this IL-6-induced Bax phosphorylation and promoted cell death.	ly-2940002	28-38	BCL2-associated X protein	Mus musculus	65-68
19556852-7	2009	Tea polyphenols treatment along with DMBA exposure resulted in upregulation of p53, and proapoptotic protein Bax, whereas enhanced expression of antiapoptotic proteins, Bcl-2 and survivin by DMBA were downregulated.	Polyphenols	4-15	BCL2-associated X protein	Mus musculus	109-112
19556852-7	2009	Tea polyphenols treatment along with DMBA exposure resulted in upregulation of p53, and proapoptotic protein Bax, whereas enhanced expression of antiapoptotic proteins, Bcl-2 and survivin by DMBA were downregulated.	9,10-Dimethyl-1,2-benzanthracene	37-41	BCL2-associated X protein	Mus musculus	109-112
19382207-6	2009	Ethanol induced dephosphorylation of GSK3beta at Ser9 and the activation of Bax as well as caspase-3 in the developing mouse brain.	Ethanol	0-7	BCL2-associated X protein	Mus musculus	76-79
19470390-4	2009	MAIN METHODS: Farnesol at three different doses 25, 50 and 100 mg/kg body weight was topically applied to the mouse skin, 30 min prior to TPA (2 microg/200 microl acetone) to evaluate edema, hyperplasia, expression of cyclooxygenase-2 (COX-2), oxidative stress response and hyperproliferation, and expression of Ras, Raf, p-ERK1/2, Bax and Bcl-2 in DMBA/TPA-induced tumors.	Farnesol	14-22	BCL2-associated X protein	Mus musculus	332-335
19439408-9	2009	Suppression of HSP70 expression in vitro stimulated indomethacin-induced apoptosis and activation of Bax but not the endoplasmic reticulum stress response.	Indomethacin	52-64	BCL2-associated X protein	Mus musculus	101-104
19439408-11	2009	The results of this study provide direct genetic evidence that expression of HSP70 confers gastric protection against indomethacin-induced lesions by inhibiting the activation of Bax.	Indomethacin	118-130	BCL2-associated X protein	Mus musculus	179-182
19393233-5	2009	Feeding of this synthetic coumarin induced positive modulations in expression of all biomarkers in DMBA administered mice, giving clues on its possible signaling pathway(s) - primarily through down-regulation of Aryl hydrocarbon receptor and PCNA and up-regulation of apoptotic proteins like Bax, Bad, Cytochrome c, Apaf, Caspase-3 and Caspase-9, resulting in an appreciable reduction in growth of papilloma in mice.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	99-103	BCL2-associated X protein	Mus musculus	292-295
19232459-9	2009	The findings of this study indicate that mouse testicular Leydig cells adapt to chronic cadmium exposure by increasing cell survival through increased expression of Bcl-2, and decreased expression of Bax.	Cadmium	88-95	BCL2-associated X protein	Mus musculus	200-203
19620044-6	2009	In the presence of glucose above 16.7 mmol/L, the percentages of apoptotic islet cells increased with glucose concentration, but insulin secretion and IRS2 expression decreased; Bax expression significantly increased in the presence of high-concentration glucose.	Glucose	19-26	BCL2-associated X protein	Mus musculus	178-181
19429258-8	2009	Consistently, ALDH2 transgene significantly attenuated alcohol-induced upregulation of Bax, Omi/HtrA2 and XIAP as well as downregulation of Bcl-2 and ARC without affecting alcohol-induced increase of FLIP in cerebral cortex.	Alcohols	55-62	BCL2-associated X protein	Mus musculus	87-90
19385969-0	2009	Cyclin-dependent kinase 1 inhibitor RO-3306 enhances p53-mediated Bax activation and mitochondrial apoptosis in AML.	RO 3306	36-43	BCL2-associated X protein	Mus musculus	66-69
19470789-7	2009	DIM/butyrate combination treatment induced the expression of proapoptotic Bax and Bak proteins, triggered Bax dimerization/activation, and caused release of cytochrome c and Smac proteins from mitochondria.	dim/butyrate	0-12	BCL2-associated X protein	Mus musculus	74-77
19470789-7	2009	DIM/butyrate combination treatment induced the expression of proapoptotic Bax and Bak proteins, triggered Bax dimerization/activation, and caused release of cytochrome c and Smac proteins from mitochondria.	dim/butyrate	0-12	BCL2-associated X protein	Mus musculus	106-109
19269163-6	2009	It induced early generation of reactive nitrogen and oxygen species (RNOS), thus producing oxidative stress mediated mitochondrial membrane potential (MMP) loss leading to the release of cytochrome c, the translocation of Bax to mitochondria and apoptosis-inducing factor to the nuclei.	reactive nitrogen and oxygen species	31-67	BCL2-associated X protein	Mus musculus	222-225
19431040-3	2009	We also found that PS increased the ratio of Bax/Bcl-2 and activated caspase-9 and caspase-3 but not caspase-8.	Polysaccharides	19-21	BCL2-associated X protein	Mus musculus	45-48
19409106-6	2009	The effect of MRN-100 on Bcl-2 and Bax protein levels was determined by Western blot.	mrn-100	14-21	BCL2-associated X protein	Mus musculus	35-38
19409106-8	2009	In contrast, pre-treatment of cells with MRN-100 followed by H(2)O(2) treatment results in significantly reduced levels of apoptosis.In addition, MRN-100 partially prevents H(2)O(2) -induced down-regulation of the anti-apoptotic molecule Bcl-2 and upregulation of the pro-apoptotic molecule Bax.	mrn-100	41-48	BCL2-associated X protein	Mus musculus	291-294
19409106-8	2009	In contrast, pre-treatment of cells with MRN-100 followed by H(2)O(2) treatment results in significantly reduced levels of apoptosis.In addition, MRN-100 partially prevents H(2)O(2) -induced down-regulation of the anti-apoptotic molecule Bcl-2 and upregulation of the pro-apoptotic molecule Bax.	Hydrogen Peroxide	61-69	BCL2-associated X protein	Mus musculus	291-294
19279129-5	2009	We show that cisplatin could induce Bax activation, cytochrome c release, and apoptosis in primary cultures of p53-deficient renal tubular cells, albeit at a level that was lower than in the wild-type cells.	Cisplatin	13-22	BCL2-associated X protein	Mus musculus	36-39
19279129-8	2009	Bax and Bak, two key molecules in the mitochondrial pathway of apoptosis, were interdependently activated by cisplatin, with Bax translocation to and Bax/Bak oligomerization in mitochondria, leading to cytochrome c release.	Cisplatin	109-118	BCL2-associated X protein	Mus musculus	0-3
19279129-8	2009	Bax and Bak, two key molecules in the mitochondrial pathway of apoptosis, were interdependently activated by cisplatin, with Bax translocation to and Bax/Bak oligomerization in mitochondria, leading to cytochrome c release.	Cisplatin	109-118	BCL2-associated X protein	Mus musculus	125-128
19279129-8	2009	Bax and Bak, two key molecules in the mitochondrial pathway of apoptosis, were interdependently activated by cisplatin, with Bax translocation to and Bax/Bak oligomerization in mitochondria, leading to cytochrome c release.	Cisplatin	109-118	BCL2-associated X protein	Mus musculus	125-128
19215238-10	2009	The data revealed that alcohol intake enhanced expression of p53, Omi/HtrA2, Bcl-2 and Bax without affecting XIAP expression or the Bcl-2/Bax ratio.	Alcohols	23-30	BCL2-associated X protein	Mus musculus	87-90
19272431-10	2009	These findings suggest that prenatal heroin exposure during the E9-18 period enhances neuronal apoptosis by altering the expressions of caspase-3, Bcl-2, and Bax in the mouse hippocampus, and leads to impairment in hippocampus-dependent learning and memory.	Heroin	37-43	BCL2-associated X protein	Mus musculus	158-161
19360325-10	2009	Further, in the DMBA-treated mice, apoptosis was induced by a decrease in Bcl-2 and an increase in Bax.	9,10-Dimethyl-1,2-benzanthracene	16-20	BCL2-associated X protein	Mus musculus	99-102
19269163-6	2009	It induced early generation of reactive nitrogen and oxygen species (RNOS), thus producing oxidative stress mediated mitochondrial membrane potential (MMP) loss leading to the release of cytochrome c, the translocation of Bax to mitochondria and apoptosis-inducing factor to the nuclei.	rnos	69-73	BCL2-associated X protein	Mus musculus	222-225
18656336-6	2009	The tea polyphenols inhibited inflammatory response in the lung lesions on the 9th week, when decreased expression of H-ras and c-myc and increased expression of bax were noted.	Polyphenols	8-19	BCL2-associated X protein	Mus musculus	162-165
18656336-8	2009	These observations indicate that the tea polyphenols can restrict B[a]P-induced lung carcinogenesis by differential modulation of the expression of p53 and its associated genes such as bax, bcl-2, mdm2, p21 and p27, along with H-ras, c-myc and cyclin D1, at different time points.	Polyphenols	41-52	BCL2-associated X protein	Mus musculus	185-188
19202353-3	2009	In the present study, the exposure of murine fibrosarcoma L929 cells to oridonin led to the generation of intracellular reactive oxygen species (ROS) and, subsequently, the ROS triggered apoptosis by Bax translocation, cytochrome c release and ERK activations.	Reactive Oxygen Species	173-176	BCL2-associated X protein	Mus musculus	200-203
19095349-7	2009	Marchantin C-treated xenografts showed decreased microtubules, Bcl-2 and increased cyclin B1, Bax, caspase-3, indicating that marchantin C possess the same ability to induce microtubules depolymerization and tumor cell apoptosis in tumor-bearing mice as in vitro.	marchantin C	0-12	BCL2-associated X protein	Mus musculus	94-97
19202353-3	2009	In the present study, the exposure of murine fibrosarcoma L929 cells to oridonin led to the generation of intracellular reactive oxygen species (ROS) and, subsequently, the ROS triggered apoptosis by Bax translocation, cytochrome c release and ERK activations.	oridonin	72-80	BCL2-associated X protein	Mus musculus	200-203
19374816-12	2009	Bcl-2 expression decreased (P&lt;0.01), in contrast, Bax expression increased (P&lt;0.01) in the untreated VMC group compared with that in the control group.	2-methoxy-4-(1-{2-[(2S)-1-methylpyrrolidin-2-yl]ethyl}-4-phenyl-1H-imidazol-5-yl)phenol	107-110	BCL2-associated X protein	Mus musculus	53-56
19200344-4	2009	Carbachol inhibits DomA-induced activation of Jun N-terminal (JNK) and p38 kinases, increased translocation to mitochondria of the pro-apoptotic protein Bax, and activation of caspase-3.	Carbachol	0-9	BCL2-associated X protein	Mus musculus	153-156
19200344-4	2009	Carbachol inhibits DomA-induced activation of Jun N-terminal (JNK) and p38 kinases, increased translocation to mitochondria of the pro-apoptotic protein Bax, and activation of caspase-3.	domoic acid	19-23	BCL2-associated X protein	Mus musculus	153-156
19187231-4	2009	We showed that reactive oxygen species triggered apoptosis by Bax translocation, cytochrome c release and extracellular signal-regulated kinase activation.	Reactive Oxygen Species	15-38	BCL2-associated X protein	Mus musculus	62-65
19087973-2	2009	Like AHR, BAX is also functionally required for PAH to kill oocytes.	Polycyclic Aromatic Hydrocarbons	48-51	BCL2-associated X protein	Mus musculus	10-13
19087973-3	2009	Here, we show that PAH upregulates ovarian expression of not just Bax but a large cassette of proapoptotic genes that function at multiple steps of the cell death signaling pathway.	Polycyclic Aromatic Hydrocarbons	19-22	BCL2-associated X protein	Mus musculus	66-69
19100860-9	2009	IPA extracted five gene networks: Network-1 included genes related to cancer and cell cycle arrest and associated with Bax, Btg2, Ccng1, Cdkn1a, Gadd45b, Gdf15, Hspb1, Mdm2 and Plk2 and Network-2 was related to DNA replication, recombination, repair and cell death and associated with Cyp21a1, Gdf15, Ppp1r3c, Rcan1 and Tubb2c.	ipa	0-3	BCL2-associated X protein	Mus musculus	119-122
18974775-4	2009	Here, we first show that hydrogen peroxide (H(2)O(2)) induces necrotic cell death in Bax-/- Bak-/- mouse embryonic fibroblasts through a mechanism involving PARP-1 activation and ATP depletion.	Hydrogen Peroxide	25-42	BCL2-associated X protein	Mus musculus	85-88
19228953-5	2009	Using primary neurons from mice transgenic or deficient for apoptosis-related genes, we determined that polyQ-AR apoptotic activation is fully dependent on Bax.	polyglutamine	104-109	BCL2-associated X protein	Mus musculus	156-159
19228953-0	2009	Polyglutamine-expanded androgen receptor truncation fragments activate a Bax-dependent apoptotic cascade mediated by DP5/Hrk.	polyglutamine	0-13	BCL2-associated X protein	Mus musculus	73-76
19209030-9	2009	In the cultured cells, DHA inhibited cell viability, downregulated the expression of proliferating cell nuclear antigen and cyclin D1, and upregulated p21(WAF1/CIP1); and induced apoptosis by reducing the ratio of Bcl-2/Bax and increasing the activation of caspase-9, in a dose-dependent manner.	artenimol	23-26	BCL2-associated X protein	Mus musculus	220-223
18974775-4	2009	Here, we first show that hydrogen peroxide (H(2)O(2)) induces necrotic cell death in Bax-/- Bak-/- mouse embryonic fibroblasts through a mechanism involving PARP-1 activation and ATP depletion.	Hydrogen Peroxide	44-52	BCL2-associated X protein	Mus musculus	85-88
18974775-4	2009	Here, we first show that hydrogen peroxide (H(2)O(2)) induces necrotic cell death in Bax-/- Bak-/- mouse embryonic fibroblasts through a mechanism involving PARP-1 activation and ATP depletion.	Adenosine Triphosphate	179-182	BCL2-associated X protein	Mus musculus	85-88
19995710-0	2009	Dexamethasone effects on Bax expression in the mouse testicular germ cells.	Dexamethasone	0-13	BCL2-associated X protein	Mus musculus	25-28
19918366-6	2009	The transcriptions and expressions of Bax and caspase-3 in group D were increased significantly when compared with groups A, B, and C. In conclusion, DNR-loaded MNPs-Fe3O4 can overcome MDR in vivo.	ferryl iron	166-171	BCL2-associated X protein	Mus musculus	38-41
18936150-10	2009	Memantine blocked apoptotic cell death in the GCL, increased Bcl-2 gene expression, and decreased Bax gene expression.	Memantine	0-9	BCL2-associated X protein	Mus musculus	98-101
19086074-8	2009	Doxycycline-treated laminin-alpha2-deficient muscles had increased Akt phosphorylation, decreased inflammation, and decreased levels of Bax protein, terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling-positive myonuclei, and activated caspase-3.	Doxycycline	0-11	BCL2-associated X protein	Mus musculus	136-139
19995710-2	2009	The aim of the present study was to find out whether dexamethasone (Dex), a widely used GC, would influence the apoptosis and expression of Bax, an important proapoptotic protein, in the mouse testicular germ cells.	Dexamethasone	53-66	BCL2-associated X protein	Mus musculus	140-143
19995710-2	2009	The aim of the present study was to find out whether dexamethasone (Dex), a widely used GC, would influence the apoptosis and expression of Bax, an important proapoptotic protein, in the mouse testicular germ cells.	Dexamethasone	68-71	BCL2-associated X protein	Mus musculus	140-143
19076721-0	2009	The LCB2 subunit of the sphingolip biosynthesis enzyme serine palmitoyltransferase can function as an attenuator of the hypersensitive response and Bax-induced cell death.	sphingolip	24-34	BCL2-associated X protein	Mus musculus	148-151
19076721-6	2009	Reactive oxygen species (ROS) accumulation induced by Bax was compromised in BcLCB(2)-overexpressing yeast cells.	Reactive Oxygen Species	0-23	BCL2-associated X protein	Mus musculus	54-57
19076721-6	2009	Reactive oxygen species (ROS) accumulation induced by Bax was compromised in BcLCB(2)-overexpressing yeast cells.	Reactive Oxygen Species	25-28	BCL2-associated X protein	Mus musculus	54-57
19002586-9	2008	Tumors from capsaicin treated mice demonstrated increased apoptosis, which was related to the activation of JNK and increased cytosolic protein expression of Bax, cytochrome c, AIF and cleaved caspase-3, as compared with controls.	Capsaicin	12-21	BCL2-associated X protein	Mus musculus	158-161
18791811-5	2009	Results of the western blotting showed that resveratrol treatment increased the DMBA suppressed p53 and Bax while decreased the expression of Bcl-2 and Survivin.	Resveratrol	44-55	BCL2-associated X protein	Mus musculus	104-107
18791811-5	2009	Results of the western blotting showed that resveratrol treatment increased the DMBA suppressed p53 and Bax while decreased the expression of Bcl-2 and Survivin.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	80-84	BCL2-associated X protein	Mus musculus	104-107
18948087-8	2008	Rosiglitazone-treated mice also showed significantly less number of TUNEL(+) apoptotic neurons and curtailed induction of caspase-3 and Bax, compared to vehicle control.	Rosiglitazone	0-13	BCL2-associated X protein	Mus musculus	136-139
19084052-0	2008	WITHDRAWN: Anti-tumor and proapoptotic effect of withaferin A is mediated by up-regulation of Bax and inhibition NF-kappaB in Ehrlich ascites tumor cells.	withaferin A	49-61	BCL2-associated X protein	Mus musculus	94-97
19630211-1	2008	This study hypothesized that the expression of apoptosis-regulatory genes, such as BCL-2 and BAX may be affected by genetic variation in bleomycin-induced pulmonary fibrosis in C57BL/6 and NMRI mice.	Bleomycin	137-146	BCL2-associated X protein	Mus musculus	93-96
19630211-7	2008	The expression of BAX protein was significantly (p&lt;0.05) upregulated in alveolar epithelial cells of both strains and downregulated in myofibroblasts and lymphocytes of the lung tissues of C57BL/6 mice and also in lymphocytes of NMRI mice at 2 weeks after bleomycin instillation.	Bleomycin	259-268	BCL2-associated X protein	Mus musculus	18-21
18587053-10	2008	Fas-induced proliferation and lung growth in hyperoxic newborn lungs may counteract, in part, the detrimental effects of apoptosis mediated by non-Fas pathways, such as pro-apoptotic Bax/Bcl-2 family members.	ammonium ferrous sulfate	0-3	BCL2-associated X protein	Mus musculus	183-186
18989682-11	2008	Losartan treatment was associated with a significant reduction of the bax-to-bcl-2 ratio and TNF-alpha expression after SBR compared to non-treated groups.	Losartan	0-8	BCL2-associated X protein	Mus musculus	70-73
18718527-0	2008	Bz-423 superoxide signals apoptosis via selective activation of JNK, Bak, and Bax.	Bz-423	0-6	BCL2-associated X protein	Mus musculus	78-81
18708175-6	2008	Analysis by in vivo incorporation of bromodeoxyuridine into chondrocytes within the fracture tissues indicated a highly significant increase in chondrocyte proliferation in Bax KO fractures compared to C57BL/6J fractures at day 7.	Bromodeoxyuridine	37-54	BCL2-associated X protein	Mus musculus	173-176
19031314-5	2008	Blockade of AR activity in J774A.1 cells markedly augmented the acrolein- or hydrogen peroxide-induced translocation of Bax to mitochondria along with reduced Bcl-2 and increased release of cytochrome c from the mitochodria.	Hydrogen Peroxide	77-94	BCL2-associated X protein	Mus musculus	120-123
19110998-0	2008	Diethyl maleate-induced oxidative stress leads to testicular germ cell apoptosis involving Bax and Bcl-2.	diethyl maleate	0-15	BCL2-associated X protein	Mus musculus	91-94
18718527-0	2008	Bz-423 superoxide signals apoptosis via selective activation of JNK, Bak, and Bax.	Superoxides	7-17	BCL2-associated X protein	Mus musculus	78-81
18718527-7	2008	The response of these cells to Bz-423 is critically dependent on both superoxide and JNK activation as antioxidants and the JNK inhibitor SP600125 prevents Bax translocation, cytochrome c release, and cell death.	Bz-423	31-37	BCL2-associated X protein	Mus musculus	156-159
18718527-7	2008	The response of these cells to Bz-423 is critically dependent on both superoxide and JNK activation as antioxidants and the JNK inhibitor SP600125 prevents Bax translocation, cytochrome c release, and cell death.	pyrazolanthrone	138-146	BCL2-associated X protein	Mus musculus	156-159
18789312-7	2008	Auranofin-induced apoptosis was effectively blocked by the overexpression of Bcl-2, and Bax/Bak deficient mouse embryonic fibroblasts were also resistant to apoptosis, indicating a central role for the pro-apoptotic proteins of this family in auranofin-triggered apoptosis.	Auranofin	0-9	BCL2-associated X protein	Mus musculus	88-91
18678651-8	2008	siRNA-treated BAK(-/-) BAX(-/-) double-knockout mouse embryonic fibroblasts failed to activate capase-3 or increase TUNEL staining but instead exhibited autophagy, as demonstrated by proteolytic processing of microtubule-associated protein 1 light chain 3 (LC3) and translocation of transfected green fluorescent protein-LC3 from the nucleus to punctate cytoplasmic structures.	bakuchiol	14-17	BCL2-associated X protein	Mus musculus	23-26
18723505-10	2008	Sildenafil also enhanced the Bcl-2/Bax ratio, phosphorylation of Akt, ERK1/2, and glycogen synthase kinase 3beta.	Sildenafil Citrate	0-10	BCL2-associated X protein	Mus musculus	35-38
18266059-0	2008	In vivo 5-fluorouracil-[corrected]induced apoptosis on murine thymocytes: involvement of FAS, Bax and Caspase3.	Fluorouracil	8-22	BCL2-associated X protein	Mus musculus	94-97
18266059-12	2008	This study revealed that in vivo apoptosis in normal thymus after 5-FU administration is related to FAS, Bax, and Caspase 3 co-expressions under the current experimental conditions, these findings, therefore, contribute to a new insight into the molecular mechanisms involved during 5-FU administration upon the thymus and the possible events committed in the lymphophenia associated with chemotherapy.	Fluorouracil	66-70	BCL2-associated X protein	Mus musculus	105-108
18670882-5	2008	Here we report that m38.5 protein encoded by murine cytomegalovirus, which is unrelated to vMIA in its amino acid sequence, delays death receptor ligation-induced cell death, and that m38.5 associates with Bax, recruits it to mitochondria, and blocks Bax-mediated but not Bak-mediated mitochondrial outer membrane permeabilization.	bakuchiol	272-275	BCL2-associated X protein	Mus musculus	206-209
18675323-5	2008	Therefore, we used Affymetrix and qRT-PCR technology to characterize temporal mRNA changes in striatum in response to MPTP in genetically MPTP-sensitive, C57BL/6J, and MPTP-resistant Swiss Webster and BCL2-associated X protein (Bax)-/- mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	118-122	BCL2-associated X protein	Mus musculus	201-226
18628252-9	2008	In addition, DBA treatment altered the expression of a few apoptosis-related genes such as Fas, TRAF2, bcl-2, and bax in a dose-dependent manner.	dibromoacetic acid	13-16	BCL2-associated X protein	Mus musculus	114-117
18628687-4	2008	Furthermore, 15d-PGJ2 reduced (1) spinal cord inflammation and tissue injury (histological score), (2) neutrophil infiltration (myeloperoxidase activity), (3) nuclear factor-kappaB activation, (4) expression of iNOS, nitrotyrosine and TNF-alpha, and (5) apoptosis (terminal deoxynucleotidyltransferase-mediated uridine triphosphate end labeling staining, Bax, Bcl-2, and FAS-L expression).	15-deoxyprostaglandin J2	13-21	BCL2-associated X protein	Mus musculus	355-358
18597125-3	2008	Cell cycle arrest is associated with increased levels of p21 and reduced amounts of cyclin E. RAPTA-C treatment also enhances the levels of p53, and its treatment triggers the mitochondrial apoptotic pathway, as shown by the change in Bax to Bcl-2 ratios, resulting in cytochrome c release and caspase-9 activation.	dichloro(4-cymene)(1,3,5-triaza-7-phosphatricyclo(3.3.1.1)decane)ruthenium(II)	94-101	BCL2-associated X protein	Mus musculus	235-238
18818479-4	2008	A rapid generation of reactive oxygen species (ROS) was triggered by oridonin, and subsequently up-regulation of phospho-p53 (ser 15) expression and an increased expression ratio of Bax/Bcl-2 was observed.	Reactive Oxygen Species	22-45	BCL2-associated X protein	Mus musculus	182-185
18818479-4	2008	A rapid generation of reactive oxygen species (ROS) was triggered by oridonin, and subsequently up-regulation of phospho-p53 (ser 15) expression and an increased expression ratio of Bax/Bcl-2 was observed.	Reactive Oxygen Species	47-50	BCL2-associated X protein	Mus musculus	182-185
18818479-4	2008	A rapid generation of reactive oxygen species (ROS) was triggered by oridonin, and subsequently up-regulation of phospho-p53 (ser 15) expression and an increased expression ratio of Bax/Bcl-2 was observed.	oridonin	69-77	BCL2-associated X protein	Mus musculus	182-185
18818479-9	2008	Taken together, these observations showed that oridonin-induced cell death in L929 cells involved intracellular ROS generation, activation of phospho-p53 (ser 15), and up-regulation of the Bax/Bcl-2 ratio; and the augmented cell death by z-VAD-fmk was dependent on an increased ROS production.	oridonin	47-55	BCL2-associated X protein	Mus musculus	189-192
18563851-8	2008	In mice, tumor growth increased only slightly during liposome-Bax mRNA administration and the tumor volume on day 30 (10 days after completion of administration) was 36.7% of that in the saline control group.	Sodium Chloride	187-193	BCL2-associated X protein	Mus musculus	62-65
18180697-0	2008	Edaravone prevents Fas-induced fulminant hepatic failure in mice by regulating mitochondrial Bcl-xL and Bax.	Edaravone	0-9	BCL2-associated X protein	Mus musculus	104-107
18180697-0	2008	Edaravone prevents Fas-induced fulminant hepatic failure in mice by regulating mitochondrial Bcl-xL and Bax.	ammonium ferrous sulfate	19-22	BCL2-associated X protein	Mus musculus	104-107
18180697-13	2008	Western blotting showed that the Bcl-xL-Bax ratio of the edaravone group was much higher than that of the control group.	Edaravone	57-66	BCL2-associated X protein	Mus musculus	40-43
18180697-14	2008	In conclusion, edaravone might protect hepatocytes from Fas-induced mitochondria-dependent apoptosis by regulating mitochondrial Bcl-xL and Bax.	Edaravone	15-24	BCL2-associated X protein	Mus musculus	140-143
18180697-14	2008	In conclusion, edaravone might protect hepatocytes from Fas-induced mitochondria-dependent apoptosis by regulating mitochondrial Bcl-xL and Bax.	ammonium ferrous sulfate	56-59	BCL2-associated X protein	Mus musculus	140-143
18718084-3	2008	Cell proliferation was detected by MTT method, while the concentration of IL-2 was detected by ELISA, mRNA levels of bcl-2 and cdk2 in cells treated with evodiamine were detected by RT-PCR, the apoptosis rate and intracellular reactive oxygen species (ROS) concentration were analyzed by FCM, and the protein levels of BCL-2, CDK2 and BAX were determined by fluorescence microscope.	evodiamine	154-164	BCL2-associated X protein	Mus musculus	335-338
18317887-7	2008	Therefore, we analyzed Bax and Bcl2 levels in the dorsolateral prostate of TRAMP mice fed GTP and observed a shift in balance between Bax and Bcl2 favoring apoptosis.	Guanosine Triphosphate	90-93	BCL2-associated X protein	Mus musculus	134-137
18481334-6	2008	The data indicated that methylglyoxal induced mouse Neuro-2A neuroblastoma (Neuro-2A) cell apoptosis via alternation of mitochondria membrane potential and Bax/Bcl-2 ratio, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase.	Pyruvaldehyde	24-37	BCL2-associated X protein	Mus musculus	156-159
18468506-2	2008	We found that inhibition of calpain increased oridonin-induced Bax activation, cytochrome c release and PARP cleavage, indicating that calpain plays an anti-apoptotic role in oridonin-induced L929 cell apoptosis.	oridonin	46-54	BCL2-associated X protein	Mus musculus	63-66
18717958-5	2008	UVB-induced apoptosis was less pronounced in Baicalin-treated mice epidermis, which was accompanied by less p53 accumulation and higher Bcl-2/Bax ratio compared with that of untreated mice.	baicalin	45-53	BCL2-associated X protein	Mus musculus	142-145
21141587-4	2008	RESULTS: Naoyikang could ameliorate the capacity of learning and memory of AD model mice and reduce MAO-B activity in the brain tissue and activate the activity of Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme in the brain tissue and decrease the expression of Bax mRNA, but increase the expression of Bcl-2 mRNA in the model brain tissue.	naoyikang	9-18	BCL2-associated X protein	Mus musculus	262-265
21141587-6	2008	It could modify the metabolism of monoamine neurotransmitter in brain through reducing MAO-B activity and protect neurons by activating the activity of Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme and decrease Bax expression and increase Bcl-2 expression in the model brain tissue.	monoamine	34-43	BCL2-associated X protein	Mus musculus	212-215
18468506-2	2008	We found that inhibition of calpain increased oridonin-induced Bax activation, cytochrome c release and PARP cleavage, indicating that calpain plays an anti-apoptotic role in oridonin-induced L929 cell apoptosis.	oridonin	175-183	BCL2-associated X protein	Mus musculus	63-66
18635920-7	2008	PAB had no effect on mitochondrial membrane potential (MMP), but up-regulated the expressions of Bax and Bcl-2.	pseudolaric acid B	0-3	BCL2-associated X protein	Mus musculus	97-100
18606001-10	2008	Cell treatment with 250 microM homocysteine also triggered the onset of apoptosis, as demonstrated by the increased expression of early apoptotic markers such as Bax, caspase-3 and p53.	Homocysteine	31-43	BCL2-associated X protein	Mus musculus	162-165
18635920-9	2008	Additionally, PAB inhibited the localization of Bax in mitochondria, but Bcl-2 still was in the mitochondria to sustain MMP.	pseudolaric acid B	14-17	BCL2-associated X protein	Mus musculus	48-51
18450357-9	2008	15d-PGJ2 triggered the mitochondrial apoptotic pathway indicated by enhanced Bax expression, loss of mitochondrial membrane potential, cytochrome c release, and caspase-3 activation.	15-deoxy-delta(12,14)-prostaglandin J2	0-8	BCL2-associated X protein	Mus musculus	77-80
18645028-5	2008	(-)-Gossypol blocked the interactions of Bcl-xL with Bax or Bad in cancer cells by fluorescence resonance energy transfer assay and overcame the Bcl-xL protection of FL5.12 model cells on interleukin-3 withdrawal.	Gossypol	0-12	BCL2-associated X protein	Mus musculus	53-56
20731895-7	2008	RESULTS: The tumor-inhibiting rate of paclitaxel plus LY294002 (92.47%) was significantly higher than the paclitaxel alone (65.59%)(P &lt;0.05).The protein expression of bcl-2 in paclitaxel plus LY294002 group were significantly higher, while bax was significantly lower than that in the other two groups (P &lt;0.05).	Paclitaxel	38-48	BCL2-associated X protein	Mus musculus	243-246
18627295-6	2008	In DOX B1R(-/-) mice, cardiac dysfunction was improved compared to DOX control mice, which was associated with normalization of the bax/bcl-2 ratio and interleukin 6, as well as AKT activation state.	Doxorubicin	3-6	BCL2-associated X protein	Mus musculus	132-135
18296662-11	2008	Western blot analysis showed that (+)-SKF10047 inhibited the increase in Bax after glutamate treatments.	SK and F 10047	34-46	BCL2-associated X protein	Mus musculus	73-76
18296662-11	2008	Western blot analysis showed that (+)-SKF10047 inhibited the increase in Bax after glutamate treatments.	Glutamic Acid	83-92	BCL2-associated X protein	Mus musculus	73-76
18329639-4	2008	Treatment of mice with 100, 200, or 400 mg/kg/day of paeonol significantly inhibited the growth of the HepA tumor in mice, induced HepA cell apoptosis as demonstrated by light microscopy and electron microscopy analyses, decreased the expression of Bcl-2 and increased the expression of Bax in HepA tumor tissues in a dose-related manner.	paeonol	53-60	BCL2-associated X protein	Mus musculus	287-290
20731895-7	2008	RESULTS: The tumor-inhibiting rate of paclitaxel plus LY294002 (92.47%) was significantly higher than the paclitaxel alone (65.59%)(P &lt;0.05).The protein expression of bcl-2 in paclitaxel plus LY294002 group were significantly higher, while bax was significantly lower than that in the other two groups (P &lt;0.05).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	54-62	BCL2-associated X protein	Mus musculus	243-246
18272391-0	2008	Bax deficiency promotes an up-regulation of Bim(EL) and Bak during striatal and cortical postnatal development, and after excitotoxic injury.	bakuchiol	56-59	BCL2-associated X protein	Mus musculus	0-3
18272391-2	2008	Compared with wild-type animals, Bax knockout mice showed region- and time-dependent increases in pro-apoptotic proteins Bak and Bim(EL).	bakuchiol	121-124	BCL2-associated X protein	Mus musculus	33-36
18371449-5	2008	Endogenous ROS triggered apoptosis of wild-type mES through mitochondrial translocation of p53 and BAX but inhibited Nanog expression of SIRT1(-/-) mES, indicating that SIRT1 makes mES cells sensitive to ROS and inhibits p53-mediated suppression of Nanog expression.	Reactive Oxygen Species	11-14	BCL2-associated X protein	Mus musculus	99-102
18230621-0	2008	Chelerythrine induces apoptosis through a Bax/Bak-independent mitochondrial mechanism.	chelerythrine	0-13	BCL2-associated X protein	Mus musculus	42-45
18230621-5	2008	Interestingly, chelerythrine-mediated release of cytochrome c is rapid and precedes Bax translocation and integration.	chelerythrine	15-28	BCL2-associated X protein	Mus musculus	84-87
18230621-9	2008	These results, thus, argue for the existence of an alternative Bax/Bak-independent apoptotic mechanism that involves cyclosporine A-sensitive mitochondrial membrane permeability.	Cyclosporine	117-131	BCL2-associated X protein	Mus musculus	63-66
18211809-2	2008	We report that sequence of events after exposure of mouse embryonic fibroblast (MEF) cells to actinomycin D followed the order: Bax translocation--&gt;superoxide production--&gt;cardiolipin peroxidation.	Dactinomycin	94-107	BCL2-associated X protein	Mus musculus	128-131
18211809-3	2008	Genetic ablation of Bax/Bak inhibited actinomycin D induced superoxide production and cardiolipin peroxidation.	Dactinomycin	38-51	BCL2-associated X protein	Mus musculus	20-23
18211809-3	2008	Genetic ablation of Bax/Bak inhibited actinomycin D induced superoxide production and cardiolipin peroxidation.	Superoxides	60-70	BCL2-associated X protein	Mus musculus	20-23
18211809-6	2008	In isolated mitochondria, recombinant Bax enhanced succinate induced cardiolipin oxidation and cytochrome c release.	Succinic Acid	51-60	BCL2-associated X protein	Mus musculus	38-41
18211809-8	2008	Thus, cardiolipin peroxidation may be causatively and time-dependently related to Bax/Bak effects on ROS generation and peroxidase activation of cytochrome c.	Reactive Oxygen Species	101-104	BCL2-associated X protein	Mus musculus	82-85
18418439-7	2008	Hearts of NTG diabetic mice, but not Gsalpha mice, showed increased expression of proapoptosis Bax, downregulation in Bcl2, and an increase in the Bax/Bcl2 ratio.	Nitroglycerin	10-13	BCL2-associated X protein	Mus musculus	95-98
18337425-5	2008	We confirmed the absence of PC PCD as well as the normal PCD of EGCs in Bax-KO mice.	egcs	64-68	BCL2-associated X protein	Mus musculus	72-75
18418439-7	2008	Hearts of NTG diabetic mice, but not Gsalpha mice, showed increased expression of proapoptosis Bax, downregulation in Bcl2, and an increase in the Bax/Bcl2 ratio.	Nitroglycerin	10-13	BCL2-associated X protein	Mus musculus	147-150
18380009-5	2008	Experiments with the embryonic stem cell line, ESC-B5, disclose that CTN induces apoptosis via several mechanisms, including ROS generation, increased cytoplasmic free calcium levels, intracellular nitric oxide production, enhanced Bax/Bcl-2 ratio, loss of mitochondrial membrane potential, cytochrome c release, activation of caspase-9 and caspase-3, and p21-activated protein kinase 2 and c-Jun N-terminal protein kinase activation.	Citrinin	69-72	BCL2-associated X protein	Mus musculus	232-235
18281560-8	2008	Honokiol-induced apoptosis correlated with induction of Bax, Bak, and Bad and a decrease in Bcl-xL and Mcl-1 protein levels.	honokiol	0-8	BCL2-associated X protein	Mus musculus	56-59
18191336-5	2008	RESULTS: Radiation exposure of Bax- and Bak-deficient mice, both expressing a wild-type acid sphingomyelinase (ASMase) phenotype, indicated that Bax and Bak are both mandatory, though mutually independent, for the intestinal endothelial apoptotic response.	bakuchiol	40-43	BCL2-associated X protein	Mus musculus	145-148
17996028-0	2008	6-Hydroxydopamine activates the mitochondrial apoptosis pathway through p38 MAPK-mediated, p53-independent activation of Bax and PUMA.	Oxidopamine	0-17	BCL2-associated X protein	Mus musculus	121-124
17996028-5	2008	In contrast, 6-OHDA-induced cell death was associated with a significant translocation of the pro-apoptotic Bax protein from the cytosol to mitochondria and with a significant induction of the BH3-only protein PUMA.	Oxidopamine	13-19	BCL2-associated X protein	Mus musculus	108-111
17996028-6	2008	Experiments in mouse embryonic fibroblasts deficient in Bax or PUMA demonstrated a role for both proteins in 6-OHDA-induced apoptosis.	Oxidopamine	109-115	BCL2-associated X protein	Mus musculus	56-59
17996028-8	2008	In contrast, we found that p38 mitogen-activated protein kinase (MAPK) was activated early during 6-OHDA-induced apoptosis, and that treatment with the p38 MAPK inhibitor SKF86002 potently inhibited PUMA induction, green fluorescent protein-Bax redistribution and apoptosis in response to 6-OHDA.	Oxidopamine	98-104	BCL2-associated X protein	Mus musculus	241-244
17996028-9	2008	These data demonstrate a critical involvement of p38 MAPK, PUMA, and Bax in 6-OHDA-induced apoptosis.	Oxidopamine	76-82	BCL2-associated X protein	Mus musculus	69-72
18006096-11	2008	CONCLUSIONS: The radiosensitization effect of DCQ occurs through enhancement of radiation-induced apoptosis, which correlates to the inhibition of p-Akt kinase and Bcl-X(L) and the activation of Erk and Jnk kinases, but appears independent of p53 induction or modulation of Bax/Bcl-2 gene expression.	2-benzoyl-3-phenyl-6,7-dichloroquinoxaline-1,4-dioxide	46-49	BCL2-associated X protein	Mus musculus	274-277
18281560-9	2008	Transient transfection of PC-3 cells with Bak- and Bax-targeted siRNAs and Bcl-xL plasmid conferred partial yet significant protection against honokiol-induced apoptosis.	honokiol	143-151	BCL2-associated X protein	Mus musculus	51-54
18034189-7	2008	4-OOH-CY treatment induced reactive oxygen species production, upregulation of Bax, and nuclear relocation of the mitochondrial factors apoptosis-inducing factor (AIF) and endonuclease G (EndoG).	perfosfamide	0-8	BCL2-associated X protein	Mus musculus	79-82
18056705-3	2008	Thymocytes prepared from glucose-depleted wild-type mice but not from p53-deficient mice underwent apoptosis, which was accompanied by a remarkable phosphorylation of AMPKalpha and a significant induction of p53 as well as pro-apoptotic Bax.	Glucose	25-32	BCL2-associated X protein	Mus musculus	237-240
18174271-8	2008	GCDCA induced overexpression of CHOP and Bax in isolated WT hepatocytes, whereas CHOP-deficient hepatocytes had reduced cleaved caspase-3 expression and a lower propidium iodide index after GCDCA treatment.	Glycochenodeoxycholic Acid	0-5	BCL2-associated X protein	Mus musculus	41-44
18034189-8	2008	The antioxidant N-acetyl-L-cysteine substantially inhibited conformational changes of Bax, loss of mitochondrial membrane potential, nuclear relocation of mitochondrial factors, and apoptosis induction in 4-OOH-CY-treated T cells.	Acetylcysteine	16-35	BCL2-associated X protein	Mus musculus	86-89
19112467-6	2008	Furthermore, a translocation of Bax was found, after sphingosylphosphorylcholine treatment.	sphingosine phosphorylcholine	53-80	BCL2-associated X protein	Mus musculus	32-35
18226269-5	2008	In xenogrfated tumors, curcumin upregulated the expression of TRAIL-R1/DR4, TRAIL-R2/DR5, Bax, Bak, p21/WAF1, and p27/KIP1, and inhibited the activation of NFkappaB and its gene products such as cyclin D1, VEGF, uPA, MMP-2, MMP-9, Bcl-2 and Bcl-XL.	Curcumin	23-31	BCL2-associated X protein	Mus musculus	90-93
18203299-1	2008	AIM: To investigate genistein-induced apoptosis of implanted tumors of SG7901 cells in nude mice, and the relationship between this apoptosis and expression of Bcl-2 and Bax.	Genistein	20-29	BCL2-associated X protein	Mus musculus	170-173
18203299-9	2008	The positive rate of Bcl-2 protein was decreased progressively (11.9%+/-0.9%, 5.9%+/-0.7% and 4.2%+/-0.6%), and the positive rate of bax protein was increased progressively (0.9%+/-1.7%, 24.9%+/-0.8% and 29.6%+/-1.7%) by immunohistochemical staining, with increasing dose of genistein.	Genistein	275-284	BCL2-associated X protein	Mus musculus	133-136
17582397-7	2007	There was a smaller increase of hippocampal Bax protein levels following treatment with imipramine after 1 or 14 days, and following citalopram and amitriptyline after 14 but not 1 day.	Imipramine	88-98	BCL2-associated X protein	Mus musculus	44-47
17559077-2	2008	In particular, for the first time, we demonstrated that PGF2alpha increased osteoblast survival in a dose-dependent manner and we showed that the effect is correlated with an increase in Bcl-2/Bax ratio.	Dinoprost	56-65	BCL2-associated X protein	Mus musculus	193-196
17906064-0	2008	Mitochondrial bax translocation accelerates DNA fragmentation and cell necrosis in a murine model of acetaminophen hepatotoxicity.	Acetaminophen	101-114	BCL2-associated X protein	Mus musculus	14-17
17906064-3	2008	APAP overdose induced Bax translocation from the cytosol to the mitochondria as early as 1 h after APAP injection.	Acetaminophen	0-4	BCL2-associated X protein	Mus musculus	22-25
17906064-3	2008	APAP overdose induced Bax translocation from the cytosol to the mitochondria as early as 1 h after APAP injection.	Acetaminophen	99-103	BCL2-associated X protein	Mus musculus	22-25
17906064-7	2008	Conversely, Bax gene knockout (Bax(-/-)) mice had 80% lower ALT activities, less DNA fragmentation, and less intermembrane protein release at 6 h. However, immunohistochemical staining for nitrotyrosine or APAP protein adducts did not show differences between wild-type and Bax(-/-) mice.	3-nitrotyrosine	189-202	BCL2-associated X protein	Mus musculus	12-15
17906064-10	2008	However, the persistent oxidant stress and peroxynitrite formation in mitochondria may eventually trigger the permeability transition pore opening and release intermembrane proteins independently of Bax.	Peroxynitrous Acid	43-56	BCL2-associated X protein	Mus musculus	199-202
17576196-7	2007	Vitamin E supplementation also prevented the Bax and Bcl-2/Bax ratio impairments caused by hypoxia, as well as the decrease in inner and outer mitochondrial membrane integrity.	Vitamin E	0-9	BCL2-associated X protein	Mus musculus	45-48
17576196-7	2007	Vitamin E supplementation also prevented the Bax and Bcl-2/Bax ratio impairments caused by hypoxia, as well as the decrease in inner and outer mitochondrial membrane integrity.	Vitamin E	0-9	BCL2-associated X protein	Mus musculus	59-62
17576196-8	2007	In conclusion, the results suggest that vitamin E prevents the loss of mitochondrial integrity and function, as well as the increase in Bax content, which suggests that mitochondria are involved in increased cell death induced by severe hypobaric hypoxia in mice skeletal muscle.	Vitamin E	40-49	BCL2-associated X protein	Mus musculus	136-139
17986867-7	2007	The SV40 immortalized mouse embryonic fibroblasts (MEFs) derived from Bak and Bax double knockout mice, but not Bid knockout mice, were significantly more resistant to BPDE-induced apoptosis compared with the MEFs derived from wild-type mice.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	168-172	BCL2-associated X protein	Mus musculus	78-81
17786558-4	2007	Ctx treatment also resulted in the inactivation of BCL-2 through phosphorylation at serine 70, thereby perturbing the BAX/BCL-2 rheostat, and the subsequent activation of the cytochrome c-mediated death pathway.	Serine	84-90	BCL2-associated X protein	Mus musculus	118-121
17910606-4	2007	The mitochondrial apoptotic pathway, which plays a critical role in liver cell death during malarial infection, was almost completely suppressed by melatonin as it corrects both the overexpression of Bax and down-regulation of bcl-2 as revealed by semiquantitative RT-PCR.	Melatonin	148-157	BCL2-associated X protein	Mus musculus	200-203
17942726-2	2007	A Bax-dependent increase of mitochondrial-derived reactive oxygen species (ROS) begins in these cells soon after NGF withdrawal.	Reactive Oxygen Species	50-73	BCL2-associated X protein	Mus musculus	2-5
17942726-2	2007	A Bax-dependent increase of mitochondrial-derived reactive oxygen species (ROS) begins in these cells soon after NGF withdrawal.	Reactive Oxygen Species	75-78	BCL2-associated X protein	Mus musculus	2-5
17569628-4	2007	EGCG inhibited expressions of Bcl-2 and Bcl-XL and induced expressions of Bax, Bak, Bcl-XS and PUMA.	epigallocatechin gallate	0-4	BCL2-associated X protein	Mus musculus	74-77
17569628-5	2007	Mouse embryonic fibroblasts (MEFs) derived from Bax and Bak double knockout mice exhibited greater protection against EGCG-induced apoptosis than wild-type or single knockout MEFs.	epigallocatechin gallate	118-122	BCL2-associated X protein	Mus musculus	48-51
17569628-6	2007	EGCG caused Bax activation in p53 -/- MEFs, suggesting that EGCG can induce apoptosis in the absence of p53.	epigallocatechin gallate	0-4	BCL2-associated X protein	Mus musculus	12-15
17569628-6	2007	EGCG caused Bax activation in p53 -/- MEFs, suggesting that EGCG can induce apoptosis in the absence of p53.	epigallocatechin gallate	60-64	BCL2-associated X protein	Mus musculus	12-15
17548347-6	2007	Genotoxic stress induced by camptothecin treatment of NPCs stabilized p53, which formed a complex with GSK3beta and activated Bax and caspase-3.	Camptothecin	28-40	BCL2-associated X protein	Mus musculus	126-129
17548347-7	2007	Camptothecin-induced activation of caspase-3 was reduced by GSK3 inhibitors in both bax(+)(/)(+) and bax(-/-) NPCs.	Camptothecin	0-12	BCL2-associated X protein	Mus musculus	84-87
17548347-7	2007	Camptothecin-induced activation of caspase-3 was reduced by GSK3 inhibitors in both bax(+)(/)(+) and bax(-/-) NPCs.	Camptothecin	0-12	BCL2-associated X protein	Mus musculus	101-104
18480150-7	2008	In 7,12-dimethyl benz(a)anthracene-exposed animals, downregulation approximately 30%) of antiapoptotic Bcl-2 and upregulation (approximately 60%) of pro-apoptotic Bax proteins were observed.	7,12-dimethyl benz(a	3-23	BCL2-associated X protein	Mus musculus	163-166
18480150-7	2008	In 7,12-dimethyl benz(a)anthracene-exposed animals, downregulation approximately 30%) of antiapoptotic Bcl-2 and upregulation (approximately 60%) of pro-apoptotic Bax proteins were observed.	anthracene	24-34	BCL2-associated X protein	Mus musculus	163-166
18030663-6	2007	Results of western blot analysis showed that [6]-gingerol upregulated the testosterone depleted levels of p53 in mouse prostate and upregulated its downstream regulator Bax and further activated Caspase-9 and Caspase-3 in both LNCaP cells and in mouse prostate.	gingerol	45-57	BCL2-associated X protein	Mus musculus	169-172
17914641-2	2007	To investigate the molecular mechanism of Bax-induced secondary metabolite biosynthesis, we determined the contents of nitric oxide (NO) of the transgenic Catharanthus roseus cells overexpressing a mouse Bax protein and checked the effects of NO specific scavenger 2,4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPITO) on Bax-induced terpenoid indole alkaloid (TIA) production of the cells.	Nitric Oxide	119-131	BCL2-associated X protein	Mus musculus	42-45
17914641-2	2007	To investigate the molecular mechanism of Bax-induced secondary metabolite biosynthesis, we determined the contents of nitric oxide (NO) of the transgenic Catharanthus roseus cells overexpressing a mouse Bax protein and checked the effects of NO specific scavenger 2,4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPITO) on Bax-induced terpenoid indole alkaloid (TIA) production of the cells.	1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole	265-328	BCL2-associated X protein	Mus musculus	42-45
17914641-2	2007	To investigate the molecular mechanism of Bax-induced secondary metabolite biosynthesis, we determined the contents of nitric oxide (NO) of the transgenic Catharanthus roseus cells overexpressing a mouse Bax protein and checked the effects of NO specific scavenger 2,4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPITO) on Bax-induced terpenoid indole alkaloid (TIA) production of the cells.	cpito	330-335	BCL2-associated X protein	Mus musculus	42-45
17914641-2	2007	To investigate the molecular mechanism of Bax-induced secondary metabolite biosynthesis, we determined the contents of nitric oxide (NO) of the transgenic Catharanthus roseus cells overexpressing a mouse Bax protein and checked the effects of NO specific scavenger 2,4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPITO) on Bax-induced terpenoid indole alkaloid (TIA) production of the cells.	Secologanin Tryptamine Alkaloids	352-377	BCL2-associated X protein	Mus musculus	42-45
17914641-2	2007	To investigate the molecular mechanism of Bax-induced secondary metabolite biosynthesis, we determined the contents of nitric oxide (NO) of the transgenic Catharanthus roseus cells overexpressing a mouse Bax protein and checked the effects of NO specific scavenger 2,4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPITO) on Bax-induced terpenoid indole alkaloid (TIA) production of the cells.	Secologanin Tryptamine Alkaloids	379-382	BCL2-associated X protein	Mus musculus	42-45
17914641-4	2007	Treatment of cPITO not only inhibited the Bax-triggered NO burst but also suppressed the Bax-induced TIA production.	cpito	13-18	BCL2-associated X protein	Mus musculus	42-45
17914641-4	2007	Treatment of cPITO not only inhibited the Bax-triggered NO burst but also suppressed the Bax-induced TIA production.	cpito	13-18	BCL2-associated X protein	Mus musculus	89-92
17602169-8	2007	BBN administration increased p53-mediated expression of p21, Mdm2 and Bax, and the inducible expression of p21 was significantly enhanced in Nrf2-/- mice.	Butylhydroxybutylnitrosamine	0-3	BCL2-associated X protein	Mus musculus	70-73
17974986-12	2007	Moreover, bosentan pretreatment resulted in reduced tumor necrosis factor-alpha content, lipid peroxidation, and Bax expression, as well as increased GATA-4 expression.	Bosentan	10-18	BCL2-associated X protein	Mus musculus	113-116
17618303-7	2007	The diterpenes prevented apoptosis through a mechanism compatible with the inhibition of caspase-3 activation, release of cytochrome c to the cytosol and p53 overexpression, as well as an alteration in the levels of proteins of the Bcl-2 family, in particular, the levels of Bax.	Diterpenes	4-14	BCL2-associated X protein	Mus musculus	275-278
17415663-6	2007	Collectively, ROS induced by proteasome inhibition mediates a mitochondrial dysfunction in neuronal cells that culminates in death through caspase- and Bax-independent mechanisms.	Reactive Oxygen Species	14-17	BCL2-associated X protein	Mus musculus	152-155
17635523-4	2007	The regulation of expression of Bax and Bcl-2 was also checked by western blotting after Ciprofloxacin treatment.	Ciprofloxacin	89-102	BCL2-associated X protein	Mus musculus	32-35
17372679-0	2007	Pro-apoptotic activity of imidazole derivatives mediated by up-regulation of Bax and activation of CAD in Ehrlich Ascites Tumor cells.	imidazole	26-35	BCL2-associated X protein	Mus musculus	77-80
17372679-2	2007	Delineating further into molecular mechanisms leading to apoptosis of EAT cells, we observed that imidazole derivatives induce tumor cell death by the up-regulation of proto-oncoprotein Bax, release of cytochrome c from the mitochondria which activates caspase-3 and activated caspase-3 activates CAD (Caspase Activated DNase) causes DNA fragmentation.	imidazole	98-107	BCL2-associated X protein	Mus musculus	186-189
17635523-7	2007	The two cell lines expressed the same level of Bax and Bcl-2 following stimulation by Ciprofloxacin.	Ciprofloxacin	86-99	BCL2-associated X protein	Mus musculus	47-50
17410096-0	2007	The pathological role of Bax in cisplatin nephrotoxicity.	Cisplatin	32-41	BCL2-associated X protein	Mus musculus	25-28
17909501-3	2007	The results of in situ hybridization experiments indicate that daidzein could help increase the transcriptions of bcl-2 and decrease the transcriptions of bax in those brain regions of D-galactose-treated mice.	daidzein	63-71	BCL2-associated X protein	Mus musculus	155-158
17909501-3	2007	The results of in situ hybridization experiments indicate that daidzein could help increase the transcriptions of bcl-2 and decrease the transcriptions of bax in those brain regions of D-galactose-treated mice.	Galactose	185-196	BCL2-associated X protein	Mus musculus	155-158
17909501-5	2007	These results suggest that daidzein in soybean can inhibit the D-gal induced apoptosis via Bcl-2/Bax apoptotic pathway and be a potential medical candidate for neurodegeneration therapy.	daidzein	27-35	BCL2-associated X protein	Mus musculus	97-100
17364147-8	2007	Together, these results show that sepsis increases steroid-induced thymic lymphoid cell apoptosis, which is associated with reduced SOCS-1 expression and increased Bax translocation to mitochondria.	Steroids	51-58	BCL2-associated X protein	Mus musculus	164-167
17880775-5	2007	In contrast, administration of BLM-treated mice with TDZD-8 (1 mg/kg daily) significantly reduced (I) the degree of lung injury, (II) the increase in staining (immunohistochemistry) for myeloperoxidase (MPO), nitrotyrosine, iNOS, TNF-alpha and IL-1beta and (III) the degree of apoptosis, as evaluated by Bax and Bcl-2 immunoreactivity and TUNEL staining.	Bleomycin	31-34	BCL2-associated X protein	Mus musculus	304-307
17880775-5	2007	In contrast, administration of BLM-treated mice with TDZD-8 (1 mg/kg daily) significantly reduced (I) the degree of lung injury, (II) the increase in staining (immunohistochemistry) for myeloperoxidase (MPO), nitrotyrosine, iNOS, TNF-alpha and IL-1beta and (III) the degree of apoptosis, as evaluated by Bax and Bcl-2 immunoreactivity and TUNEL staining.	4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione	53-59	BCL2-associated X protein	Mus musculus	304-307
17449502-10	2007	Moreover, transcriptional analysis by real-time RT-PCR showed an increased level of pro-apoptotic mRNA transcripts (FAS, BAX, caspase 3) in paclitaxel-treated arteries.	Paclitaxel	140-150	BCL2-associated X protein	Mus musculus	121-124
17669262-0	2007	Gene expression profiling of rewarding effect in methamphetamine treated Bax-deficient mouse.	Methamphetamine	49-64	BCL2-associated X protein	Mus musculus	73-76
17669262-3	2007	According to a previous study, Bax was involved in neurotoxicity by methamphetamine, but the function of Bax in rewarding effect has not yet been elucidated.	Methamphetamine	68-83	BCL2-associated X protein	Mus musculus	31-34
17669262-5	2007	In the present study, we treated chronic methamphetamine exposure in a Bax-deficient mouse model and examined behavioral change using a conditioned place preference (CPP) test.	Methamphetamine	41-56	BCL2-associated X protein	Mus musculus	71-74
17410096-2	2007	In cultured tubular epithelial cells, cisplatin can activate the proapoptotic protein Bax resulting in cytochrome c release, caspase activation, and apoptosis.	Cisplatin	38-47	BCL2-associated X protein	Mus musculus	86-89
17410096-3	2007	Definitive evidence for the involvement of Bax in cisplatin nephrotoxicity in vivo, however, is lacking.	Cisplatin	50-59	BCL2-associated X protein	Mus musculus	43-46
17410096-4	2007	We analyzed Bax regulation during cisplatin nephrotoxicity in wild-type mice and determined the pathological role of Bax using mice in which this gene was knocked out.	Cisplatin	34-43	BCL2-associated X protein	Mus musculus	12-15
17410096-5	2007	In wild-type mice, cisplatin induced Bax in renal tubular cells which became active, accumulated in the mitochondria, and was accompanied by acute kidney injury.	Cisplatin	19-28	BCL2-associated X protein	Mus musculus	37-40
17410096-6	2007	Compared with the wild-type mice renal function, as measured by blood urea nitrogen and serum creatinine, was partially but significantly preserved in Bax knockout mice.	Creatinine	94-104	BCL2-associated X protein	Mus musculus	151-154
17410096-8	2007	Additionally, cisplatin-induced cytochrome c release was attenuated in the Bax-deficient mice.	Cisplatin	14-23	BCL2-associated X protein	Mus musculus	75-78
17410096-10	2007	Collectively, our results provide compelling evidence for a role of Bax and its related apoptotic pathway in cisplatin nephrotoxicity.	Cisplatin	109-118	BCL2-associated X protein	Mus musculus	68-71
17718425-6	2007	Elevated expression of Bax was obviously observed after DOX treatment, while this elevation was prevented by MT induction by Zinc.	Doxorubicin	56-59	BCL2-associated X protein	Mus musculus	23-26
17718425-8	2007	CONCLUSION: These findings suggest that metallothionein induced by Zinc exhibits protective effects on the cardiac apoptosis of DOX, which might be mediated through the prevention of Bax protein up-regulation by DOX and associated elevation of Bax/Bcl-2 ratio.	Doxorubicin	128-131	BCL2-associated X protein	Mus musculus	183-186
17718425-8	2007	CONCLUSION: These findings suggest that metallothionein induced by Zinc exhibits protective effects on the cardiac apoptosis of DOX, which might be mediated through the prevention of Bax protein up-regulation by DOX and associated elevation of Bax/Bcl-2 ratio.	Doxorubicin	128-131	BCL2-associated X protein	Mus musculus	244-247
17718425-8	2007	CONCLUSION: These findings suggest that metallothionein induced by Zinc exhibits protective effects on the cardiac apoptosis of DOX, which might be mediated through the prevention of Bax protein up-regulation by DOX and associated elevation of Bax/Bcl-2 ratio.	Doxorubicin	212-215	BCL2-associated X protein	Mus musculus	183-186
17318368-5	2007	Immunoblotting analysis also indicated that ajoene plus t10,c12CLA caused a greater increase in phosphorylation of c-Jun N-terminal kinase (JNK) and Bax expression and a greater release of mitochondrial proteins (cytochrome c, AIF) than additive responses to each compound alone.	ajoene	44-50	BCL2-associated X protein	Mus musculus	149-152
17384938-1	2007	OBJECTIVES: This study analyzes the effects of prolonged administration of methadone and withdrawal on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and caspase-8) and the mitochondrial (Bcl-2, Bcl-x(L), Bad, and Bax) apoptotic pathways.	Methadone	75-84	BCL2-associated X protein	Mus musculus	319-322
17589894-0	2007	Effect of targeted magnetic nanoparticles containing 5-FU on expression of bcl-2, bax and caspase 3 in nude mice with transplanted human liver cancer.	Fluorouracil	53-57	BCL2-associated X protein	Mus musculus	82-85
17589894-9	2007	CONCLUSION: The targeted magnetic nanoparticles containing 5-FU can improve the chemotherapeutic effect of 5-FU against hepatocellular carcinoma by decreasing the expression of bcl-2 gene, and increasing the expression of bax and caspase 3 genes.	Fluorouracil	59-63	BCL2-associated X protein	Mus musculus	222-225
17589894-9	2007	CONCLUSION: The targeted magnetic nanoparticles containing 5-FU can improve the chemotherapeutic effect of 5-FU against hepatocellular carcinoma by decreasing the expression of bcl-2 gene, and increasing the expression of bax and caspase 3 genes.	Fluorouracil	107-111	BCL2-associated X protein	Mus musculus	222-225
17367743-5	2007	We found that ROS levels were enhanced in livers of MnSOD(-/-) mice which were reduced in size and displayed signs of liver failure such as intracellular protein droplets, increased apoptotic bodies and Bax levels as well as multinuclear hepatocytes.	Reactive Oxygen Species	14-17	BCL2-associated X protein	Mus musculus	203-206
17277231-8	2007	The present study demonstrates the role of Bax and Bak as a critical regulator of curcumin-induced apoptosis and over-expression of Smac as interventional approaches to deal with Bax- and/or Bak-deficient chemoresistant cancers for curcumin-based therapy.	Curcumin	82-90	BCL2-associated X protein	Mus musculus	43-46
17331071-4	2007	Experiments in embryonic stem cells (ESC-B5) showed that CTN induces apoptosis via ROS (reactive oxygen species) generation, increased Bax/Bcl-2 ratio, loss of MMP (mitochondrial membrane potential), induction of cytochrome c release, and activation of caspase 3.	Citrinin	57-60	BCL2-associated X protein	Mus musculus	135-138
17277231-8	2007	The present study demonstrates the role of Bax and Bak as a critical regulator of curcumin-induced apoptosis and over-expression of Smac as interventional approaches to deal with Bax- and/or Bak-deficient chemoresistant cancers for curcumin-based therapy.	Curcumin	232-240	BCL2-associated X protein	Mus musculus	43-46
17277231-0	2007	Bax and Bak genes are essential for maximum apoptotic response by curcumin, a polyphenolic compound and cancer chemopreventive agent derived from turmeric, Curcuma longa.	Curcumin	66-74	BCL2-associated X protein	Mus musculus	0-3
17418876-4	2007	Treatment of the mice with AG126 and AG556 significantly reduced the degree of (1) spinal cord inflammation and tissue injury (histological score), (2) neutrophil infiltration (myeloperoxidase activity), (3) iNOS, nitrotyrosine, and PARP expression and (4) apoptosis (TUNEL staining and Bax and Bcl-2 expression).	AG 127	27-32	BCL2-associated X protein	Mus musculus	287-290
17277231-2	2007	The objective of this study was to examine the molecular mechanisms by which multidomain pro-apoptotic Bcl-2 family members Bax and Bak regulate curcumin-induced apoptosis using mouse embryonic fibroblasts (MEFs) deficient in Bax, Bak or both genes.	Curcumin	145-153	BCL2-associated X protein	Mus musculus	124-127
17277231-3	2007	Curcumin treatment resulted an increase in the protein levels of both Bax and Bak, and mitochondrial translocation and activation of Bax in MEFs to trigger drop in mitochondrial membrane potential, cytosolic release of apoptogenic molecules [cytochrome c and second mitochondria-derived activator of caspases (Smac)/direct inhibitor of apoptosis protein-binding protein with low isoelectric point], activation of caspase-9 and caspase-3 and ultimately apoptosis.	Curcumin	0-8	BCL2-associated X protein	Mus musculus	70-73
17277231-3	2007	Curcumin treatment resulted an increase in the protein levels of both Bax and Bak, and mitochondrial translocation and activation of Bax in MEFs to trigger drop in mitochondrial membrane potential, cytosolic release of apoptogenic molecules [cytochrome c and second mitochondria-derived activator of caspases (Smac)/direct inhibitor of apoptosis protein-binding protein with low isoelectric point], activation of caspase-9 and caspase-3 and ultimately apoptosis.	Curcumin	0-8	BCL2-associated X protein	Mus musculus	133-136
17277231-4	2007	Furthermore, MEFs derived from Bax and Bak double-knockout (DKO) mice exhibited even greater protection against curcumin-induced release of cytochrome c and Smac, activation of caspase-3 and caspase-9 and induction of apoptosis compared with wild-type MEFs or single-knockout Bax(-/-) or Bak(-/-) MEFs.	Curcumin	112-120	BCL2-associated X protein	Mus musculus	31-34
17277231-4	2007	Furthermore, MEFs derived from Bax and Bak double-knockout (DKO) mice exhibited even greater protection against curcumin-induced release of cytochrome c and Smac, activation of caspase-3 and caspase-9 and induction of apoptosis compared with wild-type MEFs or single-knockout Bax(-/-) or Bak(-/-) MEFs.	Curcumin	112-120	BCL2-associated X protein	Mus musculus	276-279
17089128-10	2007	Administration of STAT3 antisense oligonucleotide successfully induced apoptosis of LPMCs and counteracted the unbalanced expressions of Bcl-2 and Bax in LPMCs from colitis.	Oligonucleotides	34-49	BCL2-associated X protein	Mus musculus	147-150
17161385-9	2007	Finally, the METH injection was associated with increased expression of the proapoptotic proteins, Bax and Bid, but with decreased expression of the antideath protein, Bcl2.	Methamphetamine	13-17	BCL2-associated X protein	Mus musculus	99-102
17418876-4	2007	Treatment of the mice with AG126 and AG556 significantly reduced the degree of (1) spinal cord inflammation and tissue injury (histological score), (2) neutrophil infiltration (myeloperoxidase activity), (3) iNOS, nitrotyrosine, and PARP expression and (4) apoptosis (TUNEL staining and Bax and Bcl-2 expression).	AG 556	37-42	BCL2-associated X protein	Mus musculus	287-290
17265069-9	2007	The identification of the germ-cell apoptotic pathway induced after testicular IR, including the key players in the pathway subsequent to ROS (BAX, caspase 9, and caspase 2), aids our understanding of IR injury in the testis and provides a wider background for the development of therapeutic interventions to rescue testis function.	Reactive Oxygen Species	138-141	BCL2-associated X protein	Mus musculus	143-146
17448893-8	2007	The mitochondria from the ethanol-fed Sod1-/- mice had elevated levels of cleaved Bax, Bak, Bcl-xl, and adenine nucleotide translocator.	Ethanol	26-33	BCL2-associated X protein	Mus musculus	82-85
17448893-9	2007	Immunoprecipitation studies revealed increased association of Bax and Bak with the adenine nucleotide translocator.	Adenine Nucleotides	83-101	BCL2-associated X protein	Mus musculus	62-65
17208988-6	2007	Ten days post-MI, apoptosis among granulation tissue cells was significantly suppressed in the olmesartan-treated hearts, where expression of Fas, Bax, procaspase-3, and Daxx and activation of caspase-3, c-Jun NH(2)-terminal kinase, and c-Jun were all significantly attenuated.	olmesartan	95-105	BCL2-associated X protein	Mus musculus	147-150
17230516-8	2007	More importantly, vaccination with E7-presenting DCs transfected with BAK/BAX siRNA generated a strong therapeutic effect against an E7-expressing tumor in vaccinated mice, compared with DCs transfected with control siRNA.	bakuchiol	70-73	BCL2-associated X protein	Mus musculus	74-77
17223243-3	2007	MC-LR treatment (60 microg/kg of body weight) for 12h prompted large amount of ROS generation in mice liver, upregulated the expression of Bax and Bid, caused the mitochondrial membrane potential (MMP) loss and hepatocyte apoptosis as well as liver injury.	cyanoginosin LR	0-5	BCL2-associated X protein	Mus musculus	139-142
17655156-8	2007	CONCLUSION: Taspine has antitumor effect on the S180 sarcoma, and the mechanism may be through the way of decreasing the expressing of the VEGF, bFGF, Bcl-2 and Bax and inducing the vascular endothelial cell apoptosis.	taspine	12-19	BCL2-associated X protein	Mus musculus	161-164
17404107-4	2007	One such lead compound is the benzenesulfonyl derivative TW-37, which was designed to target the BH3-binding groove in Bcl-2 where proapoptotic Bcl-2 proteins, such as Bak, Bax, Bid, and Bim bind.	TW-37	57-62	BCL2-associated X protein	Mus musculus	173-176
17404107-4	2007	One such lead compound is the benzenesulfonyl derivative TW-37, which was designed to target the BH3-binding groove in Bcl-2 where proapoptotic Bcl-2 proteins, such as Bak, Bax, Bid, and Bim bind.	BH 3	97-100	BCL2-associated X protein	Mus musculus	173-176
17447031-2	2007	To investigate the effects of Bax on the biosynthesis of clinically important natural products in plant cells, we generate transgenic Catharanthus roseus cells overexpressing a mouse Bax protein under the beta-estradiol-inducible promoter.	Estradiol	205-219	BCL2-associated X protein	Mus musculus	183-186
17447031-5	2007	Northern and Western blotting results show that expression of mammalian Bax induces transcriptional activation of Tdc and Str, two key genes in terpenoid indole alkaloid biosynthetic pathway of Catharanthus roseus cells, and stimulates the accumulation of defense-related protein PR1 in the cells, showing that the mouse Bax triggers the defense responses of Catharanthus roseus cells and activates the terpenoid indole alkaloid biosynthetic pathway.	Secologanin Tryptamine Alkaloids	144-169	BCL2-associated X protein	Mus musculus	321-324
17447031-5	2007	Northern and Western blotting results show that expression of mammalian Bax induces transcriptional activation of Tdc and Str, two key genes in terpenoid indole alkaloid biosynthetic pathway of Catharanthus roseus cells, and stimulates the accumulation of defense-related protein PR1 in the cells, showing that the mouse Bax triggers the defense responses of Catharanthus roseus cells and activates the terpenoid indole alkaloid biosynthetic pathway.	Terpenes	144-153	BCL2-associated X protein	Mus musculus	321-324
17447031-5	2007	Northern and Western blotting results show that expression of mammalian Bax induces transcriptional activation of Tdc and Str, two key genes in terpenoid indole alkaloid biosynthetic pathway of Catharanthus roseus cells, and stimulates the accumulation of defense-related protein PR1 in the cells, showing that the mouse Bax triggers the defense responses of Catharanthus roseus cells and activates the terpenoid indole alkaloid biosynthetic pathway.	Indole Alkaloids	154-169	BCL2-associated X protein	Mus musculus	321-324
17097638-0	2007	Bax affects production of reactive oxygen by the mitochondria of non-apoptotic neurons.	reactive oxygen	26-41	BCL2-associated X protein	Mus musculus	0-3
17209037-9	2007	Finally, they demonstrate that Bax, Bid, and MMP-12 play similar roles in bleomycin-induced fibrosis, thereby highlighting the importance of this Bid-activated, Bax-mediated pathway and downstream MMP-12 in a variety of fibrogenic settings.	Bleomycin	74-83	BCL2-associated X protein	Mus musculus	31-34
17209037-9	2007	Finally, they demonstrate that Bax, Bid, and MMP-12 play similar roles in bleomycin-induced fibrosis, thereby highlighting the importance of this Bid-activated, Bax-mediated pathway and downstream MMP-12 in a variety of fibrogenic settings.	Bleomycin	74-83	BCL2-associated X protein	Mus musculus	161-164
17295509-9	2007	The induction of apoptosis in 3T3-L1 preadipocytes by capsaicin was mediated through the activation of caspase-3, Bax, and Bak, and then through the cleavage of PARP and the down-regulation of Bcl-2.	Capsaicin	54-63	BCL2-associated X protein	Mus musculus	114-117
17303011-10	2007	CONCLUSION: These results demonstrated that MK-AS was an effective antitumor antisense oligonucleotide in vivo in mice; its antitumor effect is associated with the increase of pro-apoptotic proteins, such as p53, Bax, and caspase-3, and the decrease of the anti-apoptotic protein, Bcl-2.	mk-as	44-49	BCL2-associated X protein	Mus musculus	213-216
17097638-3	2007	A Bax-dependent increase of mitochondrial-derived reactive oxygen species (ROS) that is an important component of the apoptotic cascade in these cells begins soon after NGF withdrawal.	Reactive Oxygen Species	50-73	BCL2-associated X protein	Mus musculus	2-5
17097638-3	2007	A Bax-dependent increase of mitochondrial-derived reactive oxygen species (ROS) that is an important component of the apoptotic cascade in these cells begins soon after NGF withdrawal.	Reactive Oxygen Species	75-78	BCL2-associated X protein	Mus musculus	2-5
17097638-4	2007	Here we report that Bax can also influence mitochondrial production of ROS in non-apoptotic sympathetic neurons.	Reactive Oxygen Species	71-74	BCL2-associated X protein	Mus musculus	20-23
17097638-7	2007	To enhance any effects that Bax might have on ROS levels in NGF-replete cells we exposed cultures to the ATP synthase inhibitor, oligomycin.	Oligomycins	129-139	BCL2-associated X protein	Mus musculus	28-31
17097638-9	2007	NGF-replete neurons from mice in which bax had been deleted had much higher levels of mitochondrial-derived ROS when treated with oligomycin than did bax wild-type cells.	Reactive Oxygen Species	108-111	BCL2-associated X protein	Mus musculus	39-42
17097638-9	2007	NGF-replete neurons from mice in which bax had been deleted had much higher levels of mitochondrial-derived ROS when treated with oligomycin than did bax wild-type cells.	Oligomycins	130-140	BCL2-associated X protein	Mus musculus	39-42
17097638-10	2007	Oligomycin treatment also caused greater hyperpolarization of DeltaPsi(m) in bax-deleted cells than in wild-type cells.	Oligomycins	0-10	BCL2-associated X protein	Mus musculus	77-80
17097638-11	2007	These findings indicate that Bax can affect mitochondrial ROS production in non-apoptotic neurons and may do so by altering DeltaPsi(m).	Reactive Oxygen Species	58-61	BCL2-associated X protein	Mus musculus	29-32
17316905-3	2007	Novel synthetic analogues of the endogenous neurosteroids allopregnanolone and dehydroepiandrostrone, inhibited excitotoxic cell death of P19-N neurons, by directly maintaining the activation of PKB/Akt kinase and interfering with the intrinsic mitochondrial apoptotic pathway, preserving cytochrome c in the mitochondria and Bax in the cytoplasm.	Pregnanolone	58-74	BCL2-associated X protein	Mus musculus	326-329
17316905-3	2007	Novel synthetic analogues of the endogenous neurosteroids allopregnanolone and dehydroepiandrostrone, inhibited excitotoxic cell death of P19-N neurons, by directly maintaining the activation of PKB/Akt kinase and interfering with the intrinsic mitochondrial apoptotic pathway, preserving cytochrome c in the mitochondria and Bax in the cytoplasm.	dehydroepiandrostrone	79-100	BCL2-associated X protein	Mus musculus	326-329
17041754-11	2006	Taken together, our study suggests that in vivo EGCG could induce apoptosis in S180 cells through alteration in G2/M phase of the cell cycle by up-regulation of p53, bax and down-regulation of c-myc, bcl-2 and U1B, U4-U6 UsnRNAs.	epigallocatechin gallate	48-52	BCL2-associated X protein	Mus musculus	166-169
17304106-3	2007	Treatment of the mice with z-VAD-fmk, a potent broad specific caspase inhibitor, significantly reduced the degree of (1) spinal cord inflammation and tissue injury (histological score), (2) neutrophil infiltration (myeloperoxidase activity), (3) nitrotyrosine formation, and (4) apoptosis (TUNEL staining and Bax and Bcl-2 expression).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	27-36	BCL2-associated X protein	Mus musculus	309-312
17207636-4	2007	Administration of phenyl-N-tert-butylnitrone (PBN), a potent ROS scavenger, reduced the development of thermal hyperalgesia and mechanical allodynia at 1 and 3 days post-CCI, and decreased the mRNA levels of bax, apaf-1, and caspase-9.	phenyl-N-tert-butylnitrone	18-44	BCL2-associated X protein	Mus musculus	208-211
17207636-4	2007	Administration of phenyl-N-tert-butylnitrone (PBN), a potent ROS scavenger, reduced the development of thermal hyperalgesia and mechanical allodynia at 1 and 3 days post-CCI, and decreased the mRNA levels of bax, apaf-1, and caspase-9.	phenyl-N-tert-butylnitrone	46-49	BCL2-associated X protein	Mus musculus	208-211
17584059-5	2007	Another stable non-toxic and non-polar lipophilic chelate, Copper(II)2(3,5-ditertiarybutylsalicylate)4, was found to prevent Bax-initiated and caspases-3-activation mediated apoptosis.	copper(ii)2(3,5-ditertiarybutylsalicylate)4	59-102	BCL2-associated X protein	Mus musculus	125-128
17340578-7	2007	In DMBA treated animals, downregulation of antiapoptotic Bcl-2 and upregulation of proapoptotic Bax and Caspase 3 in mouse liver was observed.	9,10-Dimethyl-1,2-benzanthracene	3-7	BCL2-associated X protein	Mus musculus	96-99
17135272-9	2007	Carbon monoxide inhibited the activation of Bid and the expression and mitochondrial translocation of Bax, whereas promoted Bcl-X(L)/Bax interaction and increased Bad phosphorylation.	Carbon Monoxide	0-15	BCL2-associated X protein	Mus musculus	102-105
17135272-9	2007	Carbon monoxide inhibited the activation of Bid and the expression and mitochondrial translocation of Bax, whereas promoted Bcl-X(L)/Bax interaction and increased Bad phosphorylation.	Carbon Monoxide	0-15	BCL2-associated X protein	Mus musculus	133-136
17135272-10	2007	We also show that carbon monoxide promoted an interaction of heme oxygenase-1 with Bax.	Carbon Monoxide	18-33	BCL2-associated X protein	Mus musculus	83-86
17234790-5	2007	Studies employing Bax and/or Bak knockout mouse embryonic fibroblasts (MEFs) confirm that Bax is required for ABT-737+/-roscovitine lethality, whereas Bak is primarily involved in potentiation of ABT-737-induced apoptosis by Mcl-1 down-regulation.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	110-113	BCL2-associated X protein	Mus musculus	90-93
17234790-5	2007	Studies employing Bax and/or Bak knockout mouse embryonic fibroblasts (MEFs) confirm that Bax is required for ABT-737+/-roscovitine lethality, whereas Bak is primarily involved in potentiation of ABT-737-induced apoptosis by Mcl-1 down-regulation.	Roscovitine	120-131	BCL2-associated X protein	Mus musculus	90-93
17622766-7	2007	Quantitative RT-PCR further showed that DHA remarkably downregulated the expression of antiapoptotic bcl-2 mRNA, but upregulated that of the proapoptotic gene bax mRNA.	artenimol	40-43	BCL2-associated X protein	Mus musculus	159-162
17121905-11	2006	CONCLUSIONS: The present study indicates that DATS administration inhibits growth of PC-3 xenografts in vivo in association with induction of Bax and Bak.	diallyl trisulfide	46-50	BCL2-associated X protein	Mus musculus	142-145
17157251-5	2006	Nonetheless, cBAK requires activation by truncated BID to induce cytochrome c release in mitochondria isolated from bak/bax double-knockout mouse embryonic fibroblasts.	cbak	13-17	BCL2-associated X protein	Mus musculus	120-123
17097561-0	2006	The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized.	BH 3	4-7	BCL2-associated X protein	Mus musculus	99-102
17097561-0	2006	The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	16-19	BCL2-associated X protein	Mus musculus	99-102
17097561-2	2006	Of seven putative BH3 mimetics tested, only ABT-737 triggered Bax/Bak-mediated apoptosis.	BH 3	18-21	BCL2-associated X protein	Mus musculus	62-65
17097561-2	2006	Of seven putative BH3 mimetics tested, only ABT-737 triggered Bax/Bak-mediated apoptosis.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	44-47	BCL2-associated X protein	Mus musculus	62-65
17116975-6	2006	In L929 cells treated with oridonin alone, the activated ERK decreased the ratio of Bcl-2/Bax by mediating the phosphorylation of Bcl-2, resulting in apoptosis; the Ras inhibitor manumycin A and Raf inhibitor GW5074 failed to inhibit this apoptosis, indicating that there is a signal other than Ras/Raf pathway activated ERK.	oridonin	27-35	BCL2-associated X protein	Mus musculus	90-93
16916958-3	2006	Our group previously demonstrated that in the thymus, MEL inhibits the release of Cytochrome C from mitochondria and the dexamethasone-dependent increase of bax mRNA levels.	Melatonin	54-57	BCL2-associated X protein	Mus musculus	157-160
16916958-3	2006	Our group previously demonstrated that in the thymus, MEL inhibits the release of Cytochrome C from mitochondria and the dexamethasone-dependent increase of bax mRNA levels.	Dexamethasone	121-134	BCL2-associated X protein	Mus musculus	157-160
17076657-0	2006	Recombinant human granulocyte colony-stimulating factor protects against MPTP-induced dopaminergic cell death in mice by altering Bcl-2/Bax expression levels.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	73-77	BCL2-associated X protein	Mus musculus	136-139
17076657-7	2006	G-CSF significantly prevented MPTP-induced loss of tyrosine hydroxylase-positive neurons (p &lt; 0.05), increased Bcl-2 protein and decreased Bax protein expression.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	30-34	BCL2-associated X protein	Mus musculus	142-145
17116975-6	2006	In L929 cells treated with oridonin alone, the activated ERK decreased the ratio of Bcl-2/Bax by mediating the phosphorylation of Bcl-2, resulting in apoptosis; the Ras inhibitor manumycin A and Raf inhibitor GW5074 failed to inhibit this apoptosis, indicating that there is a signal other than Ras/Raf pathway activated ERK.	manumycin	179-190	BCL2-associated X protein	Mus musculus	90-93
16935937-0	2006	Gossypol induces Bax/Bak-independent activation of apoptosis and cytochrome c release via a conformational change in Bcl-2.	Gossypol	0-8	BCL2-associated X protein	Mus musculus	17-20
17121941-6	2006	The SV40-immortalized mouse embryonic fibroblasts derived from Bax and Bak double knockout mice were significantly more resistant to BITC-induced DNA fragmentation compared with wild-type mouse embryonic fibroblasts.	benzyl isothiocyanate	133-137	BCL2-associated X protein	Mus musculus	63-66
16935937-4	2006	We found that gossypol, but not other Bcl-2-interacting molecules, induced cyto c release and loss of mitochondrial membrane potential (delta psi m) independently of mPTP and Bak/Bax activation.	Gossypol	14-22	BCL2-associated X protein	Mus musculus	179-182
16935937-5	2006	Furthermore, we found that gossypol induced an allosteric change in Bcl-2 in both bak(-/-)/bax(-/-) cells and Bcl-2 overexpressing cells.	Gossypol	27-35	BCL2-associated X protein	Mus musculus	91-94
16880202-5	2006	Aspirin exposure also resulted in an increase in the half-life of pd1EGFP, a model substrate of proteasome, as well as various intracellular substrates like Bax, IkappaB-alpha, p53, and p27(kip1).	Aspirin	0-7	BCL2-associated X protein	Mus musculus	157-160
16797631-0	2006	Trimethyltin-induced apoptosis is associated with upregulation of inducible nitric oxide synthase and Bax in a hippocampal cell line.	trimethyltin	0-12	BCL2-associated X protein	Mus musculus	102-105
16797631-8	2006	It was concluded that excessive ROS generation initiated the apoptotic cell death by upregulating iNOS followed by increased Bax expression which then led to loss of DeltaPsim and caspase-executed cell death.	Reactive Oxygen Species	32-35	BCL2-associated X protein	Mus musculus	125-128
16483740-4	2006	Also, a different pattern of intracellular localization of p65 in WT cells as well as IkappaBalpha and Bax in both cell lines was detected in response to MTX.	Methotrexate	154-157	BCL2-associated X protein	Mus musculus	103-106
16712891-5	2006	atRA-induced apoptosis was associated with upregulation of bcl-2, translocation of bax protein to the mitochondria from the cytosol, activation of caspase-3 and cytochrome c release into cytosol.	Tretinoin	0-4	BCL2-associated X protein	Mus musculus	83-86
16896890-9	2006	CLA-treated LL2 tumors showed decrease of PPARgamma and EGFR proteins and increase of BAX protein in comparison with untreated tumors.	Linoleic Acids, Conjugated	0-3	BCL2-associated X protein	Mus musculus	86-89
16462815-3	2006	Haloperidol-induced apoptosis is mediated by the sigma2 (sigma2) receptor system and does not involve the expected antagonism of the dopamine D(2) receptor, nor is it influenced by Vitamin E- or p53/Bax-mediated events.	Haloperidol	0-11	BCL2-associated X protein	Mus musculus	199-202
16951520-4	2006	RESULTS: Resveratrol of every dosage could improve the performance records of behavior tests in AD mice,could inhibit the SOD vitality and the MDA level both in the serum and in the brain, and could suppress the acetylcholinesterase vitality and the bax expression.	Resveratrol	9-20	BCL2-associated X protein	Mus musculus	250-253
16886631-10	2006	Moreover, sulindac sulfide activated caspases 3 and 8, decreased the levels of Bax and Bid proteins, caused cleavage of PARP and increased the expressions of the bax and caspase 3 genes.	sulindac sulfide	10-26	BCL2-associated X protein	Mus musculus	79-82
16886631-10	2006	Moreover, sulindac sulfide activated caspases 3 and 8, decreased the levels of Bax and Bid proteins, caused cleavage of PARP and increased the expressions of the bax and caspase 3 genes.	sulindac sulfide	10-26	BCL2-associated X protein	Mus musculus	162-165
16716514-3	2006	The purpose of the present study was to analyse the effects of naltrexone on the expression levels of proteins regulating the extrinsic (FasL and Fas) and the mitochondrial (Bcl-2, Bcl-xL, Bad and Bax) apoptotic pathways, as well as the active fragment of the executioner caspase-3 in the mouse brain.	Naltrexone	63-73	BCL2-associated X protein	Mus musculus	197-200
16716514-4	2006	Western blotting showed that a single injection of naltrexone (1 mg/kg) induced a down-regulation of the pro-apototic proteins Fas, FasL, Bad and Bax.	Naltrexone	51-61	BCL2-associated X protein	Mus musculus	146-149
16617056-9	2006	Studies using mouse embryonic fibroblasts deficient for both Bax and Bak indicate the contribution of both Bax and Bak in mediating cell death induced by resveratrol and the existence of Bax/Bak-independent cell death possibly through caspase-8- or caspase-2-mediated mitochondria-independent downstream caspase processing.	Resveratrol	154-165	BCL2-associated X protein	Mus musculus	61-64
16617056-9	2006	Studies using mouse embryonic fibroblasts deficient for both Bax and Bak indicate the contribution of both Bax and Bak in mediating cell death induced by resveratrol and the existence of Bax/Bak-independent cell death possibly through caspase-8- or caspase-2-mediated mitochondria-independent downstream caspase processing.	Resveratrol	154-165	BCL2-associated X protein	Mus musculus	107-110
16617056-9	2006	Studies using mouse embryonic fibroblasts deficient for both Bax and Bak indicate the contribution of both Bax and Bak in mediating cell death induced by resveratrol and the existence of Bax/Bak-independent cell death possibly through caspase-8- or caspase-2-mediated mitochondria-independent downstream caspase processing.	Resveratrol	154-165	BCL2-associated X protein	Mus musculus	107-110
16696956-6	2006	Rosiglitazone treatment reduced TUNEL(+)/activated caspase-3(+) cells, MPO(+)/Ox-42(+) inflammatory cell infiltrations, caspase-3 activity, and Bax(+) cells, as compared to the ischemia-vehicle group.	Rosiglitazone	0-13	BCL2-associated X protein	Mus musculus	144-147
16738485-0	2006	Prion protein protects against ethanol-induced Bax-mediated cell death in vivo.	Ethanol	31-38	BCL2-associated X protein	Mus musculus	47-50
16738485-2	2006	To determine whether prion protein can protect against Bax-mediated cell death in vivo, wild-type, null and prion over-expressing mice were subjected to Bax-dependent ethanol induced neuronal apoptotic cell death and the brains were immunostained for active caspase-3 as a downstream marker of Bax activation.	Ethanol	167-174	BCL2-associated X protein	Mus musculus	153-156
16738485-2	2006	To determine whether prion protein can protect against Bax-mediated cell death in vivo, wild-type, null and prion over-expressing mice were subjected to Bax-dependent ethanol induced neuronal apoptotic cell death and the brains were immunostained for active caspase-3 as a downstream marker of Bax activation.	Ethanol	167-174	BCL2-associated X protein	Mus musculus	153-156
16738485-3	2006	Bax activation occurs in all ethanol-injected mice independent of their genotype.	Ethanol	29-36	BCL2-associated X protein	Mus musculus	0-3
16723081-8	2006	Furthermore, FLZ prevented the increase of AChE and Bax, and the decrease of Bcl-2 immunoreactive cells in the CA1 region of the hippocampus, and reduced the increase of MDA content in the hippocampus in mice injected with Abeta(25-35).	flz	13-16	BCL2-associated X protein	Mus musculus	52-55
16621521-7	2006	Furthermore estradiol-induced apoptosis shown by with nuclear condensation and Bax/Bcl2 ratio.	Estradiol	12-21	BCL2-associated X protein	Mus musculus	79-82
16778361-4	2006	These changes of Bax were attenuated by pretreatment with SNP at a low-nontoxic concentration (100 microM) or dibutyryl cGMP (DBcGMP), a cell-permeable cGMP analogue.	dibutyryl-cGMP	110-124	BCL2-associated X protein	Mus musculus	17-20
16778361-4	2006	These changes of Bax were attenuated by pretreatment with SNP at a low-nontoxic concentration (100 microM) or dibutyryl cGMP (DBcGMP), a cell-permeable cGMP analogue.	dbcgmp	126-132	BCL2-associated X protein	Mus musculus	17-20
16778361-4	2006	These changes of Bax were attenuated by pretreatment with SNP at a low-nontoxic concentration (100 microM) or dibutyryl cGMP (DBcGMP), a cell-permeable cGMP analogue.	Cyclic GMP	120-124	BCL2-associated X protein	Mus musculus	17-20
16778361-5	2006	SB203580, a p38 mitogen-activated protein kinase (MAP kinase) inhibitor, blocked the effects of 4 mM SNP on Bax translocation and cell viability.	SB 203580	0-8	BCL2-associated X protein	Mus musculus	108-111
16778361-7	2006	These findings suggest that the NO/cGMP signaling pathway inhibits NO-induced apoptosis of macrophages by suppressing the p38 MAP kinase activation, which results in N-terminal conformational change of Bax and its translocation to mitochondria.	Cyclic GMP	35-39	BCL2-associated X protein	Mus musculus	202-205
16413235-8	2006	Western analysis revealed that DHT decreased Bcl-2 resulting in a significantly increased Bax/Bcl-2 ratio.	Dihydrotestosterone	31-34	BCL2-associated X protein	Mus musculus	90-93
16513270-0	2006	Neuroprotective effects of ebselen are associated with the regulation of Bcl-2 and Bax proteins in cultured mouse cortical neurons.	ebselen	27-34	BCL2-associated X protein	Mus musculus	83-86
16513270-2	2006	In this study, we sought to determine the relationship between alterations in the expression of Bcl-2 and Bax proteins and intracellular levels of calcium and the protective effects of ebselen with a concentration range of 0.01-20 microM against glutamate toxicity in cultured mouse cortical neurons.	ebselen	185-192	BCL2-associated X protein	Mus musculus	106-109
16513270-4	2006	Pretreatment with ebselen (8 microM) also prevented apoptotic alterations, completely reversed the suppression of Bcl-2 expression, and significantly inhibited Bax overexpression, but did not alter elevated intracellular concentrations of calcium induced by glutamate.	ebselen	18-25	BCL2-associated X protein	Mus musculus	160-163
16513270-6	2006	These results indicate that the neuroprotective effects of ebselen at low doses are associated with the regulation of Bcl-2 and Bax proteins but appear to be independent of glutamate-mediated elevation of intracellular calcium, suggesting that different mechanisms are involved in the actions of low and high dose regimens.	ebselen	59-66	BCL2-associated X protein	Mus musculus	128-131
16413235-11	2006	Increased Bax/Bcl-2 ratio was essential since either Bcl-2 overexpression or Bax downregulation by RNA interference (RNAi) partially abrogated or reversed DHT-enhanced osteoblastic apoptosis.	Dihydrotestosterone	155-158	BCL2-associated X protein	Mus musculus	10-13
16413235-11	2006	Increased Bax/Bcl-2 ratio was essential since either Bcl-2 overexpression or Bax downregulation by RNA interference (RNAi) partially abrogated or reversed DHT-enhanced osteoblastic apoptosis.	Dihydrotestosterone	155-158	BCL2-associated X protein	Mus musculus	77-80
16488414-5	2006	In contrast, only when treated with 4-HC, caspase-9 activation and the increase in the intracellular expression of Bax were detected.	4-hydroxycyclophosphamide	36-40	BCL2-associated X protein	Mus musculus	115-118
16288207-7	2006	ODQ prolonged p53 half-life, induced phosphorylation of p53 on Ser15, and upregulated the p53-dependent gene products p21, murine double minute-2, and the proapoptotic, p53-responsive gene product Bax.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	0-3	BCL2-associated X protein	Mus musculus	197-200
17028925-5	2006	We found that the reduction of pulmonary colonies grown in EFA-deficient animals was associated with a high expression of apoptotic activity as revealed by the presence of apoptotic nuclei and a high immunoreactivity for bax.	Fatty Acids, Essential	59-62	BCL2-associated X protein	Mus musculus	221-224
16542588-0	2006	Inducing apoptosis and upregulation of Bax and Fas ligand expression by allicin in hepatocellular carcinoma in Balb/c nude mice.	allicin	72-79	BCL2-associated X protein	Mus musculus	39-42
16112698-9	2006	Folic acid also reduced VPA-induced alterations in p53, NF-kappaB, Pim-1, c-Myb, and Bax/Bcl-2 protein levels, while pantothenic acid prevented VPA-induced alterations in NF-kappaB, Pim-1, and c-Myb.	Folic Acid	0-10	BCL2-associated X protein	Mus musculus	85-88
16112698-9	2006	Folic acid also reduced VPA-induced alterations in p53, NF-kappaB, Pim-1, c-Myb, and Bax/Bcl-2 protein levels, while pantothenic acid prevented VPA-induced alterations in NF-kappaB, Pim-1, and c-Myb.	Valproic Acid	24-27	BCL2-associated X protein	Mus musculus	85-88
16562676-5	2006	RESULTS: In the YCF group, the escape latency was significantly shortened, the time of swim in the platform quadrant significantly increased, the apoptosis rate of hippocampus neural decreased; the level of Bcl-2 mRNA and the rate of Bcl-2/Bax increased, and the level of Bax mRNA decreased.	(2e)-N-Hydroxy-2-[1-(4-{[(4-{(1e)-1-[2-(N'-Hydroxycarbamimidoyl)hydrazinylidene]ethyl} Phenyl)carbamoyl]amino}phenyl)ethylidene]hydrazinecarboximidamide	16-19	BCL2-associated X protein	Mus musculus	240-243
16562676-5	2006	RESULTS: In the YCF group, the escape latency was significantly shortened, the time of swim in the platform quadrant significantly increased, the apoptosis rate of hippocampus neural decreased; the level of Bcl-2 mRNA and the rate of Bcl-2/Bax increased, and the level of Bax mRNA decreased.	(2e)-N-Hydroxy-2-[1-(4-{[(4-{(1e)-1-[2-(N'-Hydroxycarbamimidoyl)hydrazinylidene]ethyl} Phenyl)carbamoyl]amino}phenyl)ethylidene]hydrazinecarboximidamide	16-19	BCL2-associated X protein	Mus musculus	272-275
16475703-6	2006	Western blotting also showed that berberine increased the levels of Bax and cytochrome c and decreased the levels of Bcl-2 in both cell lines.	Berberine	34-43	BCL2-associated X protein	Mus musculus	68-71
16215995-5	2006	bax knock-out and wild-type mice pups were exposed to ethanol via vapor inhalation during the maximal period of neonatal cerebellar ethanol sensitivity and cerebellar tissue was subsequently assessed for Purkinje and granule cell number and ethanol-mediated generation of reactive oxygen species (ROS).	Ethanol	54-61	BCL2-associated X protein	Mus musculus	0-3
16337883-8	2006	In addition, transgenic mice administered melatonin (10 mg/kg) showed a significant reduction in upregulated expression of Bax, caspase-3 and Par-4, indicating inhibited triggering of neuronal apoptosis.	Melatonin	42-51	BCL2-associated X protein	Mus musculus	123-126
16679553-3	2006	Iron-induced mitochondrial damage and apoptosis were characterized by reactive oxygen species production, increased metallothionein and glutathione synthesis, caspase- 3 activation, NF-kappaB induction, and decreased Bcl-2 expression, without any significant change in Bax expression.	Iron	0-4	BCL2-associated X protein	Mus musculus	269-272
16140583-4	2006	The mechanism of morphine suppression of immunity might be through the suppression of E7-specific CD8+ T lymphocyte proliferation and the promotion of apoptosis of these cells by the Bcl-2 and Bax pathways.	Morphine	17-25	BCL2-associated X protein	Mus musculus	193-196
16888403-5	2006	RESULTS: The ratio of Bcl-2 to Bax expression levels significantly increased with 400-ppb FA exposure in OVA-immunized mice but not in mice without OVA immunization, although differences in each protein level were not significant among groups.	400-ppb fa	82-92	BCL2-associated X protein	Mus musculus	31-34
16143399-7	2006	Ceramide induced an increase in Bax expression, depolarization of mitochondrial membrane potential, and caspase activation.	Ceramides	0-8	BCL2-associated X protein	Mus musculus	32-35
16888403-0	2006	Inhalation of low-level formaldehyde increases the Bcl-2/Bax expression ratio in the hippocampus of immunologically sensitized mice.	Formaldehyde	24-36	BCL2-associated X protein	Mus musculus	57-60
16289892-8	2006	Alpha-linolenic acid- and riluzole treatment were associated with a reduction in cytopathological features of cell injury, including DNA fragmentation and Bax expression in the cortex and the caudate putamen.	alpha-Linolenic Acid	0-20	BCL2-associated X protein	Mus musculus	155-158
16289892-8	2006	Alpha-linolenic acid- and riluzole treatment were associated with a reduction in cytopathological features of cell injury, including DNA fragmentation and Bax expression in the cortex and the caudate putamen.	Riluzole	26-34	BCL2-associated X protein	Mus musculus	155-158
17177630-9	2006	There was a four-fold increase in Bax/Bcl-2 ratio in the heart of PB and PB+Stress treated mice while an attenuation was observed in aortic endothelium.	Pyridostigmine Bromide	66-68	BCL2-associated X protein	Mus musculus	34-37
17177630-9	2006	There was a four-fold increase in Bax/Bcl-2 ratio in the heart of PB and PB+Stress treated mice while an attenuation was observed in aortic endothelium.	Pyridostigmine Bromide	73-75	BCL2-associated X protein	Mus musculus	34-37
16418768-4	2005	In addition, z-VAD-fmk plus TNFalpha increased Bax expression without affecting Bcl-2 and cytochrome expression.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	13-22	BCL2-associated X protein	Mus musculus	47-50
17374968-7	2006	Interestingly, both proapoptotic (p53 and Bax) and antiapoptotic (Bcl-2 and MDM2)genes were downregulated in osteocytes treated with high-dose steroid hormones in the hypoxic environment.	Steroids	143-159	BCL2-associated X protein	Mus musculus	42-45
16418769-8	2005	In addition, oridonin increased the ratio of Bax/Bcl-2 protein expression, but TNFalpha did not.	oridonin	13-21	BCL2-associated X protein	Mus musculus	45-48
16272691-6	2005	Moreover, a higher dose of oridonin promoted p53 phosphorylation, increased Bax expression and subsequently induced death of low sensitive L929 cells, however, it had no effect on Bcl-2 expression.	oridonin	27-35	BCL2-associated X protein	Mus musculus	76-79
16309240-8	2005	Western blot analysis showed that apoptosis was induced by an increased expression of Bax and decreased expression of Bcl-2 after treatment with Ritonavir and ionizing radiation.	Ritonavir	145-154	BCL2-associated X protein	Mus musculus	86-89
16272691-7	2005	The increased Bcl-2/Bax ratio in oridonin low sensitive L929 cells did not inhibit caspase-9 or -3 activation, but suppressed the cleavage of poly (ADP-ribose) polymerase (PARP), indicating the existence of caspase-9 or -3 independent PARP activation.	oridonin	33-41	BCL2-associated X protein	Mus musculus	20-23
16334562-2	2005	METHODS: The effect of salidroside on peripheral blood cells, BMCs, and bone marrow cell cycle in bone marrow depressed anemia mice was detected by automatic blood cell analysator, white blood count and flow cytometry (FCM)respectively,and the expression of Bcl-2 and Bax of BMCs was detected by immunohistochemistry method simultaneously.	rhodioloside	23-34	BCL2-associated X protein	Mus musculus	268-271
16275996-7	2005	On the other hand, SV40 immortalized mouse embryonic fibroblasts derived from Bax-Bak double knockout mice were significantly more resistant to guggulsterone-induced cell killing compared with wild-type cells.	bakuchiol	82-85	BCL2-associated X protein	Mus musculus	78-81
16275996-7	2005	On the other hand, SV40 immortalized mouse embryonic fibroblasts derived from Bax-Bak double knockout mice were significantly more resistant to guggulsterone-induced cell killing compared with wild-type cells.	pregna-4,17-diene-3,16-dione	144-157	BCL2-associated X protein	Mus musculus	78-81
16254338-12	2005	In addition, the expression of F1L was essential to inhibit tBid-induced cytochrome c release in both wild-type murine embryonic fibroblasts (MEFs) and Bax-deficient MEFs, indicating that F1L could inhibit apoptosis in the presence and absence of Bax.	tBID	60-64	BCL2-associated X protein	Mus musculus	152-155
16254338-12	2005	In addition, the expression of F1L was essential to inhibit tBid-induced cytochrome c release in both wild-type murine embryonic fibroblasts (MEFs) and Bax-deficient MEFs, indicating that F1L could inhibit apoptosis in the presence and absence of Bax.	tBID	60-64	BCL2-associated X protein	Mus musculus	247-250
16254338-13	2005	tBid-induced Bak oligomerization and N-terminal exposure of Bak in Bax-deficient MEFs were inhibited during virus infection, as assessed by cross-linking and limited trypsin proteolysis.	tBID	0-4	BCL2-associated X protein	Mus musculus	67-70
16081520-0	2005	Methoxychlor directly affects ovarian antral follicle growth and atresia through Bcl-2- and Bax-mediated pathways.	Methoxychlor	0-12	BCL2-associated X protein	Mus musculus	92-95
16334562-4	2005	Additionally, the expression of Bcl-2 in BMCs was increased in low-dose and high-dose salidroside groups, especially the increase was significant in the low-dose salidroside group; moreover, the expression of Bax in BMCs was reduced significantly in both low-dose and high-dose salidroside groups.	rhodioloside	86-97	BCL2-associated X protein	Mus musculus	209-212
16334562-4	2005	Additionally, the expression of Bcl-2 in BMCs was increased in low-dose and high-dose salidroside groups, especially the increase was significant in the low-dose salidroside group; moreover, the expression of Bax in BMCs was reduced significantly in both low-dose and high-dose salidroside groups.	rhodioloside	162-173	BCL2-associated X protein	Mus musculus	209-212
16334562-4	2005	Additionally, the expression of Bcl-2 in BMCs was increased in low-dose and high-dose salidroside groups, especially the increase was significant in the low-dose salidroside group; moreover, the expression of Bax in BMCs was reduced significantly in both low-dose and high-dose salidroside groups.	rhodioloside	162-173	BCL2-associated X protein	Mus musculus	209-212
16334562-5	2005	CONCLUSION: These data suggest that salidroside may promote the recovery of hematopoietic function of the bone marrow depressed anemia in mice by ending off G0/G1-phase arrest, accelerating G0/G1-S phase and S-G2/M phase transition, up-regulating Bcl-2 expression, down-regulating Bax expression, and inhibiting BMCs apoptosis.	rhodioloside	36-47	BCL2-associated X protein	Mus musculus	281-284
16191100-0	2005	Effect of IL-2-Bax, a novel interleukin-2-receptor-targeted chimeric protein, on bleomycin lung injury.	Bleomycin	81-90	BCL2-associated X protein	Mus musculus	15-18
16148050-8	2005	Furthermore, fibroblast cells deficient in Bax and Bak, but not Bid, were resistant to bleomycin-induced cell death.	Bleomycin	87-96	BCL2-associated X protein	Mus musculus	43-46
16148050-10	2005	Bleomycin-induced Bax activation was prevented by the expression of a dominant negative JNK in MLE-12 cells.	Bleomycin	0-9	BCL2-associated X protein	Mus musculus	18-21
16191100-8	2005	Bleomycin induced a BAL lymphocytosis that was significantly attenuated by IL-2-Bax and IL-2-PE66(4Glu).	Bleomycin	0-9	BCL2-associated X protein	Mus musculus	80-83
16191100-10	2005	These results show that IL-2-Bax reduces the lymphocytic infiltration of the lungs in response to bleomycin, but this effect is not accompanied by a decrease in lung fibrosis.	Bleomycin	98-107	BCL2-associated X protein	Mus musculus	29-32
15987750-10	2005	Dexamethasone also lowered the increase in the proapoptotic Bax, which was increased by PA, and increased expression of the antiapoptotic Bcl-xL protein.	Dexamethasone	0-13	BCL2-associated X protein	Mus musculus	60-63
15987750-10	2005	Dexamethasone also lowered the increase in the proapoptotic Bax, which was increased by PA, and increased expression of the antiapoptotic Bcl-xL protein.	Puromycin Aminonucleoside	88-90	BCL2-associated X protein	Mus musculus	60-63
15789364-7	2005	The doxazosin treatment did not further decrease the expression of an already low level of Bcl-2 in all prostate tumors, but it increased the expression of Bax, and the activation of caspase-3, and the cleavage of a downstream substrate, PARP.	Doxazosin	4-13	BCL2-associated X protein	Mus musculus	156-159
16123348-4	2005	Moreover, exposure to a chronically high dose of glucose decreases interactions between GCK and mitochondria with an increase in Bax binding to mitochondria and cytochrome C release.	Glucose	49-56	BCL2-associated X protein	Mus musculus	129-132
16123348-8	2005	Our results show that this may be one mechanism by which glucose is toxic to beta-cells and suggests a novel approach to prevent and treat diabetes by manipulating Bax- and GCK-controlled signaling to promote apoptosis or proliferation.	Glucose	57-64	BCL2-associated X protein	Mus musculus	164-167
16077961-5	2005	Similarly, although etoposide induced-apoptosis was inhibited in Bax(-/-)/Bak(-/-)mouse embryonic fibroblasts, autophagy was not inhibited, which was regulated by Bcl-xL.	Etoposide	20-29	BCL2-associated X protein	Mus musculus	65-68
16188096-1	2005	OBJECTIVE: To study DNA damage, Bcl-2 and Bax expression, and ultrastructure change in spermatogenic cell of mice by cadmium exposure.	Cadmium	117-124	BCL2-associated X protein	Mus musculus	42-45
16046310-9	2005	3,4-DGE results in Bax oligomerization, release of cytochrome c from mitochondria, activation of caspases-9 and -3, and Bid proteolysis.	3,4-dideoxyglucosone-3-ene	0-7	BCL2-associated X protein	Mus musculus	19-22
16046310-12	2005	In contrast, antagonism of Bax by a Ku-70-derived peptide or antisense oligonucleotides prevented both apoptosis and cell death.	ku-70-derived peptide	36-57	BCL2-associated X protein	Mus musculus	27-30
16046310-13	2005	In conclusion, 3,4-DGE promotes apoptosis of cultured renal parenchymal cells by a Bax- and caspase-dependent mechanism.	3,4-dideoxyglucosone-3-ene	15-22	BCL2-associated X protein	Mus musculus	83-86
15979664-4	2005	In mouse embryonic fibroblasts, 10 microM As(III) stimulated cytochrome c release and apoptosis via a Bax/Bak-dependent mechanism.	as(iii)	42-49	BCL2-associated X protein	Mus musculus	102-105
16188096-10	2005	CONCLUSION: Cadmium exposure will cause the DNA break, Bcl-2 and Bax protein abnormal expression and ultrastructural change in spermatogenic cell.	Cadmium	12-19	BCL2-associated X protein	Mus musculus	65-68
15916740-8	2005	Picroside II 10 mg/kg was found to protect hepatocytes against apoptosis in a dose-dependent manner; it up-regulated the expression of bcl-2 genes, thus increased the bcl-2/bax ratio.	picroside II	0-12	BCL2-associated X protein	Mus musculus	173-176
15919200-6	2005	The presence of trastuzumab markedly attenuated the relative increase on p27 expression and the Bax:Bcl2 ratio induced by gefitinib.	Gefitinib	122-131	BCL2-associated X protein	Mus musculus	96-99
15621629-11	2005	In summary, ginsenoside Re showed protection from MPTP-induced apoptosis in the PD model mouse nigral neurons and this effect may be attributable to upregulating the expression of Bcl-2 protein, downregulating the expression of Bax, and iNOS protein, and inhibiting the activation of caspase-3.	Ginsenosides	12-23	BCL2-associated X protein	Mus musculus	228-231
15824117-8	2005	Even a single injection of paraquat + maneb in the non-transgenic treated group modulated several key pro- and anti-apoptotic proteins, including Bax, Bad, Bcl-xL, and upstream stress-induced cascade.	Paraquat	27-35	BCL2-associated X protein	Mus musculus	146-149
15716857-7	2005	The potential mechanism by which JNK promoted Bax translocation after ischemia was further studied using coimmunoprecipitation, and the results revealed that JNK activation caused serine phosphorylation of 14-3-3, a cytoplasmic sequestration protein of Bax, leading to Bax disassociation from 14-3-3 and subsequent translocation to mitochondria.	Serine	180-186	BCL2-associated X protein	Mus musculus	46-49
15769983-5	2005	We also found that manumycin induced translocation of Bcl-2-associated X protein (Bax), another possible mediator of cytochrome c release, from the cytosol to the mitochondria.	manumycin	19-28	BCL2-associated X protein	Mus musculus	54-80
15914633-11	2005	KCl-mediated MMP-9 upregulation was associated with an increase in proapoptotic protein Bax and apoptotic death of cells in the ganglion cell (GCL) and inner nuclear layer (INL), and subsequent loss of NF-L-positive ganglion cells and calretinin-positive amacrine cells.	Potassium Chloride	0-3	BCL2-associated X protein	Mus musculus	88-91
15769983-0	2005	Bcl-2-associated X protein is the main mediator of manumycin a-induced apoptosis in anaplastic thyroid cancer cells.	manumycin	51-62	BCL2-associated X protein	Mus musculus	0-26
15769983-5	2005	We also found that manumycin induced translocation of Bcl-2-associated X protein (Bax), another possible mediator of cytochrome c release, from the cytosol to the mitochondria.	manumycin	19-28	BCL2-associated X protein	Mus musculus	82-85
15769983-6	2005	Silencing Bax with a specific small interfering RNA blocked manumycin-induced mitochondrial condensation and cytochrome c release, arguing the dependence of manumycin-induced apoptosis on Bax.	manumycin	60-69	BCL2-associated X protein	Mus musculus	10-13
15769983-6	2005	Silencing Bax with a specific small interfering RNA blocked manumycin-induced mitochondrial condensation and cytochrome c release, arguing the dependence of manumycin-induced apoptosis on Bax.	manumycin	157-166	BCL2-associated X protein	Mus musculus	10-13
15769983-6	2005	Silencing Bax with a specific small interfering RNA blocked manumycin-induced mitochondrial condensation and cytochrome c release, arguing the dependence of manumycin-induced apoptosis on Bax.	manumycin	157-166	BCL2-associated X protein	Mus musculus	188-191
15769983-7	2005	Using a binary adenoviral vector system, we found that overexpression of Bax enhanced manumycin-induced apoptosis of ATC cells, and the combination of manumycin and overexpression of Bax increased inhibition of ATC xenograft growth in nude mice.	manumycin	86-95	BCL2-associated X protein	Mus musculus	73-76
15769983-7	2005	Using a binary adenoviral vector system, we found that overexpression of Bax enhanced manumycin-induced apoptosis of ATC cells, and the combination of manumycin and overexpression of Bax increased inhibition of ATC xenograft growth in nude mice.	manumycin	86-95	BCL2-associated X protein	Mus musculus	183-186
15769983-8	2005	Thus, we concluded that manumycin-induced apoptosis in ATC cells was primarily mediated by Bax and that increasing Bax expression may sensitize ATC cells to manumycin.	manumycin	24-33	BCL2-associated X protein	Mus musculus	91-94
15769983-8	2005	Thus, we concluded that manumycin-induced apoptosis in ATC cells was primarily mediated by Bax and that increasing Bax expression may sensitize ATC cells to manumycin.	manumycin	157-166	BCL2-associated X protein	Mus musculus	115-118
15899861-2	2005	Activation of the TNF-R1 receptor results in the cleavage of BID into truncated BID (tBID), which translocates to the mitochondria and induces the activation of BAX or BAK.	tBID	85-89	BCL2-associated X protein	Mus musculus	161-164
15854745-5	2005	In addition, it was found that pre-treatment with melatonin inhibits Abeta-induced increase in the levels of bax mRNA and that it enhances the level of bcl-2 expression.	Melatonin	50-59	BCL2-associated X protein	Mus musculus	109-112
15731293-8	2005	Moreover, Bax knockout mice showed resistance to AMPH-induced apoptotic cell death but not to AMPH-induced destruction of dopaminergic terminals.	Amphetamine	49-53	BCL2-associated X protein	Mus musculus	10-13
15851100-0	2005	Old yellow enzyme interferes with Bax-induced NADPH loss and lipid peroxidation in yeast.	NADP	46-51	BCL2-associated X protein	Mus musculus	34-37
15851100-3	2005	In knockout experiments, only deletion of OYE3, coding for yeast Old yellow enzyme, attenuated the rate of Bax-induced growth arrest, cell death and NADPH decrease.	NADP	149-154	BCL2-associated X protein	Mus musculus	107-110
15855635-7	2005	In dominant-negative CREB-transfected cells, dibutyryl cAMP no longer prevented cell injury or inhibited changes in mRNA expression of Bcl-2 and Bax.	dibutyryl	45-54	BCL2-associated X protein	Mus musculus	145-148
15855635-7	2005	In dominant-negative CREB-transfected cells, dibutyryl cAMP no longer prevented cell injury or inhibited changes in mRNA expression of Bcl-2 and Bax.	Cyclic AMP	55-59	BCL2-associated X protein	Mus musculus	145-148
15855635-8	2005	In mice with unilateral renal occlusion, ioversol increased urinary excretion of N-acetyl-beta-d-glucosaminidase with concomitant decreases in Bcl-2 mRNA, increases in Bax mRNA, activation of caspase-3, and induction of apoptosis in tubular and interstitial cells.	ioversol	41-49	BCL2-associated X protein	Mus musculus	168-171
15833884-0	2005	Flavokawain A, a novel chalcone from kava extract, induces apoptosis in bladder cancer cells by involvement of Bax protein-dependent and mitochondria-dependent apoptotic pathway and suppresses tumor growth in mice.	flavokawain A	0-13	BCL2-associated X protein	Mus musculus	111-114
15875769-8	2005	In the amifostine treatment group before irradiation, the increased rate of p53 and Bax was suppressed, particularly in the LDs-treated group.	Amifostine	7-17	BCL2-associated X protein	Mus musculus	84-87
15833884-4	2005	These effects of flavokawain A are accompanied by a time-dependent decrease in Bcl-x(L), a decrease in the association of Bcl-x(L) to Bax, and an increase in the active form of Bax protein.	flavokawain A	17-30	BCL2-associated X protein	Mus musculus	134-137
15833884-4	2005	These effects of flavokawain A are accompanied by a time-dependent decrease in Bcl-x(L), a decrease in the association of Bcl-x(L) to Bax, and an increase in the active form of Bax protein.	flavokawain A	17-30	BCL2-associated X protein	Mus musculus	177-180
15814648-0	2005	Caspase-dependent apoptosis induction by phenethyl isothiocyanate, a cruciferous vegetable-derived cancer chemopreventive agent, is mediated by Bak and Bax.	phenethyl isothiocyanate	41-65	BCL2-associated X protein	Mus musculus	152-155
15790513-8	2005	These results demonstrated that SN could induce apoptosis of macrophages through activation of ERK, and ERK activation might partially involve in the increased expression of p27 and Bax in apoptotic macrophages.	sinomenine	32-34	BCL2-associated X protein	Mus musculus	182-185
15668244-8	2005	An early increase in Bcl-2 to Bax ratio with sildenafil treatment was also observed in myocytes after SI-RO.	Sildenafil Citrate	45-55	BCL2-associated X protein	Mus musculus	30-33
15814648-5	2005	The SV40 immortalized mouse embryonic fibroblasts derived from Bak and Bax double knockout mice were significantly more resistant to PEITC-induced DNA fragmentation compared with wild-type or Bak-/- mouse embryonic fibroblasts.	phenethyl isothiocyanate	133-138	BCL2-associated X protein	Mus musculus	71-74
15814648-8	2005	CONCLUSION: The results of the present study indicate that caspase-dependent apoptosis by PEITC is mediated by Bak and Bax proteins.	phenethyl isothiocyanate	90-95	BCL2-associated X protein	Mus musculus	119-122
15831280-8	2005	It was also shown that nicotine increases the mRNA level of bax and decreases that of bcl-2.	Nicotine	23-31	BCL2-associated X protein	Mus musculus	60-63
15831280-10	2005	CONCLUSION(S): Nicotine appears to activate specific intracellular death-related pathways, probably by bax-dependent activation of caspase-3, inducing apoptosis in Leydig cells.	Nicotine	15-23	BCL2-associated X protein	Mus musculus	103-106
15846091-0	2005	Indirect effects of Bax and Bak initiate the mitochondrial alterations that lead to cytochrome c release during arsenic trioxide-induced apoptosis.	Arsenic Trioxide	112-128	BCL2-associated X protein	Mus musculus	20-23
15846091-4	2005	At clinically achievable concentrations, arsenic stimulated cytochrome c release and apoptosis via a Bax/Bak-dependent mechanism.	Arsenic	41-48	BCL2-associated X protein	Mus musculus	101-104
15868939-0	2005	Involvement of Bax, Bcl-2 and caspase 3 in hydroxyurea- or etoposide-induced apoptosis of mouse interleukin-3-dependent lymphoma cells.	Hydroxyurea	43-54	BCL2-associated X protein	Mus musculus	15-18
15868939-0	2005	Involvement of Bax, Bcl-2 and caspase 3 in hydroxyurea- or etoposide-induced apoptosis of mouse interleukin-3-dependent lymphoma cells.	Etoposide	59-68	BCL2-associated X protein	Mus musculus	15-18
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	142-145	BCL2-associated X protein	Mus musculus	90-93
15730564-3	2005	We and others, have previously reported that in a stable HT22 neuronal cell line, glutamate induces apoptosis as indicated by DNA fragmentation and up- and down-regulation of Bax (pro-apoptotic), and Bcl-2 (anti-apoptotic) genes respectively.	Glutamic Acid	82-91	BCL2-associated X protein	Mus musculus	175-178
15545281-0	2005	Taurine monochloramine activates a cell death pathway involving Bax and Caspase-9.	N-chlorotaurine	0-22	BCL2-associated X protein	Mus musculus	64-67
15545281-8	2005	TauNHCl treatment results in a conformational change in BAX that is associated with its activation.	taunhcl	0-7	BCL2-associated X protein	Mus musculus	56-59
15389801-10	2005	Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL-induced apoptosis in cancer cells through up-regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation.	Paclitaxel	24-34	BCL2-associated X protein	Mus musculus	203-206
15389801-10	2005	Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL-induced apoptosis in cancer cells through up-regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation.	Vincristine	36-47	BCL2-associated X protein	Mus musculus	203-206
15389801-10	2005	Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL-induced apoptosis in cancer cells through up-regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation.	Vinblastine	49-60	BCL2-associated X protein	Mus musculus	203-206
15389801-10	2005	Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL-induced apoptosis in cancer cells through up-regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation.	Etoposide	62-71	BCL2-associated X protein	Mus musculus	203-206
15389801-10	2005	Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL-induced apoptosis in cancer cells through up-regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation.	Doxorubicin	73-84	BCL2-associated X protein	Mus musculus	203-206
15389801-10	2005	Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL-induced apoptosis in cancer cells through up-regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation.	Camptothecin	90-102	BCL2-associated X protein	Mus musculus	203-206
15756018-8	2005	Treatment of EGCG-rich GTP in drinking water to 4T1 cells bearing BALB/c mice resulted in reduction of tumor growth accompanied with increase in Bax/Bcl-2 ratio, reduction in proliferating cell nuclear antigen and activation of caspase 3 in tumors.	epigallocatechin gallate	13-17	BCL2-associated X protein	Mus musculus	145-148
15756018-8	2005	Treatment of EGCG-rich GTP in drinking water to 4T1 cells bearing BALB/c mice resulted in reduction of tumor growth accompanied with increase in Bax/Bcl-2 ratio, reduction in proliferating cell nuclear antigen and activation of caspase 3 in tumors.	epigallocatechin gallate	23-26	BCL2-associated X protein	Mus musculus	145-148
15756018-8	2005	Treatment of EGCG-rich GTP in drinking water to 4T1 cells bearing BALB/c mice resulted in reduction of tumor growth accompanied with increase in Bax/Bcl-2 ratio, reduction in proliferating cell nuclear antigen and activation of caspase 3 in tumors.	Water	39-44	BCL2-associated X protein	Mus musculus	145-148
15694660-3	2005	We now show that in murine thymocytes, sulindac sulfide-induced cell death is p53, bax, Fas, and FasL independent.	sulindac sulfide	39-55	BCL2-associated X protein	Mus musculus	83-86
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Doxycycline	281-284	BCL2-associated X protein	Mus musculus	90-93
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Doxycycline	176-179	BCL2-associated X protein	Mus musculus	90-93
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	274-277	BCL2-associated X protein	Mus musculus	90-93
15672541-9	2004	Elevated p53, Bax, cytochrome c, caspase-3 and active fragments of caspase-3 protein were observed in the cells exposed to levodopa.	Levodopa	123-131	BCL2-associated X protein	Mus musculus	14-17
15578100-0	2004	Prostaglandin E2 reduces radiation-induced epithelial apoptosis through a mechanism involving AKT activation and bax translocation.	Dinoprostone	0-16	BCL2-associated X protein	Mus musculus	113-116
15578100-3	2004	Apoptosis in Bax(-/-) mice receiving 12 Gy was approximately 50% less than in WT mice, and the ability of dmPGE2 to attenuate apoptosis was lost in Bax(-/-) mice.	16,16-Dimethylprostaglandin E2	106-112	BCL2-associated X protein	Mus musculus	148-151
15578100-4	2004	Positional analysis revealed that apoptosis in the Bax(-/-) mice was diminished only in the bax-expressing cells of the lower crypts and that in WT mice, dmPGE2 decreased apoptosis only in the bax-expressing cells.	16,16-Dimethylprostaglandin E2	154-160	BCL2-associated X protein	Mus musculus	193-196
15578100-9	2004	Treatment with dmPGE2 did not alter bax or bcl-x expression but suppressed bax translocation to the mitochondrial membrane.	16,16-Dimethylprostaglandin E2	15-21	BCL2-associated X protein	Mus musculus	75-78
15578100-11	2004	The in vitro studies indicate that dmPGE2, most likely by signaling through the E prostaglandin receptor EP2, reduces radiation-induced apoptosis through transactivation of the EGFR and enhanced activation of AKT and that this results in reduced bax translocation to the mitochondria.	16,16-Dimethylprostaglandin E2	35-41	BCL2-associated X protein	Mus musculus	246-249
15525693-10	2005	Expression of bcl-2 was significantly increased in MXC- and HPTE-treated cells, while bax was decreased in MXC- and HPTE-treated cells compared to controls.	2,2-bis(4-hydroxyphenyl)-1,1,1-trichloroethane	116-120	BCL2-associated X protein	Mus musculus	86-89
15499039-4	2005	Activation of Bax also occurs in free cholesterol-loaded and oxysterol-treated mouse macrophages.	Cholesterol	38-49	BCL2-associated X protein	Mus musculus	14-17
15499039-4	2005	Activation of Bax also occurs in free cholesterol-loaded and oxysterol-treated mouse macrophages.	Oxysterols	61-70	BCL2-associated X protein	Mus musculus	14-17
15588723-4	2005	Here, we show that the molecular pathway leading to TFEC-mediated cell death is associated with an early cytosolic to mitochondrial translocation of BAX, a pro-apoptotic member of the BCL-2 family.	S-(1,1,2,2-Tetrafluoroethyl)cysteine	52-56	BCL2-associated X protein	Mus musculus	149-152
15588723-5	2005	Immunoblot analyses indicated movement of BAX (21 kDa) to the mitochondrial fraction after exposure to a cytotoxic concentration of TFEC (250 microM).	S-(1,1,2,2-Tetrafluoroethyl)cysteine	132-136	BCL2-associated X protein	Mus musculus	42-45
15588723-8	2005	Hence, TFEC-induced necrotic cell death in the TAMH cell line is mediated by BAX and antagonized by the anti-apoptotic BCL-2 family member, BCL-xL.	S-(1,1,2,2-Tetrafluoroethyl)cysteine	7-11	BCL2-associated X protein	Mus musculus	77-80
15657349-5	2005	As expected (-)-gossypol induced complete cytochrome c release from mitochondria, increased caspases-3 and -9 activity, and caused apoptotic death without affecting protein levels of Bcl-2, Bcl-X(L), Bax, and Bak.	Gossypol	12-24	BCL2-associated X protein	Mus musculus	200-203
15554929-5	2004	In wild-type mice, TNBS treatment resulted in colonic ulceration and marked apoptosis, which was associated with decreased colon content of the antiapoptotic protein Bcl-2, whereas the proapoptotic Bax was unchanged.	Trinitrobenzenesulfonic Acid	19-23	BCL2-associated X protein	Mus musculus	198-201
15488733-4	2004	Staurosporine-mediated activation of the pro-apoptotic BCL-2 family member, BAX, was inhibited in the epithelial cell line infected for 32 h with the lymphogranuloma venereum (LGV/L2) but not the murine pneumonitis (MoPn) strain of C. trachomatis, but inhibition of staurosporine-mediated BAX activation disappeared after 48 h of infection with the LGV/L2 strain.	Staurosporine	0-13	BCL2-associated X protein	Mus musculus	76-79
15272317-1	2004	Photoreceptors of bax(-/-)bak(-/-) but neither bax(-/-) mice nor bak(-/-) mice are protected from developmental apoptosis, suggesting that bax(-/-)bak(-/-) photoreceptors may also be protected from pathologic apoptosis.	bakuchiol	26-29	BCL2-associated X protein	Mus musculus	18-21
15557813-7	2004	Furthermore, pretreatment of LLC cells with ceramide/DMS not only increased the protein expression level of Bax, but also decreased Bcl-2 after gamma-irradiation.	Ceramides	44-52	BCL2-associated X protein	Mus musculus	108-111
15488733-4	2004	Staurosporine-mediated activation of the pro-apoptotic BCL-2 family member, BAX, was inhibited in the epithelial cell line infected for 32 h with the lymphogranuloma venereum (LGV/L2) but not the murine pneumonitis (MoPn) strain of C. trachomatis, but inhibition of staurosporine-mediated BAX activation disappeared after 48 h of infection with the LGV/L2 strain.	Staurosporine	0-13	BCL2-associated X protein	Mus musculus	289-292
15488733-4	2004	Staurosporine-mediated activation of the pro-apoptotic BCL-2 family member, BAX, was inhibited in the epithelial cell line infected for 32 h with the lymphogranuloma venereum (LGV/L2) but not the murine pneumonitis (MoPn) strain of C. trachomatis, but inhibition of staurosporine-mediated BAX activation disappeared after 48 h of infection with the LGV/L2 strain.	Staurosporine	266-279	BCL2-associated X protein	Mus musculus	76-79
15488733-6	2004	These results suggest that the ability to inhibit staurosporine-mediated BAX activation or to activate BAX due to the infection itself may vary as a function of the chlamydial strain.	Staurosporine	50-63	BCL2-associated X protein	Mus musculus	73-76
15467189-11	2004	Moreover, oridonin increased the ratio of Bax/Bcl-2 protein expression, whereas it had no effect on the expression of Bcl-xL.	oridonin	10-18	BCL2-associated X protein	Mus musculus	42-45
15180944-10	2004	Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release.	Lovastatin	83-93	BCL2-associated X protein	Mus musculus	56-59
15180944-10	2004	Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release.	Lovastatin	83-93	BCL2-associated X protein	Mus musculus	181-184
15180944-10	2004	Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release.	Lovastatin	109-119	BCL2-associated X protein	Mus musculus	56-59
15180944-10	2004	Since immunoelectron microscopy showed translocation of Bax to the mitochondria in lovastatin-treated cells, lovastatin-induced apoptosis may, therefore, be ultimately dependent on Bax induction of cytochrome c release.	Lovastatin	109-119	BCL2-associated X protein	Mus musculus	181-184
15380639-9	2004	Apoptosis was manifested by elevation of bax and bad mRNA levels, which was much more rapid and intense in the case of free doxorubicin and HYD conjugate.	Doxorubicin	124-135	BCL2-associated X protein	Mus musculus	41-44
15213903-5	2004	RESULTS: For the saline-treated mice, increased cellular apoptosis, suppressed expression of p53 and bcl-2 (with decreased bcl-2 to bax ratio) and increased caspase-3 activity were found for the I/R-injured small intestine.	Sodium Chloride	17-23	BCL2-associated X protein	Mus musculus	132-135
15604726-0	2004	Bax-induced cell death of Arabidopsis is meditated through reactive oxygen-dependent and -independent processes.	reactive	59-67	BCL2-associated X protein	Mus musculus	0-3
15604726-0	2004	Bax-induced cell death of Arabidopsis is meditated through reactive oxygen-dependent and -independent processes.	Oxygen	68-74	BCL2-associated X protein	Mus musculus	0-3
15604726-6	2004	Bax expression was followed by reactive oxygen species (ROS) accumulation.	Reactive Oxygen Species	31-54	BCL2-associated X protein	Mus musculus	0-3
15604726-6	2004	Bax expression was followed by reactive oxygen species (ROS) accumulation.	Reactive Oxygen Species	56-59	BCL2-associated X protein	Mus musculus	0-3
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	46-66	BCL2-associated X protein	Mus musculus	93-96
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	46-66	BCL2-associated X protein	Mus musculus	128-131
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	68-71	BCL2-associated X protein	Mus musculus	93-96
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	68-71	BCL2-associated X protein	Mus musculus	128-131
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Reactive Oxygen Species	141-144	BCL2-associated X protein	Mus musculus	93-96
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Reactive Oxygen Species	141-144	BCL2-associated X protein	Mus musculus	128-131
15604726-8	2004	However, some population of the ROS depleted cells still induced cell death, indicating that there is a process that Bax-mediated plant cell death is independent of ROS accumulation.	Reactive Oxygen Species	32-35	BCL2-associated X protein	Mus musculus	117-120
15604726-10	2004	Over-expression of a key redox-regulator, Arabidopsis nucleoside diphosphate kinase 2 (AtNDPK2) down-regulated ROS accumulation and suppressed Bax-mediated cell death and transient expression of Arabidopsis Bax inhibitor-1 (AtBI-1) substantially suppressed Bax-induced cell death without altering cellular ROS level.	Reactive Oxygen Species	111-114	BCL2-associated X protein	Mus musculus	207-210
15604726-10	2004	Over-expression of a key redox-regulator, Arabidopsis nucleoside diphosphate kinase 2 (AtNDPK2) down-regulated ROS accumulation and suppressed Bax-mediated cell death and transient expression of Arabidopsis Bax inhibitor-1 (AtBI-1) substantially suppressed Bax-induced cell death without altering cellular ROS level.	Reactive Oxygen Species	306-309	BCL2-associated X protein	Mus musculus	207-210
15604726-11	2004	Taken together, our results collectively suggest that the Bax-mediated cell death and its suppression in plants is mediated by ROS-dependent and -independent processes.	Reactive Oxygen Species	127-130	BCL2-associated X protein	Mus musculus	58-61
15256477-0	2004	Stimulatory effect of topical application of caffeine on UVB-induced apoptosis in the epidermis of p53 and Bax knockout mice.	Caffeine	45-53	BCL2-associated X protein	Mus musculus	107-110
15256477-6	2004	Topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(-/-) mice with UVB enhanced the UVB-induced increases in apoptotic sunburn cells at 6 h by 214% and 467%, respectively, and topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(-/-) mice with UVB enhanced the UVB-induced increase in caspase 3 (active form) positive cells at 6 h by 253% and 750%, respectively.	Caffeine	23-31	BCL2-associated X protein	Mus musculus	65-68
15256477-6	2004	Topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(-/-) mice with UVB enhanced the UVB-induced increases in apoptotic sunburn cells at 6 h by 214% and 467%, respectively, and topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(-/-) mice with UVB enhanced the UVB-induced increase in caspase 3 (active form) positive cells at 6 h by 253% and 750%, respectively.	Caffeine	23-31	BCL2-associated X protein	Mus musculus	77-80
15256477-6	2004	Topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(-/-) mice with UVB enhanced the UVB-induced increases in apoptotic sunburn cells at 6 h by 214% and 467%, respectively, and topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(-/-) mice with UVB enhanced the UVB-induced increase in caspase 3 (active form) positive cells at 6 h by 253% and 750%, respectively.	Caffeine	23-31	BCL2-associated X protein	Mus musculus	77-80
15256477-6	2004	Topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(-/-) mice with UVB enhanced the UVB-induced increases in apoptotic sunburn cells at 6 h by 214% and 467%, respectively, and topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(-/-) mice with UVB enhanced the UVB-induced increase in caspase 3 (active form) positive cells at 6 h by 253% and 750%, respectively.	Caffeine	23-31	BCL2-associated X protein	Mus musculus	77-80
15256477-7	2004	The results indicate that UVB-induced increases in apoptosis in the epidermis of wild-type mice are predominantly (but not entirely) by p53- and Bax-dependent pathways and that topical application of caffeine can enhance UVB-induced increases in apoptosis by p53- and Bax-independent pathways.	Caffeine	200-208	BCL2-associated X protein	Mus musculus	145-148
15256477-7	2004	The results indicate that UVB-induced increases in apoptosis in the epidermis of wild-type mice are predominantly (but not entirely) by p53- and Bax-dependent pathways and that topical application of caffeine can enhance UVB-induced increases in apoptosis by p53- and Bax-independent pathways.	Caffeine	200-208	BCL2-associated X protein	Mus musculus	268-271
15225679-5	2004	Four genes, BAX, calcyclin, osteopontin and Cu-Zn superoxide dismutase (SOD1), identified by the microarray as showing changes in mRNA level with nicotine treatment were investigated in detail.	Nicotine	146-154	BCL2-associated X protein	Mus musculus	12-15
15225679-6	2004	RT-PCR showed that nicotine exposure resulted in significant decreases in mRNA levels for BAX, calcyclin and osteopontin, but nicotine did not affect the mRNA level of SOD1.	Nicotine	19-27	BCL2-associated X protein	Mus musculus	90-93
15225679-7	2004	Nicotine-induced changes in BAX, calcyclin and osteopontin mRNAs showed a general correlation with stimulation of branching, implying a common mechanism for effects of nicotine on branching and on gene expression.	Nicotine	0-8	BCL2-associated X protein	Mus musculus	28-31
15225679-8	2004	BAX, calcyclin and osteopontin mRNA levels were found to be developmentally regulated, but only the effect of nicotine on BAX mRNA was parallel to the developmental change in vivo, suggesting that nicotine action cannot be explained simply as a stimulation of the embryonic lung"s developmental program.	Nicotine	110-118	BCL2-associated X protein	Mus musculus	122-125
15213903-7	2004	CONCLUSIONS: The results of our study suggest that I/R-induced apoptosis of the mouse small intestine may be related to p53 and bcl-2 suppression (with decreased bcl-2 to bax ratio) and activation of caspase 3 and that such apoptosis seems to be suppressed by FBS treatment.	r	53-54	BCL2-associated X protein	Mus musculus	171-174
15111020-10	2004	Striatal Bcl-2 was significantly decreased, while Bax was increased in MPTP treated mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	71-75	BCL2-associated X protein	Mus musculus	50-53
14973267-11	2004	Mice that overexpressed Bcl-2 or mice that were deficient in Bax were protected from MXC-induced atresia.	Methoxychlor	85-88	BCL2-associated X protein	Mus musculus	61-64
15172982-3	2004	DETA-NO-treated DCs became resistant to tumor-induced apoptosis because DETA-NO prevented tumor-induced changes in the expression of Bcl-2, Bax, and Bcl-xL; activation of caspase-9; and a reduction in the mitochondrial membrane potential.	DETA-NO	0-7	BCL2-associated X protein	Mus musculus	140-143
15172982-3	2004	DETA-NO-treated DCs became resistant to tumor-induced apoptosis because DETA-NO prevented tumor-induced changes in the expression of Bcl-2, Bax, and Bcl-xL; activation of caspase-9; and a reduction in the mitochondrial membrane potential.	DETA-NO	72-79	BCL2-associated X protein	Mus musculus	140-143
15111020-11	2004	Lithium treatment not only increased striatal Bcl-2 in control mice, but also prevented its reduction as induced by MPTP, and an opposing effect was seen with Bax.	Lithium	0-7	BCL2-associated X protein	Mus musculus	159-162
15111020-12	2004	The neuroprotective action of lithium in this model of Parkinson"s disease has been attributed to its antiapoptotic activity which among other factors includes induction of Bcl-2 and reduction of Bax.	Lithium	30-37	BCL2-associated X protein	Mus musculus	196-199
32585786-10	2004	Striatal Bcl-2 was significantly decreased, while Bax was increased in MPTP treated mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	71-75	BCL2-associated X protein	Mus musculus	50-53
14766674-2	2004	Administration of DOX (22.5 mg/kg ip) in mice upregulated the mRNA levels of Bax and MDM2, whereas PFT-alpha attenuated those levels when administered at a total dose of 4.4 mg/kg at 30 min before and 3 h after DOX challenge.	Doxorubicin	18-21	BCL2-associated X protein	Mus musculus	77-80
32585786-11	2004	Lithium treatment not only increased striatal Bcl-2 in control mice, but also prevented its reduction as induced by MPTP, and an opposing effect was seen with Bax.	Lithium	0-7	BCL2-associated X protein	Mus musculus	159-162
32585786-12	2004	The neuroprotective action of lithium in this model of Parkinson"s disease has been attributed to its antiapoptotic activity which among other factors includes induction of Bcl-2 and reduction of Bax.	Lithium	30-37	BCL2-associated X protein	Mus musculus	196-199
15125997-5	2004	BaP also induced the mitochondrial dysfunction, including transition of mitochondria membrane potential and cytosolic release of cytochrome c. Furthermore, a decrease in the expression of Bcl-2 to Bax ratio and phosphorylation of p53(Ser 15) were observed in BaP-treated cells.	Benzo(a)pyrene	0-3	BCL2-associated X protein	Mus musculus	197-200
15140181-0	2004	Nitric oxide-induced cell death of cerebrocortical murine astrocytes is mediated through p53- and Bax-dependent pathways.	Nitric Oxide	0-12	BCL2-associated X protein	Mus musculus	98-101
15050406-5	2004	Of the 23 marker genes, 6 (bax, c-fos, E124, hsf1, ikBa, and p57) were significantly (Mann-Whitney U tests, P &lt; 0.05) overexpressed in BZ-exposed mice.	Benzene	138-140	BCL2-associated X protein	Mus musculus	27-30
14750167-6	2004	The impact of Bax/Bcl-xL expression on gemcitabine-sensitivity in vivo was evaluated in orthotopic Colo357 tumors in SCID mice.	gemcitabine	39-50	BCL2-associated X protein	Mus musculus	14-17
14752510-0	2004	hsp70-DnaJ chaperone pair prevents nitric oxide- and CHOP-induced apoptosis by inhibiting translocation of Bax to mitochondria.	Nitric Oxide	35-47	BCL2-associated X protein	Mus musculus	107-110
14766674-5	2004	The protein levels of Bax and MDM2 were elevated by DOX and attenuated by PFT-alpha.	Doxorubicin	52-55	BCL2-associated X protein	Mus musculus	22-25
14718643-10	2004	Finally, thymocytes from mice exposed perinatally to TCDD showed higher levels of Fas, TRAIL, and DR5 mRNA, but the levels of Bcl-2, Bcl-xL, and Bax were either unaltered or changed moderately.	Polychlorinated Dibenzodioxins	53-57	BCL2-associated X protein	Mus musculus	145-148
15052282-5	2004	Catecholamine-treated mice had decreased Bcl-2 and increased Bax and BNIP1 expression, suggesting mitochondria-dependent apoptosis pathway activation.	Catecholamines	0-13	BCL2-associated X protein	Mus musculus	61-64
14744910-2	2004	METHODS: Retinal detachments were created in adult wild-type and Bax-deficient mice by subretinal injection of 1.4% sodium hyaluronate.	Hyaluronic Acid	116-134	BCL2-associated X protein	Mus musculus	65-68
14627695-0	2004	c-Myc sensitization to oxygen deprivation-induced cell death is dependent on Bax/Bak, but is independent of p53 and hypoxia-inducible factor-1.	Oxygen	23-29	BCL2-associated X protein	Mus musculus	77-80
14627695-10	2004	Thus, oxygen deprivation-induced cell death in fibroblasts with deregulated expression of c-Myc is independent of p53 or HIF-1 status, but is dependent on the Bcl-2 family member Bax or Bak to initiate mitochondrial dependent cell death.	Oxygen	6-12	BCL2-associated X protein	Mus musculus	179-182
14500572-0	2004	Involvement of Bax protein in the prevention of glucocorticoid-induced thymocytes apoptosis by melatonin.	Melatonin	95-104	BCL2-associated X protein	Mus musculus	15-18
14617800-6	2004	Phosphorylation of the transcription factor STAT3 on Ser-727, mediated by the extracellular signal-regulated kinase MAP kinase pathway, may contribute to the decrease in both Bax and Fas expression in p38 alpha-/- cells.	Serine	53-56	BCL2-associated X protein	Mus musculus	175-178
14559920-6	2004	These responses would be expected to activate the pro-apoptotic multi-BCL homology domain proteins BAX and BAK, leading to the previously reported release of cytochrome c observed during oxysterol-induced apoptosis.	Oxysterols	187-196	BCL2-associated X protein	Mus musculus	99-102
14559920-7	2004	Somewhat surprisingly, small interfering RNA knockdown of BAX resulted in a complete block of the induction of apoptosis by 25-hydroxycholesterol.	25-hydroxycholesterol	124-145	BCL2-associated X protein	Mus musculus	58-61
14695654-6	2004	The changes of Bax levels induced by etoposide that we have observed seemed to be modulated by this cytokine.	Etoposide	37-46	BCL2-associated X protein	Mus musculus	15-18
14500572-10	2004	In summary, the present results suggest that the antiapoptotic effect of melatonin on glucocorticoid-treated thymocytes would be a consequence of an inhibition of the mitochondrial pathway, presumably through the regulation of Bax protein levels.	Melatonin	73-82	BCL2-associated X protein	Mus musculus	227-230
14638906-9	2003	Apoptosis induced by CsA is associated with the translocation of Bax to the mitochondria and Bax antisense oligodeoxynucleotides protected from CsA-induced apoptosis.	Cyclosporine	21-24	BCL2-associated X protein	Mus musculus	65-68
14693041-10	2003	CONCLUSIONS: In HT22 mouse hippocampal cells, glutamate induced apoptosis that was associated with DNA fragmentation, morphological changes and up-regulation of the pro-apoptotic protein Bax and down-regulation of the anti-apoptotic protein Bcl-2.	Glutamic Acid	46-55	BCL2-associated X protein	Mus musculus	187-190
14638906-9	2003	Apoptosis induced by CsA is associated with the translocation of Bax to the mitochondria and Bax antisense oligodeoxynucleotides protected from CsA-induced apoptosis.	Cyclosporine	21-24	BCL2-associated X protein	Mus musculus	93-96
14638906-9	2003	Apoptosis induced by CsA is associated with the translocation of Bax to the mitochondria and Bax antisense oligodeoxynucleotides protected from CsA-induced apoptosis.	Cyclosporine	144-147	BCL2-associated X protein	Mus musculus	93-96
14531950-0	2003	Nimesulide inhibits tumor growth in mice implanted hepatoma: overexpression of Bax over Bcl-2.	nimesulide	0-10	BCL2-associated X protein	Mus musculus	79-82
14580681-4	2003	We also demonstrated that the rapid EPE-induced increase in hydrogen peroxide levels caused the translocation of Bax to mitochondria, and then mitochondrial cytochrome c was released.	Hydrogen Peroxide	60-77	BCL2-associated X protein	Mus musculus	113-116
12915712-5	2003	Cadmium also induced embryonic growth retardation, as well as a significant upregulation of p53, p21, and Bax transcription levels.	Cadmium	0-7	BCL2-associated X protein	Mus musculus	106-109
14531950-5	2003	Nimesulide also decreased cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2) and Bcl-2 expression, while increased the level of Bax protein.	nimesulide	0-10	BCL2-associated X protein	Mus musculus	127-130
14531950-6	2003	CONCLUSION: Nimesulide suppresses tumor growth and induces apoptosis by inhibiting COX-2 and PGE2 expression, which may be related to overexpression of Bax over Bcl-2.	nimesulide	12-22	BCL2-associated X protein	Mus musculus	152-155
14502238-0	2003	Ethanol-induced neuronal apoptosis in vivo requires BAX in the developing mouse brain.	Ethanol	0-7	BCL2-associated X protein	Mus musculus	52-55
14502238-8	2003	Therefore, it appears that ethanol-induced neuroapoptosis is an intrinsic pathway-mediated phenomenon involving Bax-induced disruption of mitochondrial membranes and cytochrome c release as early events leading to caspase-3 activation.	Ethanol	27-34	BCL2-associated X protein	Mus musculus	112-115
12939598-8	2003	After 12 to 28 days of treatment, administration of tacrine increased p53, Bax, mitochondrial permeability transition, cytosolic cytochrome c, and caspase-3 activity and triggered hepatocyte apoptosis and/or necrosis.	Tacrine	52-59	BCL2-associated X protein	Mus musculus	75-78
14507967-7	2003	When cultured oligodendrocytes were exposed to staurosporine or cyclosporin A, drugs known to stimulate apoptosis in oligodendrocytes, those from Bax-/- mice but not from Bax+/+ or Bax+/- mice were resistant to the apoptotic death.	Staurosporine	47-60	BCL2-associated X protein	Mus musculus	146-149
14507967-7	2003	When cultured oligodendrocytes were exposed to staurosporine or cyclosporin A, drugs known to stimulate apoptosis in oligodendrocytes, those from Bax-/- mice but not from Bax+/+ or Bax+/- mice were resistant to the apoptotic death.	Cyclosporine	64-77	BCL2-associated X protein	Mus musculus	146-149
12928149-9	2003	(e) p53-mediated caspase 11 activation, aside from p53-mediated Bax gene induction, may be an important pathway for cellular apoptosis after benzene exposure.	Benzene	141-148	BCL2-associated X protein	Mus musculus	64-67
12902978-6	2003	Similarly, murine embryonic fibroblasts lacking Bax undergo apoptosis when exposed to the combination of PS-341 and TRAIL; however, fibroblasts lacking Bak are significantly resistant.	Bortezomib	105-111	BCL2-associated X protein	Mus musculus	48-51
12907610-0	2003	Induction of apoptosis by caffeine is mediated by the p53, Bax, and caspase 3 pathways.	Caffeine	26-34	BCL2-associated X protein	Mus musculus	59-62
12852832-6	2003	A "ladder" pattern representing fragmentation of DNA into oligonucleosome length fragments was observed after 6 h of staurosporine treatment and sustained until 24 h. The Bax expression increased significantly at 6 h after exposure to staurosporine, peaked at 12 h compared with vehicle cultures, and decreased at 24 h. The Bcl-2 expression increased and reached the highest level at 3 h. It was then decreased gradually but still higher than normal expression level.	Staurosporine	117-130	BCL2-associated X protein	Mus musculus	171-174
12852832-6	2003	A "ladder" pattern representing fragmentation of DNA into oligonucleosome length fragments was observed after 6 h of staurosporine treatment and sustained until 24 h. The Bax expression increased significantly at 6 h after exposure to staurosporine, peaked at 12 h compared with vehicle cultures, and decreased at 24 h. The Bcl-2 expression increased and reached the highest level at 3 h. It was then decreased gradually but still higher than normal expression level.	Staurosporine	235-248	BCL2-associated X protein	Mus musculus	171-174
12738797-6	2003	Serotonin binding to 5-HT2B-receptor activates ERK kinases to inhibit Bax expression induced by serum deprivation.	Serotonin	0-9	BCL2-associated X protein	Mus musculus	70-73
12813466-3	2003	HCQ also induces mitochondrial membrane permeabilization (MMP), as indicated by the insertion of Bax into mitochondrial membranes, the conformational activation of Bax within mitochondria, the release of cytochrome c from mitochondria, and the loss of the mitochondrial transmembrane potential.	Hydroxychloroquine	0-3	BCL2-associated X protein	Mus musculus	97-100
12787408-12	2003	Simvastatin appears to alter the balance between cell-life and death-promoting genes, as reflected by the decreased Bcl-xL/Bax ratio.	Simvastatin	0-11	BCL2-associated X protein	Mus musculus	123-126
12831782-9	2003	Finally, POX treatment also resulted in a time-dependent up-regulation and translocation of the proapoptotic molecule Bax to mitochondria.	Paraoxon	9-12	BCL2-associated X protein	Mus musculus	118-121
12831782-10	2003	Inhibition of this event by zVAD-fmk suggests that the activation and translocation of Bax to mitochondria is subsequent to activation of the caspase cascades.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	28-36	BCL2-associated X protein	Mus musculus	87-90
12813466-3	2003	HCQ also induces mitochondrial membrane permeabilization (MMP), as indicated by the insertion of Bax into mitochondrial membranes, the conformational activation of Bax within mitochondria, the release of cytochrome c from mitochondria, and the loss of the mitochondrial transmembrane potential.	Hydroxychloroquine	0-3	BCL2-associated X protein	Mus musculus	164-167
12813466-6	2003	Mouse embryonic fibroblasts lacking the expression of both Bax and Bak are resistant against hydroxychloroquine-induced apoptosis.	Hydroxychloroquine	93-111	BCL2-associated X protein	Mus musculus	59-62
12813466-8	2003	The data reported herein indicate that LMP does not suffice to trigger caspase activation and that Bax/Bak-dependent MMP is a critical step of LMP-induced cell death.	bakuchiol	103-106	BCL2-associated X protein	Mus musculus	99-102
12813466-8	2003	The data reported herein indicate that LMP does not suffice to trigger caspase activation and that Bax/Bak-dependent MMP is a critical step of LMP-induced cell death.	(2~{s},3~{r},4~{s})-2-[(2~{s},3~{r})-1,3-Bis(Oxidanyl)-1-Oxidanylidene-Butan-2-Yl]-4-[(3~{s},5~{s})-5-(Dimethylcarbamoyl)pyrrolidin-3-Yl]sulfanyl-3-Methyl-3,4-Dihydro-2~{h}-Pyrrole-5-Carboxylic Acid	143-146	BCL2-associated X protein	Mus musculus	99-102
12782000-9	2003	BH4 treatment led to increases in the ratio of Bax/Bcl-x(L) mRNA and protein levels.	sapropterin	0-3	BCL2-associated X protein	Mus musculus	47-50
12742833-4	2003	Superior cardiac function of Bax(-/-) hearts after I/R was accompanied by a decrease in creatine kinase release, caspase 3 activity, irreversible ischemic injury, and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cardiomyocytes.	deoxyuridine triphosphate	228-232	BCL2-associated X protein	Mus musculus	29-32
12718432-2	2003	Three days to 12 weeks after MPTP treatment, a detectable reduction of tyrosine hydroxylase immunoreactivity in the amacrine cells was observed, with an increase of Bcl-2 expression in the Muller glial cells, and a de novo expression of Bad and Bax in the retinal ganglion cells, optic nerve fibers and plexiform layers.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	29-33	BCL2-associated X protein	Mus musculus	245-248
12663524-11	2003	These findings thus suggest involvement of Bax and apoptosis in tumors developing after sulindac treatment in this mouse model.	Sulindac	88-96	BCL2-associated X protein	Mus musculus	43-46
14690559-12	2003	CONCLUSION: Melatonin may induce apoptosis in the hepatocarcinoma cells which is concentration- and time-dependent, in which bcl-2 and bax are involved.	Melatonin	12-21	BCL2-associated X protein	Mus musculus	135-138
12624178-2	2003	Mouse embryonic fibroblasts deficient for BAX and BAK (DKO cells) were found to have a reduced resting concentration of calcium in the ER ([Ca2+]er) that results in decreased uptake of Ca2+ by mitochondria after Ca2+ release from the ER.	Calcium	120-127	BCL2-associated X protein	Mus musculus	42-53
12624178-4	2003	In contrast, targeting of BAX to mitochondria selectively restored apoptosis to "BH3-only" signals.	BH 3	81-84	BCL2-associated X protein	Mus musculus	26-29
12654481-7	2003	The paraquat-mediated gene or protein expression of proapoptotic Bax, Bcl-w, and Bcl-X(S), cell survival/death factors GADD45, MDM2, c-Myc, and caspase-3 was upregulated, but that of antiapoptotic Bcl-2 was downregulated in the GPX1-/- mice vs. the WT mice.	Paraquat	4-12	BCL2-associated X protein	Mus musculus	65-68
12971412-6	2003	The p53-dependent apoptosis related Bax proteins on formalin-fixed paraffin-embedded sections were stained by the avidin-biotin peroxidase complex method.	Formaldehyde	52-60	BCL2-associated X protein	Mus musculus	36-39
12540825-9	2003	These findings extend our in vitro retinal studies with Pb(2+) and Ca(2+) and suggest that developmental lead exposure produced rod-selective apoptosis without mitochondrial swelling by translocating cytosolic Bax to the mitochondria, which likely sensitized the Pb(2+) and Ca(2+) overloaded rod mitochondria to release cytochrome c. These results have relevance for therapies in a wide variety of progressive retinal and neuronal degenerations where Ca(2+) overload, lead exposure, andor mitochondrial dysfunction occur.	Lead	263-265	BCL2-associated X protein	Mus musculus	210-213
12576521-6	2003	The reduction in ACO expression in the hearts of 10-day etomoxir-treated mice was accompanied by an increase in the mRNA expression of the antioxidant enzyme glutathione peroxidase and the cardiac marker of oxidative stress bax.	etomoxir	56-64	BCL2-associated X protein	Mus musculus	224-227
12971412-6	2003	The p53-dependent apoptosis related Bax proteins on formalin-fixed paraffin-embedded sections were stained by the avidin-biotin peroxidase complex method.	Paraffin	67-75	BCL2-associated X protein	Mus musculus	36-39
12697689-5	2003	Calcitriol-induced cell death was regulated by members of the Bcl-2 family of apoptosis regulatory proteins, as shown by calcitriol-induced up-regulation of proapoptotic Bax and Bak and the lack of calcitriol-induced cytotoxicity in Bcl-2-overexpressing insulinoma cells.	Calcitriol	0-10	BCL2-associated X protein	Mus musculus	170-173
12244308-3	2002	We found that the development and selection of Bak(-/-)Bax(-/-) thymocytes was disrupted, with altered representation of thymic subsets and resistance to both death-by-neglect and antigen receptor-induced apoptosis.	bakuchiol	47-50	BCL2-associated X protein	Mus musculus	55-58
12697689-5	2003	Calcitriol-induced cell death was regulated by members of the Bcl-2 family of apoptosis regulatory proteins, as shown by calcitriol-induced up-regulation of proapoptotic Bax and Bak and the lack of calcitriol-induced cytotoxicity in Bcl-2-overexpressing insulinoma cells.	Calcitriol	121-131	BCL2-associated X protein	Mus musculus	170-173
12402257-5	2002	MPTP caused an increase in the level of the proapoptotic protein Bax, which was prevented by giving mice PFT-alpha and Z-1-117.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	BCL2-associated X protein	Mus musculus	65-68
12488331-0	2003	Bax, caspase-2, and caspase-3 are required for ovarian follicle loss caused by 4-vinylcyclohexene diepoxide exposure of female mice in vivo.	4-vinyl-1-cyclohexene dioxide	79-107	BCL2-associated X protein	Mus musculus	0-3
12488331-2	2003	It has been reported that VCD-induced follicle loss occurs via a cell death process involving elevated expression of Bax, a proapoptotic Bcl-2 family member, and increased caspase-3-like activity.	4-vinyl-1-cyclohexene dioxide	26-29	BCL2-associated X protein	Mus musculus	117-120
12488331-8	2003	By contrast, the extent of VCD-induced primordial follicle depletion in Bax-deficient mice (45 +/- 11%) was significantly (P &lt; 0.05) lower than that in wild-type females (85 +/- 2%).	4-vinyl-1-cyclohexene dioxide	27-30	BCL2-associated X protein	Mus musculus	72-75
12239316-8	2002	Infection of BAX knockout mice with dsNSV demonstrated that endogenous BAX also enhances the survival of animals but has no effect on paralysis.	dsnsv	36-41	BCL2-associated X protein	Mus musculus	13-16
12239316-8	2002	Infection of BAX knockout mice with dsNSV demonstrated that endogenous BAX also enhances the survival of animals but has no effect on paralysis.	dsnsv	36-41	BCL2-associated X protein	Mus musculus	71-74
12234259-5	2002	Using formalin-fixed lung tissues (n = 45), our results showed a significant difference in the percentage of Mphis stained for Bcl-2 or MAgs and Bax (P &lt; 0.0001).	Formaldehyde	6-14	BCL2-associated X protein	Mus musculus	145-148
12244308-4	2002	Elimination of Bak(-/-)Bax(-/-) T cells that responded to endogenous superantigen was also reduced.	bakuchiol	15-18	BCL2-associated X protein	Mus musculus	23-26
12160618-11	2002	The changes in mitogen-induced proliferation in DES-treated female mice were not mirrored by similar changes in the relative numbers of CD90(+) or CD45R(+) cells, or in ratios of anti-apoptotic Bcl-2 to apoptotic Bax proteins.	Diethylstilbestrol	48-51	BCL2-associated X protein	Mus musculus	213-216
12175898-7	2002	We also demonstrated that treatment with 10 microM TET caused not only induction of p53, p21(waf1), and Bax, but also nuclear translocation of p53 and hypo-phosphorylation of pRb concurrently.	tetrandrine	51-54	BCL2-associated X protein	Mus musculus	104-107
12200191-7	2002	Evidence has emerged to suggest that Bcl-2, Bax, JNK, and caspases are implicated in neurotoxic effects due to in vivo MPTP administration to mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	119-123	BCL2-associated X protein	Mus musculus	44-47
12163104-0	2002	Alcohol induces apoptosis in TM3 mouse Leydig cells via bax-dependent caspase-3 activation.	Alcohols	0-7	BCL2-associated X protein	Mus musculus	56-59
12213925-1	2002	The murine proapoptotic protein Bax was expressed in Kluyveromyces lactis to investigate its effect on cell survival and production of reactive oxygen species (ROS).	Reactive Oxygen Species	135-158	BCL2-associated X protein	Mus musculus	32-35
12213925-1	2002	The murine proapoptotic protein Bax was expressed in Kluyveromyces lactis to investigate its effect on cell survival and production of reactive oxygen species (ROS).	Reactive Oxygen Species	160-163	BCL2-associated X protein	Mus musculus	32-35
12213925-2	2002	Bax expression decreased the number of cells capable of growing and forming colonies, and it increased the number of cells producing ROS, as detected by both dihydrorhodamine 123 fluorescence and the intracellular content of SH groups.	Reactive Oxygen Species	133-136	BCL2-associated X protein	Mus musculus	0-3
12213925-2	2002	Bax expression decreased the number of cells capable of growing and forming colonies, and it increased the number of cells producing ROS, as detected by both dihydrorhodamine 123 fluorescence and the intracellular content of SH groups.	dihydrorhodamine 123	158-174	BCL2-associated X protein	Mus musculus	0-3
12163104-3	2002	In addition, it was shown that ethanol induces increases in levels of bax and caspase-3 and a decrease in bcl-2 expression.	Ethanol	31-38	BCL2-associated X protein	Mus musculus	70-73
12163104-4	2002	Based on the results, alcohol appears to activate specific intracellular death-related pathways leading to bax-dependant caspase-3 activation and the induction of apoptosis in Leydig cells.	Alcohols	22-29	BCL2-associated X protein	Mus musculus	107-110
12027451-0	2002	The p53 stabilizing compound CP-31398 induces apoptosis by activating the intrinsic Bax/mitochondrial/caspase-9 pathway.	CP 31398	29-37	BCL2-associated X protein	Mus musculus	84-87
12169271-5	2002	The level of cyclobutane pyrimidine dimers remaining was twofold greater in UVR-treated primary keratinocytes from bax-deficient mice than that of control cells at 48 h (P &lt; 0.03).	cyclobutane pyrimidine	13-35	BCL2-associated X protein	Mus musculus	115-118
12151527-2	2002	After NGF withdrawal, Bax translocates from the cytoplasm to the mitochondria of these cells and induces release of the proapoptotic protein cytochrome c. Here, we report that withdrawing NGF from mouse sympathetic neurons caused an increase of mitochondria-derived reactive oxygen species (ROS).	Reactive Oxygen Species	266-289	BCL2-associated X protein	Mus musculus	22-25
12151527-2	2002	After NGF withdrawal, Bax translocates from the cytoplasm to the mitochondria of these cells and induces release of the proapoptotic protein cytochrome c. Here, we report that withdrawing NGF from mouse sympathetic neurons caused an increase of mitochondria-derived reactive oxygen species (ROS).	Reactive Oxygen Species	291-294	BCL2-associated X protein	Mus musculus	22-25
12151527-4	2002	Bax deletion blocked death and prevented the ROS burst.	Reactive Oxygen Species	45-48	BCL2-associated X protein	Mus musculus	0-3
12151527-6	2002	A similar ROS burst in cerebellar granule neurons undergoing apoptosis was also blocked by Bax deletion.	Reactive Oxygen Species	10-13	BCL2-associated X protein	Mus musculus	91-94
12151527-7	2002	These findings indicate that Bax lies upstream from increased ROS in NGF-deprived neurons and suggest that the Bax-induced ROS burst is both necessary and sufficient for cytochrome c redistribution in these cells.	Reactive Oxygen Species	62-65	BCL2-associated X protein	Mus musculus	111-114
12151527-7	2002	These findings indicate that Bax lies upstream from increased ROS in NGF-deprived neurons and suggest that the Bax-induced ROS burst is both necessary and sufficient for cytochrome c redistribution in these cells.	Reactive Oxygen Species	123-126	BCL2-associated X protein	Mus musculus	29-32
12151527-7	2002	These findings indicate that Bax lies upstream from increased ROS in NGF-deprived neurons and suggest that the Bax-induced ROS burst is both necessary and sufficient for cytochrome c redistribution in these cells.	Reactive Oxygen Species	123-126	BCL2-associated X protein	Mus musculus	111-114
12492115-8	2002	Cisplatin induced p53 and its downstream targets, p21(Cip1) (p21) and Bax, in both cell populations.	Cisplatin	0-9	BCL2-associated X protein	Mus musculus	70-73
12027451-7	2002	Taken together, our results indicate that CP-31398 induces p53-dependent apoptosis by activating the Bax/mitochondrial/caspase-9 pathway.	CP 31398	42-50	BCL2-associated X protein	Mus musculus	101-104
11805084-2	2002	tBID translocates to the mitochondria to induce the oligomerization of BAX or BAK, resulting in the release of cytochrome c (Cyt c).	tBID	0-4	BCL2-associated X protein	Mus musculus	71-74
12039857-5	2002	Although dexamethasone induced transcription of the proapoptotic gene bax, there was no increase of Bax protein levels.	Dexamethasone	9-22	BCL2-associated X protein	Mus musculus	70-73
12579811-8	2002	The mechanism of anticancer effect of artesunate may be related to down-regulation of the expression of PCNA and Bcl-2 genes and up-regulation of the expression of Bax gene.	Artesunate	38-48	BCL2-associated X protein	Mus musculus	164-167
12123203-9	2002	The ratio between bax and bcl-2 protein increased significantly in the CsA group (5.3-fold), compared with the VH group.	Cyclosporine	71-74	BCL2-associated X protein	Mus musculus	18-21
12128097-5	2002	In utero RA-treatment resulted in decreased expression of max, mad, caspases, bax, and bad genes at 48 h. Terminal uridinetriphosphate nick end-labeling (TUNEL) analysis revealed increased apoptosis at 24-48 h, followed by decreased apoptosis 72 h after in utero RA-exposure, which correlated with the decreased expression of pro-apoptotic genes noted at 48 h. Further investigations are needed to understand the role of Myc family genes during RA-mediated teratogenesis.	Tretinoin	9-11	BCL2-associated X protein	Mus musculus	78-81
11904448-4	2002	The two parent proteins increase the acetyl-DEVD-al-sensitive caspase-3-like activity in both HEK293 cells and Telencephalon specific murine neurons, modulate Bax and bcl-2 expressions, and enhance cytochrome C translocation into the cytosol.	acetyl-devd-al	37-51	BCL2-associated X protein	Mus musculus	159-162
12043192-0	2002	Changes of bcl-2 and bax mRNA expressions in the ethanol-treated mouse brain.	Ethanol	49-56	BCL2-associated X protein	Mus musculus	21-24
12043192-1	2002	To characterize the biochemical mechanism of cell death induced by ethanol intoxication, we examined expression of mRNAs of bcl-2 and bax genes in the brain, which are related to apoptosis, by using the reverse transcription-polymerase chain reaction method (RT-PCR).	Ethanol	67-74	BCL2-associated X protein	Mus musculus	134-137
12043192-6	2002	We found that bcl-2 or bax mRNA expressions in the brain were changed after short-term ethanol exposure.	Ethanol	87-94	BCL2-associated X protein	Mus musculus	23-26
12043192-7	2002	These results suggest that bcl-2 or bax may have functional significance about ethanol intoxication.	Ethanol	79-86	BCL2-associated X protein	Mus musculus	36-39
12207051-5	2002	ES cells exposed to 1 microM all-trans-retinoic acid on day 8, 9 and 10 of differentiation revealed increased expression of Bax and Bad compared to the vehicle-treated cells.	Tretinoin	29-52	BCL2-associated X protein	Mus musculus	124-127
11919514-7	2002	Diazoxide increased the levels of Bcl2 and inhibited the association of Bax with mitochondria in neurons exposed to an apoptotic insult, suggesting that activation of mitochondrial ATP-sensitive potassium channels may stabilize mitochondrial function by differentially modulating proapoptotic and antiapoptotic proteins.	Diazoxide	0-9	BCL2-associated X protein	Mus musculus	72-75
11906184-5	2002	In addition, flow cytometry analyses revealed that treatment with BPA resulted in G2-to-M arrest, which was most prominent at 48 h. BPA increased the expression of Bax and concomitantly decreased the expression of Bcl2 at both protein and mRNA levels of granulosa cells.	bisphenol A	66-69	BCL2-associated X protein	Mus musculus	164-167
11906184-5	2002	In addition, flow cytometry analyses revealed that treatment with BPA resulted in G2-to-M arrest, which was most prominent at 48 h. BPA increased the expression of Bax and concomitantly decreased the expression of Bcl2 at both protein and mRNA levels of granulosa cells.	bisphenol A	132-135	BCL2-associated X protein	Mus musculus	164-167
11796517-9	2002	We conclude that a central role exists for the AHR in transducing the actions of PAHs in fetal ovarian germ cells, and that the proapoptotic Bcl-2 family member, Bax, is a required mediator of PAH-induced oocyte loss in female fetuses exposed to PAHs in utero.	Polycyclic Aromatic Hydrocarbons	81-84	BCL2-associated X protein	Mus musculus	162-165
12579951-9	2002	Pretreatment with 0.1 mmol.L-1 tacrine significantly increased the expression of Bcl-2 protein level and delayed the staurosporine-induced increase of Bax protein expression.	Staurosporine	117-130	BCL2-associated X protein	Mus musculus	151-154
11533046-11	2001	Thus, FC loading, perhaps via increased levels of Bax and/or cholesterol overloading of mitochondria, triggers cytochrome c release and activation of caspase-9 and the effector caspases, leading to macrophage apoptosis.	Fc(alpha) receptor	6-8	BCL2-associated X protein	Mus musculus	50-53
11698144-1	2001	We investigated whether single injection of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) (20 mg/kg) will alter the expression of pro-apoptotic genes, namely, the c-fos, c-jun, and bax, in the striatum, cortex, and cerebellum of adult male C57BL/6 mice using reverse transcription-polymerase chain reaction assay.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	44-89	BCL2-associated X protein	Mus musculus	188-191
11698144-1	2001	We investigated whether single injection of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) (20 mg/kg) will alter the expression of pro-apoptotic genes, namely, the c-fos, c-jun, and bax, in the striatum, cortex, and cerebellum of adult male C57BL/6 mice using reverse transcription-polymerase chain reaction assay.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	91-95	BCL2-associated X protein	Mus musculus	188-191
12416267-0	2002	Genistein-induced apoptosis of p815 mastocytoma cells is mediated by Bax and augmented by a proteasome inhibitor, lactacystin.	Genistein	0-9	BCL2-associated X protein	Mus musculus	69-72
12416267-6	2002	Genistein treatment resulted in the increase of Bax expression and its translocation into mitochondria, whereas expression levels of Bcl-2 remained unchanged.	Genistein	0-9	BCL2-associated X protein	Mus musculus	48-51
12416267-9	2002	Taken together, genistein-induced apoptosis of p815 mastocytoma cells is at least in part mediated by proteasome, Bax, apoptosis-inducing factor, and caspase and augmented by cotreatment with a proteasome inhibitor, lactacystin.	Genistein	16-25	BCL2-associated X protein	Mus musculus	114-117
11728455-0	2001	The Arabidopsis thaliana ethylene-responsive element binding protein (AtEBP) can function as a dominant suppressor of Bax-induced cell death of yeast.	ethylene	25-33	BCL2-associated X protein	Mus musculus	118-121
11698144-0	2001	Sequential up-regulation of the c-fos, c-jun and bax genes in the cortex, striatum and cerebellum induced by a single injection of a low dose of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	145-189	BCL2-associated X protein	Mus musculus	49-52
11698144-0	2001	Sequential up-regulation of the c-fos, c-jun and bax genes in the cortex, striatum and cerebellum induced by a single injection of a low dose of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	191-195	BCL2-associated X protein	Mus musculus	49-52
11597570-0	2001	Cisplatin-induced apoptosis by translocation of endogenous Bax in mouse collecting duct cells.	Cisplatin	0-9	BCL2-associated X protein	Mus musculus	59-62
11676493-5	2001	Probing further into the molecular signals leading to apoptosis of EAC cells, we observed that curcumin is causing tumor cell death by the up-regulation of the proto-oncoprotein Bax, release of cytochrome c from the mitochondria, and activation of caspase-3.	Curcumin	95-103	BCL2-associated X protein	Mus musculus	178-181
11597570-8	2001	Cisplatin induced the translocation of endogenous Bax from the cytosolic to the membrane fractions and, subsequently, the release of cytochrome c. Overexpression of Bcl-2 blocked cisplatin-induced apoptosis and Bax translocation.	Cisplatin	0-9	BCL2-associated X protein	Mus musculus	50-53
11597570-8	2001	Cisplatin induced the translocation of endogenous Bax from the cytosolic to the membrane fractions and, subsequently, the release of cytochrome c. Overexpression of Bcl-2 blocked cisplatin-induced apoptosis and Bax translocation.	Cisplatin	0-9	BCL2-associated X protein	Mus musculus	211-214
11597570-8	2001	Cisplatin induced the translocation of endogenous Bax from the cytosolic to the membrane fractions and, subsequently, the release of cytochrome c. Overexpression of Bcl-2 blocked cisplatin-induced apoptosis and Bax translocation.	Cisplatin	179-188	BCL2-associated X protein	Mus musculus	50-53
11597570-8	2001	Cisplatin induced the translocation of endogenous Bax from the cytosolic to the membrane fractions and, subsequently, the release of cytochrome c. Overexpression of Bcl-2 blocked cisplatin-induced apoptosis and Bax translocation.	Cisplatin	179-188	BCL2-associated X protein	Mus musculus	211-214
11597570-9	2001	These observations suggest that the subcellular redistribution of Bax is a critical event in the apoptosis induced by cisplatin.	Cisplatin	118-127	BCL2-associated X protein	Mus musculus	66-69
11544288-6	2001	In vitro, TNF enhanced the Fas-mediated apoptosis of unactivated T cells through decreased intracellular levels of FLIP and increased production of the pro-apoptotic molecule Bax.	ammonium ferrous sulfate	27-30	BCL2-associated X protein	Mus musculus	175-178
11567994-10	2001	Bax(-/-) mice survived the lethal regimen only when given PEG-rmMGDF; however, these Bax(-/-) mice showed more rapid hematopoietic recovery than did identically-treated wild-type mice.	peg-rmmgdf	58-68	BCL2-associated X protein	Mus musculus	0-3
11589996-2	2001	In the present study, we have investigated the implication of three molecules of this cascade, p53, Bax and caspase-3, in neuronal death induced by kainic acid (KA) administration in mouse hippocampus.	Kainic Acid	148-159	BCL2-associated X protein	Mus musculus	100-103
11585626-5	2001	Increased expression of the anti-apoptotic factor Bcl-2 or loss of pro-apoptotic Bax expression attenuated dopamine-induced apoptosis, suggesting the apoptosis proceeds through a mitochondrial pathway.	Dopamine	107-115	BCL2-associated X protein	Mus musculus	81-84
11481222-8	2001	Here we report that a toxic regimen of METH did cause significant increases in the pro-death Bcl-2 family genes BAD, BAX, and BID.	Methamphetamine	39-43	BCL2-associated X protein	Mus musculus	117-120
11759827-7	2001	Doxorubicin treatment induced Bax expression and down-regulated Bcl-2 expression.	Doxorubicin	0-11	BCL2-associated X protein	Mus musculus	30-33
11479581-2	2001	Mice lacking either Ahr or the pro-apoptotic protein Bax have an increased number of primordial follicles, and these mutant oocytes are resistant to PAH toxicity.	Polycyclic Aromatic Hydrocarbons	149-152	BCL2-associated X protein	Mus musculus	53-56
11455387-6	2001	Here we show that an exposure of mice to PAHs induces the expression of Bax in oocytes, followed by apoptosis.	Polycyclic Aromatic Hydrocarbons	41-45	BCL2-associated X protein	Mus musculus	72-75
11479581-3	2001	A new study shows that the Bax promoter contains two core Ahr response elements, which are required for PAH stimulation of Bax promoter activity in oocytes.	Polycyclic Aromatic Hydrocarbons	104-107	BCL2-associated X protein	Mus musculus	27-30
11479581-3	2001	A new study shows that the Bax promoter contains two core Ahr response elements, which are required for PAH stimulation of Bax promoter activity in oocytes.	Polycyclic Aromatic Hydrocarbons	104-107	BCL2-associated X protein	Mus musculus	123-126
11479581-4	2001	Thus, the toxic effects of PAH in oocytes are mediated directly by Ahr induction of the Bax pathway.	Polycyclic Aromatic Hydrocarbons	27-30	BCL2-associated X protein	Mus musculus	88-91
11494143-9	2001	Furthermore, IL-3-dependent cells from Bax-null mice activated caspases after hydroxyurea treatment and show the same sensitivity to a variety of cytotoxic drugs.	Hydroxyurea	78-89	BCL2-associated X protein	Mus musculus	39-42
11422623-6	2001	The expression of bax in the SSa-treated group at 5 and 14 h after treatment of SSa was markedly higher than those of the non-treated group, respectively (P &lt; 0.01), but there was no significant difference in the expression of p53 between the SSa-treated group and the non-treated group.	SerSA	29-32	BCL2-associated X protein	Mus musculus	18-21
11384644-12	2001	CONCLUSION(S): These results indicate that the cGMP pathway might be involved in the NO-regulated embryonic development, but not in NO-induced apoptosis, for which P53/Bax pathway might be involved.	Cyclic GMP	47-51	BCL2-associated X protein	Mus musculus	168-171
11422623-6	2001	The expression of bax in the SSa-treated group at 5 and 14 h after treatment of SSa was markedly higher than those of the non-treated group, respectively (P &lt; 0.01), but there was no significant difference in the expression of p53 between the SSa-treated group and the non-treated group.	SerSA	80-83	BCL2-associated X protein	Mus musculus	18-21
11422623-6	2001	The expression of bax in the SSa-treated group at 5 and 14 h after treatment of SSa was markedly higher than those of the non-treated group, respectively (P &lt; 0.01), but there was no significant difference in the expression of p53 between the SSa-treated group and the non-treated group.	SerSA	80-83	BCL2-associated X protein	Mus musculus	18-21
11164179-9	2001	Ionomycin treatment increased the expression level of Bax protein, whereas Bcl-2 expression was not influenced.	Ionomycin	0-9	BCL2-associated X protein	Mus musculus	54-57
11259608-16	2001	In addition, at high doses, cisplatin could damage molecules involved in cellular energy supply (i.e., ATP) and also proteins directly or indirectly involved in the apoptotic process (i.e., p53, Bax, Bcl-2, and caspases), leading to necrotic cell death.	Cisplatin	28-37	BCL2-associated X protein	Mus musculus	195-198
11226731-4	2001	Paraffin sections of the fetal brains on embryonic day (ED) 10, 12, 14, 16 and 18 were applied for the immunostains of Bcl-2 and Bax.	Paraffin	0-8	BCL2-associated X protein	Mus musculus	129-132
11226327-0	2001	Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson"s disease.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	60-105	BCL2-associated X protein	Mus musculus	0-3
11226327-3	2001	In adult mice, there is an up-regulation of Bax in the SNpc after MPTP administration and a decrease in Bcl-2.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	66-70	BCL2-associated X protein	Mus musculus	44-47
11226327-5	2001	We also show that mutant mice lacking Bax are significantly more resistant to MPTP than their wild-type littermates.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	78-82	BCL2-associated X protein	Mus musculus	38-41
11226327-6	2001	This study demonstrates that Bax plays a critical role in the MPTP neurotoxic process and suggests that targeting Bax may provide protective benefit in the treatment of Parkinson"s disease.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	62-66	BCL2-associated X protein	Mus musculus	29-32
11226327-6	2001	This study demonstrates that Bax plays a critical role in the MPTP neurotoxic process and suggests that targeting Bax may provide protective benefit in the treatment of Parkinson"s disease.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	62-66	BCL2-associated X protein	Mus musculus	114-117
10982793-3	2000	In the current study, we investigated the mechanism by which tBid regulated cytochrome c release in terms of its relationship to mitochondrial permeability transition and Bax, another Bcl-2 family protein.	tBID	61-65	BCL2-associated X protein	Mus musculus	171-174
11343247-8	2001	However, 4 repeated doses of phorone (causing more prolonged glutathione depletion) increased Bax and Fas-mediated toxicity.	phorone	29-36	BCL2-associated X protein	Mus musculus	94-97
11343247-8	2001	However, 4 repeated doses of phorone (causing more prolonged glutathione depletion) increased Bax and Fas-mediated toxicity.	Glutathione	61-72	BCL2-associated X protein	Mus musculus	94-97
11343247-10	2001	Thiol depletion could cause oxidative stress that requires several hours to increase p53; the latter induces Bax, which translocates to mitochondria after Fas stimulation.	Sulfhydryl Compounds	0-5	BCL2-associated X protein	Mus musculus	109-112
11254887-4	2001	In addition, the role of apoptosis inhibitors (Bcl-2 and Bcl-x) and the apoptosis inducer (Bax) in CsA induced-apoptosis was evaluated.	Cyclosporine	99-102	BCL2-associated X protein	Mus musculus	91-94
11254887-5	2001	The expression of Bcl-2 and Bax proteins were high in LBC cells and following CsA treatment the expression of these proteins as well as Bcl-XL decreased.	Cyclosporine	78-81	BCL2-associated X protein	Mus musculus	28-31
11172605-3	2001	The human gastric cancer cell line, MKN45 was transplanted into nude mice, and the intratumoral administration of bax gene was performed using the bax cDNA plasmid complexed with a cationic lipopolyamine.	lipopolyamine	190-203	BCL2-associated X protein	Mus musculus	114-117
11242124-4	2001	RESULTS: Hepatocyte apoptosis was induced in BalB/c mice pretreated with TNF-alpha plus D-galactosamine, accompanying the enhanced expression of Bax, Bak proteins in hepatocytes.	Galactosamine	88-103	BCL2-associated X protein	Mus musculus	145-148
11242124-6	2001	CONCLUSIONS: The enhanced expression of Bax, Bak proteins may play a role in hepatocyte apoptosis induced by TNF-alpha and D-galactosamine.	Galactosamine	123-138	BCL2-associated X protein	Mus musculus	40-43
10995754-3	2000	Similar to wild-type mice, embryos from streptozotocin-induced diabetic Bax -/- mice experienced a significant decrease in glucose transport compared with embryos from non-diabetic Bax -/- mice.	Streptozocin	40-54	BCL2-associated X protein	Mus musculus	72-75
10995754-3	2000	Similar to wild-type mice, embryos from streptozotocin-induced diabetic Bax -/- mice experienced a significant decrease in glucose transport compared with embryos from non-diabetic Bax -/- mice.	Glucose	123-130	BCL2-associated X protein	Mus musculus	72-75
10995754-6	2000	These findings suggest that hyperglycemia by decreasing glucose transport acts as a cell death signal to trigger a BAX-dependent apoptotic cascade in the murine blastocyst.	Glucose	56-63	BCL2-associated X protein	Mus musculus	115-118
11140697-4	2000	Adult mice exposed to greater than 95% oxygen concentrations for 48 to 88 hours had increased whole-lung mRNA levels of Bax and Bcl-X(L), no change in Bak, Bad, or Bcl-2, and decreased levels of Bcl-w and Bfl-1.	Oxygen	39-45	BCL2-associated X protein	Mus musculus	120-123
11175253-0	2000	Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c. We review data supporting a model in which activated tBID results in an allosteric activation of BAK, inducing its intramembranous oligomerization into a proposed pore for cytochrome c efflux.	tBID	175-179	BCL2-associated X protein	Mus musculus	63-66
11175253-2	2000	tBID induces oligomerization of BAK, and both Bid and Bak knockout mice indicate the importance of this event in the release of cytochrome c. In parallel, the full pro-apoptotic member BAX, which is highly homologous to BAK, rapidly forms pores in liposomes that release intravesicular FITC-cytochrome c approximately 20A.	tBID	0-4	BCL2-associated X protein	Mus musculus	185-188
11175253-2	2000	tBID induces oligomerization of BAK, and both Bid and Bak knockout mice indicate the importance of this event in the release of cytochrome c. In parallel, the full pro-apoptotic member BAX, which is highly homologous to BAK, rapidly forms pores in liposomes that release intravesicular FITC-cytochrome c approximately 20A.	Fluorescein-5-isothiocyanate	286-290	BCL2-associated X protein	Mus musculus	185-188
11201044-9	2000	These results suggest that butyric-acid-mediated apoptosis of murine T-cells takes place via a pathway that is independent of p53, and is followed by the p53-regulated proteins Bax and p21WAF1/CIP1, which lower the levels of the apoptosis antagonists Bcl-2 and Bcl-XL in cells.	Butyric Acid	27-39	BCL2-associated X protein	Mus musculus	177-180
11006354-6	2000	Notably, hepatic transcript levels for Bax were higher in TNFR DKO mice treated with DMN compared to identically treated WT mice.	Dimethylnitrosamine	85-88	BCL2-associated X protein	Mus musculus	39-42
11139284-3	2000	The cleavage product of caspase-8, tBID, induced insertion of BAX into mitochondria in vivo, and reconstitution in vitro showed that tBID, either directly or indirectly, relieved inhibition of the BAX transmembrane signal-anchor by the NH2-terminal domain, resulting in integration of BAX into mitochondrial membrane.	tBID	133-137	BCL2-associated X protein	Mus musculus	197-200
11139284-3	2000	The cleavage product of caspase-8, tBID, induced insertion of BAX into mitochondria in vivo, and reconstitution in vitro showed that tBID, either directly or indirectly, relieved inhibition of the BAX transmembrane signal-anchor by the NH2-terminal domain, resulting in integration of BAX into mitochondrial membrane.	tBID	133-137	BCL2-associated X protein	Mus musculus	197-200
11074301-2	2000	Some authors have proposed that apoptosis is dependent on induction of the mitochondrial permeability transition pore (PTP), and that activators of apoptosis such as Bax work through activation of PTP, whereas inhibitors of apoptosis such as Bcl-2 work through inhibition of PTP, and the consequent activation or inhibition of PTP-dependent release of mitochondrial apoptotic factors, including cytochrome c. PTP opening is classically measured by a light-scattering assay of large-amplitude swelling of rodent liver mitochondria in sucrose media.	Sucrose	533-540	BCL2-associated X protein	Mus musculus	166-169
11139284-3	2000	The cleavage product of caspase-8, tBID, induced insertion of BAX into mitochondria in vivo, and reconstitution in vitro showed that tBID, either directly or indirectly, relieved inhibition of the BAX transmembrane signal-anchor by the NH2-terminal domain, resulting in integration of BAX into mitochondrial membrane.	tBID	35-39	BCL2-associated X protein	Mus musculus	62-65
11139284-3	2000	The cleavage product of caspase-8, tBID, induced insertion of BAX into mitochondria in vivo, and reconstitution in vitro showed that tBID, either directly or indirectly, relieved inhibition of the BAX transmembrane signal-anchor by the NH2-terminal domain, resulting in integration of BAX into mitochondrial membrane.	tBID	35-39	BCL2-associated X protein	Mus musculus	197-200
11139284-3	2000	The cleavage product of caspase-8, tBID, induced insertion of BAX into mitochondria in vivo, and reconstitution in vitro showed that tBID, either directly or indirectly, relieved inhibition of the BAX transmembrane signal-anchor by the NH2-terminal domain, resulting in integration of BAX into mitochondrial membrane.	tBID	35-39	BCL2-associated X protein	Mus musculus	197-200
11139284-3	2000	The cleavage product of caspase-8, tBID, induced insertion of BAX into mitochondria in vivo, and reconstitution in vitro showed that tBID, either directly or indirectly, relieved inhibition of the BAX transmembrane signal-anchor by the NH2-terminal domain, resulting in integration of BAX into mitochondrial membrane.	tBID	133-137	BCL2-associated X protein	Mus musculus	62-65
11055382-9	2000	The level of expression of Bax in cells treated with either of these chalcones was markedly elevated and the level of Bcl-XL decreased slightly.	Chalcones	69-78	BCL2-associated X protein	Mus musculus	27-30
11006977-0	2000	p53 and Bax implication in NMDA induced-apoptosis in mouse hippocampus.	N-Methylaspartate	27-31	BCL2-associated X protein	Mus musculus	8-11
10984511-5	2000	More than half of colon and gastric cancers of the MMP contain BAX frameshifts in a (G)(8) mononucleotide tract.	mononucleotide	91-105	BCL2-associated X protein	Mus musculus	63-66
11055382-12	2000	It was supposed that isoliquiritigenin induces apoptosis in B16 cells by a mechanism involving inhibition of glucose transmembrane transport and promotion of Bax expression.	isoliquiritigenin	21-38	BCL2-associated X protein	Mus musculus	158-161
11055382-13	2000	On the other hand, it was suggested that butein induces apoptosis via down-regulation of Bcl-2 expression and promotion of Bax expression.	butein	41-47	BCL2-associated X protein	Mus musculus	123-126
10809959-13	2000	Morphine increased J774 cell expression of bax.	Morphine	0-8	BCL2-associated X protein	Mus musculus	43-46
10867640-0	2000	Copper induces apoptosis in BA/F3beta cells: Bax, reactive oxygen species, and NFkappaB are involved.	Copper	0-6	BCL2-associated X protein	Mus musculus	45-48
10875441-5	2000	It was attenuated in cortical cell cultures prepared from mice null for the bax gene, and by the caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-CH2F (ZVAD, 100 microM), but not by the NMDA receptor antagonist, D-2-amino-5-phosphonovalerate (D-APV, 200 microM ).	2-amino-4-oxo-5-phosphonopentanoic acid	212-241	BCL2-associated X protein	Mus musculus	76-79
10875441-5	2000	It was attenuated in cortical cell cultures prepared from mice null for the bax gene, and by the caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-CH2F (ZVAD, 100 microM), but not by the NMDA receptor antagonist, D-2-amino-5-phosphonovalerate (D-APV, 200 microM ).	2-amino-4-oxo-5-phosphonopentanoic acid	243-248	BCL2-associated X protein	Mus musculus	76-79
10875441-6	2000	In contrast, the neuronal death induced by 50 microM Zn2+ was characterized by plasma membrane disruption and random DNA fragmentation; this death was attenuated by D-APV, but exhibited little sensitivity to ZVAD or deletion of bax.	Zinc	53-57	BCL2-associated X protein	Mus musculus	228-231
10809959-14	2000	Interestingly, morphine-induced bax expression was inhibited by anti-TGF-beta Ab.	Morphine	15-23	BCL2-associated X protein	Mus musculus	32-35
10809959-15	2000	As both morphine-induced J774 cell apoptosis and bax expression were inhibited by anti-TGF-beta Ab, it appears that morphine-induced J774 cell apoptosis may be mediated through the generation of TGF-beta.	Morphine	116-124	BCL2-associated X protein	Mus musculus	49-52
10758335-3	2000	The results showed that (1) simultaneous incubation with carbachol dose- and time-dependently blocked the specific DNA ladder formation induced by exposure to A(beta31-35) and (2) the A(beta31-35)-induced downregulation of bcl-2 and upregulations of bax, p53, and c-fos genes were reversed or ameliorated by the coadministration of carbachol.	Carbachol	57-66	BCL2-associated X protein	Mus musculus	250-253
10792780-4	2000	MNU effectively induced hair follicular cell apoptosis at the anagen stage by up-regulation of Bax protein without down-modulation of Bcl-2 protein.	Methylnitrosourea	0-3	BCL2-associated X protein	Mus musculus	95-98
10760524-0	2000	The cytotoxic action of Bax on yeast cells does not require mitochondrial ADP/ATP carrier but may be related to its import to the mitochondria.	Adenosine Diphosphate	74-77	BCL2-associated X protein	Mus musculus	24-27
10760524-0	2000	The cytotoxic action of Bax on yeast cells does not require mitochondrial ADP/ATP carrier but may be related to its import to the mitochondria.	Adenosine Triphosphate	78-81	BCL2-associated X protein	Mus musculus	24-27
10760524-2	2000	The cytotoxic effect of Bax on yeast does not require functional oxidative phosphorylation, respiration, or mitochondrial proteins (ADP/ATP carriers) implicated in the formation of the permeability transition pore in mammalian mitochondria.	Adenosine Triphosphate	136-139	BCL2-associated X protein	Mus musculus	24-27
14634326-2	1999	Ether lipid-resistant S49ar cells were cross-resistant to extracellular stress factors (cold shock, heat shock, H2O2, dimethylsulfoxide) and to radiation-induced apoptosis but not to physiological apoptotic signals (dexamethasone, growth factor deprivation, thapsigargin, C2-ceramide) and expressed similar levels of the apoptosis-regulating proteins Bcl-2, Bcl-X, Bax, Bad and Bak as did the parent S49wt cells.	ether lipid	0-11	BCL2-associated X protein	Mus musculus	365-368
10712780-11	2000	The mechanism of arsenic trioxide may mainly be inducing liver cancer cells to undergo apoptosis, which may be related to downregulate the expression of bcl-2 genes and upregulate the expression of bax genes.	Arsenic Trioxide	17-33	BCL2-associated X protein	Mus musculus	198-201
10620504-9	2000	In cytosolic extracts from mouse liver, Bax migrated at a molecular mass of 24000 Da on gel filtration, whereas after incubation of the cytosol with 2% octyl glucoside Bax migrated at approximately 140000 Da.	octyl-beta-D-glucoside	152-167	BCL2-associated X protein	Mus musculus	168-171
10619357-8	1999	Testosterone administration induced a significant increase in the lacrimal gland content of Bax mRNA, but a striking decrease in the lacrimal tissue level of bcl-2 mRNA in F1 and C3H mice.	Testosterone	0-12	BCL2-associated X protein	Mus musculus	92-95
10537165-6	1999	As early as 6 h, Western blots demonstrated a dose-dependent decrease in the Bcl-2/Bax ratio, which reached a minimum of 0.18 in osteoblasts treated with 1000 nM corticosterone for 72 h. This reduction in Bcl-2/Bax was abolished by treating osteoblasts simultaneously with 17beta-estradiol, but not with 17alpha-estradiol.	Corticosterone	162-176	BCL2-associated X protein	Mus musculus	83-86
10537165-6	1999	As early as 6 h, Western blots demonstrated a dose-dependent decrease in the Bcl-2/Bax ratio, which reached a minimum of 0.18 in osteoblasts treated with 1000 nM corticosterone for 72 h. This reduction in Bcl-2/Bax was abolished by treating osteoblasts simultaneously with 17beta-estradiol, but not with 17alpha-estradiol.	Corticosterone	162-176	BCL2-associated X protein	Mus musculus	211-214
10537165-6	1999	As early as 6 h, Western blots demonstrated a dose-dependent decrease in the Bcl-2/Bax ratio, which reached a minimum of 0.18 in osteoblasts treated with 1000 nM corticosterone for 72 h. This reduction in Bcl-2/Bax was abolished by treating osteoblasts simultaneously with 17beta-estradiol, but not with 17alpha-estradiol.	Estradiol	273-289	BCL2-associated X protein	Mus musculus	83-86
10537165-6	1999	As early as 6 h, Western blots demonstrated a dose-dependent decrease in the Bcl-2/Bax ratio, which reached a minimum of 0.18 in osteoblasts treated with 1000 nM corticosterone for 72 h. This reduction in Bcl-2/Bax was abolished by treating osteoblasts simultaneously with 17beta-estradiol, but not with 17alpha-estradiol.	alfatradiol	304-321	BCL2-associated X protein	Mus musculus	83-86
10493969-4	1999	BCL-2 and BAX expression were lower in Tu-2449 and P497 than in SRB-10 cells.	Thiourea	39-41	BCL2-associated X protein	Mus musculus	10-13
10532544-8	1999	As Bcl-2-related proteins are involved in apoptotic process, we also evaluated their role by examining the expression of Bcl-2, Bcl-X(L), and Bax on SEB-FK506-treated murine splenic T cells.	Tacrolimus	153-158	BCL2-associated X protein	Mus musculus	142-145
10518582-5	1999	Although kainate induced the expression of bax and caspase 3 in the hippocampus of wild-type mice, these critical intracellular mediators of cell death pathways were not altered by kainate injection in the mutant mice.	Kainic Acid	9-16	BCL2-associated X protein	Mus musculus	43-46
10464378-7	1999	In both neonatal and adult mice, the labeling of dividing cells with 5-bromo-2"-deoxyuridine indicated that all Bax-positive taste cells were at least 5 days old.	Bromodeoxyuridine	69-92	BCL2-associated X protein	Mus musculus	112-115
10470825-4	1999	Constitutive overexpression of murine bax was achieved in U138 and U373 only, which resulted in an increased sensitivity of these lines to the apoptosis-inducing effect of cytosine arabinoside (ara-C).	Cytarabine	172-192	BCL2-associated X protein	Mus musculus	38-41
10470825-4	1999	Constitutive overexpression of murine bax was achieved in U138 and U373 only, which resulted in an increased sensitivity of these lines to the apoptosis-inducing effect of cytosine arabinoside (ara-C).	Cytarabine	194-199	BCL2-associated X protein	Mus musculus	38-41
10349855-0	1999	Sequential cleavage of poly(ADP-ribose)polymerase and appearance of a small Bax-immunoreactive protein are blocked by Bcl-X(L) and caspase inhibitors during staurosporine-induced dopaminergic neuronal apoptosis.	Staurosporine	157-170	BCL2-associated X protein	Mus musculus	76-79
10449034-7	1999	Phenobarbital, a potent liver tumor promoter, inhibited apoptosis in c-myc hepatocytes but not in wild-type hepatocytes, decreased p53 and bax, and increased bcl-2 protein levels.	Phenobarbital	0-13	BCL2-associated X protein	Mus musculus	139-142
10426811-4	1999	Acute treatment of B6C3F1 mice with phenobarbital resulted in increased levels of bcl-2 and decreased levels of bax protein, while acute treatment with WY-14,643 resulted in increased bcl-2 and BAG-1 protein in the liver.	Phenobarbital	36-49	BCL2-associated X protein	Mus musculus	112-115
10400666-0	1999	NH2-terminal BH4 domain of Bcl-2 is functional for heterodimerization with Bax and inhibition of apoptosis.	sapropterin	13-16	BCL2-associated X protein	Mus musculus	75-78
10400666-4	1999	Structural and functional analyses of the cleaved fragment revealed that the NH2-terminal region of Bcl-2 (1-34 amid acids) was required for its anti-apoptotic activity and heterodimerization with pro-apoptotic Bax protein.	amid acids	112-122	BCL2-associated X protein	Mus musculus	211-214
10400666-5	1999	Site-directed mutagenesis of the NH2-terminal region showed that substitutions of hydrophobic residues of BH4 domain resulted in the loss of ability to form a heterodimer with Bax.	sapropterin	106-109	BCL2-associated X protein	Mus musculus	176-179
10400666-7	1999	Our results suggest that the BH4 domain of Bcl-2 is critical for its heterodimerization with Bax and for exhibiting anti-apoptotic activity.	sapropterin	29-32	BCL2-associated X protein	Mus musculus	93-96
10349855-8	1999	The sequential cleavage of PARP and the appearance of the small Bax-immunoreactive protein in MN9D cells were blocked either by Z-VAD-fmk or by Bcl-X(L).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	128-137	BCL2-associated X protein	Mus musculus	64-67
10200338-7	1999	WAF1, c-myc and Bax mRNAs were also induced by doxorubicin in the WT cells but not in the Y8 cells.	Doxorubicin	47-58	BCL2-associated X protein	Mus musculus	16-19
10200563-7	1999	The levels of Bax and Bad proteins remained relatively constant during DMSO-induced differentiation.	Dimethyl Sulfoxide	71-75	BCL2-associated X protein	Mus musculus	14-17
10082077-9	1999	Bax deficiency also attenuated serum withdrawal- and kainate-induced apoptosis in motor neurons.	Kainic Acid	53-60	BCL2-associated X protein	Mus musculus	0-3
9875280-0	1998	Overexpression of HA-Bax but not Bcl-2 or Bcl-XL attenuates 6-hydroxydopamine-induced neuronal apoptosis.	Oxidopamine	60-77	BCL2-associated X protein	Mus musculus	21-24
9988273-4	1999	Here we show that young adult female Bax-/- mice possess threefold more primordial follicles in their ovarian reserve than their wild-type sisters, and this surfeit of follicles is maintained in advanced chronological age, such that 20-22-month-old female Bax-/- mice possess hundreds of follicles at all developmental stages and exhibit ovarian steroid-driven uterine hypertrophy.	Steroids	346-353	BCL2-associated X protein	Mus musculus	37-40
9856857-11	1998	Staurosporine (a potent inducer of apoptosis in many cell types) effectively induced neuronal cell death in wild-type, p53-deficient and Bax-deficient hippocampal neurons, indicating that all were competent to undergo programmed cell death.	Staurosporine	0-13	BCL2-associated X protein	Mus musculus	137-140
9875280-2	1998	To investigate the potential role of Bax in 6-hydroxydopamine (6-OHDA)-induced cell death, we first established and characterized a dopaminergic neuronal cell line (MN9D) stably overexpressing hemagglutinin epitope-tagged Bax (MN9D/HA-Bax) as well as control clones (MN9D/Neo).	Oxidopamine	63-69	BCL2-associated X protein	Mus musculus	37-40
9875280-4	1998	Overexpression of HA-Bax in MN9D cells was shown to attenuate 6-OHDA-induced cell death as determined by the MTT reduction assay and agarose gel analysis for DNA fragmentation.	Oxidopamine	62-68	BCL2-associated X protein	Mus musculus	21-24
9875280-4	1998	Overexpression of HA-Bax in MN9D cells was shown to attenuate 6-OHDA-induced cell death as determined by the MTT reduction assay and agarose gel analysis for DNA fragmentation.	monooxyethylene trimethylolpropane tristearate	109-112	BCL2-associated X protein	Mus musculus	21-24
9875280-4	1998	Overexpression of HA-Bax in MN9D cells was shown to attenuate 6-OHDA-induced cell death as determined by the MTT reduction assay and agarose gel analysis for DNA fragmentation.	Sepharose	133-140	BCL2-associated X protein	Mus musculus	21-24
9875280-5	1998	Western blot analysis revealed that cleavage of poly(ADP-ribose)polymerase induced by 6-OHDA was attenuated in MN9D/HA-Bax cells.	Oxidopamine	86-92	BCL2-associated X protein	Mus musculus	111-122
9637502-9	1998	A CpG ODN with a nuclease-resistant phosphorothioate backbone (S-ODN) was also active, and increased the levels of c-myc, egr-1, c-jun, bclXL, and bax mRNA and c-Myc, c-Jun, Bax, and BclXL protein in spleen B cells.	Parathion	36-52	BCL2-associated X protein	Mus musculus	147-150
9748162-3	1998	Immunodepletion of Bax from PTPC or purification of PTPC from Bax-deficient mice yielded a PTPC that could not permeabilize membranes in response to atractyloside, a proapoptotic ligand of the adenine nucleotide translocator (ANT).	Adenine Nucleotides	193-211	BCL2-associated X protein	Mus musculus	19-22
9748162-6	1998	Recombinant Bax and purified ANT, but neither of them alone, efficiently formed atractyloside-responsive channels in artificial membranes.	Atractyloside	80-93	BCL2-associated X protein	Mus musculus	12-15
9858902-4	1998	RESULTS: After hydrocortisone injection, levels of p53 and Bax, but not Bcl-2, expression were raised.	Hydrocortisone	15-29	BCL2-associated X protein	Mus musculus	59-62
9751125-3	1998	Bleomycin-induced apoptosis was accompanied by decreases in bcl-2 and bcl-xl and increases in p53, bak, and bax protein levels.	Bleomycin	0-9	BCL2-associated X protein	Mus musculus	108-111
9751125-6	1998	Phenobarbital inhibited both TGF-beta and bleomycin-induced apoptosis and the normal regulation of p53, bcl-2, and bax.	Phenobarbital	0-13	BCL2-associated X protein	Mus musculus	115-118
9792795-4	1998	A FL5.12 Bax CL16 mutant cell, ms3, which is resistant to apoptosis induced by staurosporine, retains the activity of Bax redistribution but shows no caspase-3 activity.	Staurosporine	79-92	BCL2-associated X protein	Mus musculus	9-12
9637502-9	1998	A CpG ODN with a nuclease-resistant phosphorothioate backbone (S-ODN) was also active, and increased the levels of c-myc, egr-1, c-jun, bclXL, and bax mRNA and c-Myc, c-Jun, Bax, and BclXL protein in spleen B cells.	Parathion	36-52	BCL2-associated X protein	Mus musculus	174-177
9553144-6	1998	Detergents such as Triton X-100 and Triton X-114 readily enable Bax hetero- and homodimerization.	Octoxynol	19-31	BCL2-associated X protein	Mus musculus	64-67
9852625-8	1998	Our results suggest that the therapeutic effects of bryostatin 1 in our system do not involve alterations in levels and distribution of PKC but rather a direct upregulation of bax/ bcl-2 ratios that is independent of p53.	bryostatin 1	52-64	BCL2-associated X protein	Mus musculus	176-179
9633514-4	1998	Kinetic analysis showed that the signs of apoptosis were observed not until 60 h of continued GCV treatment and preceded first by a rise in p53 protein level in 12 h and then by S-phase/G2-phase cell cycle arrest associated with corresponding increases in the level of cyclin B1 protein but no apparent change in protein level of Bax or Cdc2.	Ganciclovir	94-97	BCL2-associated X protein	Mus musculus	330-333
9553144-6	1998	Detergents such as Triton X-100 and Triton X-114 readily enable Bax hetero- and homodimerization.	Nonidet P-40	36-48	BCL2-associated X protein	Mus musculus	64-67
9553144-7	1998	However, other detergents such as polydocanol, W-1, octyl glucoside, dodecyl maltoside, Tween 20, and sodium cholate allow varying degrees of Bax hetero- and homodimerization.	Polidocanol	34-45	BCL2-associated X protein	Mus musculus	142-145
9553144-7	1998	However, other detergents such as polydocanol, W-1, octyl glucoside, dodecyl maltoside, Tween 20, and sodium cholate allow varying degrees of Bax hetero- and homodimerization.	w-1, octyl glucoside	47-67	BCL2-associated X protein	Mus musculus	142-145
9553144-7	1998	However, other detergents such as polydocanol, W-1, octyl glucoside, dodecyl maltoside, Tween 20, and sodium cholate allow varying degrees of Bax hetero- and homodimerization.	dodecyl maltoside	69-86	BCL2-associated X protein	Mus musculus	142-145
9553144-7	1998	However, other detergents such as polydocanol, W-1, octyl glucoside, dodecyl maltoside, Tween 20, and sodium cholate allow varying degrees of Bax hetero- and homodimerization.	Polysorbates	88-96	BCL2-associated X protein	Mus musculus	142-145
9553144-7	1998	However, other detergents such as polydocanol, W-1, octyl glucoside, dodecyl maltoside, Tween 20, and sodium cholate allow varying degrees of Bax hetero- and homodimerization.	Sodium Cholate	102-116	BCL2-associated X protein	Mus musculus	142-145
9553144-9	1998	Immunoprecipitation analysis with the conformation-sensitive antibody uBax 6A7 revealed that whereas Triton X-100 readily exposes the N-terminal Bax epitope (amino acid 13-19), only limited exposure of the epitope occurs in Triton X-114, polydocanol, dodecyl maltoside, and sodium cholate, and no exposure of this epitope was observed in W-1, Chaps, octyl glucoside, Tween 20, and Brij 35.	Octoxynol	101-113	BCL2-associated X protein	Mus musculus	71-74
9553144-11	1998	Sephacryl S-100 gel filtration chromatography analysis of the cytosolic Bax indicated that this protein is monomeric and displays an apparent molecular mass of 25 kDa.	sephacryl s-100	0-15	BCL2-associated X protein	Mus musculus	72-75
9628323-13	1998	The increase of Bax mRNA:GAPDH mRNA ratio was observed 3h after TGF-beta1 (1 ng/ml) administration to both the maintenance (2% FCS/RPMI) and growth promoting (10% FCS/RPMI) medium.	rpmi	131-135	BCL2-associated X protein	Mus musculus	16-19
9628323-13	1998	The increase of Bax mRNA:GAPDH mRNA ratio was observed 3h after TGF-beta1 (1 ng/ml) administration to both the maintenance (2% FCS/RPMI) and growth promoting (10% FCS/RPMI) medium.	rpmi	167-171	BCL2-associated X protein	Mus musculus	16-19
9434797-4	1998	In contrast, the content of c-myb and p53 mRNA is greater (P &lt; 0.05) in submandibular tissues of female relative to those of male mice; and (3) testosterone or cyclophosphamide treatment led to a significant (P &lt; 0.05) decline in the mRNA levels of c-myb, bcl-2, and/or AR, but an increase (P &lt; 0.05) in the mRNA amount of Bax, in lacrimal, but not in salivary, glands of female mice.	Cyclophosphamide	163-179	BCL2-associated X protein	Mus musculus	332-335
9492080-4	1998	KCl, BayK, A23187, and ionomycin elicit an elevation of cytosolic/nuclear Ca2+, which, however, is insufficient to evoke apoptosis or to alter bcl-2 or bax mRNA expression in MIN6 cells.	Potassium Chloride	0-3	BCL2-associated X protein	Mus musculus	152-155
9492080-4	1998	KCl, BayK, A23187, and ionomycin elicit an elevation of cytosolic/nuclear Ca2+, which, however, is insufficient to evoke apoptosis or to alter bcl-2 or bax mRNA expression in MIN6 cells.	Ionomycin	23-32	BCL2-associated X protein	Mus musculus	152-155
9492080-5	1998	The extracellular Ca2+ chelators, EGTA and 1,2-Bis(2-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid, tetrapotassium salt, hydrate, evoke apoptosis and also alter the ratio of bcl-2 to bax mRNA and protein concomitantly with the depletion of cytosolic/nuclear Ca2+.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	43-99	BCL2-associated X protein	Mus musculus	184-187
9492080-5	1998	The extracellular Ca2+ chelators, EGTA and 1,2-Bis(2-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid, tetrapotassium salt, hydrate, evoke apoptosis and also alter the ratio of bcl-2 to bax mRNA and protein concomitantly with the depletion of cytosolic/nuclear Ca2+.	tetrapotassium salt	101-120	BCL2-associated X protein	Mus musculus	184-187
9314540-3	1997	Within 2 h after switching to 5 mM K+, both wild-type and Bax-deficient granule cells decreased glucose uptake to &lt;20% of control.	Glucose	96-103	BCL2-associated X protein	Mus musculus	58-61
9458287-4	1998	This study shows that mitotic spindle inhibitors can induce apoptosis in fludarabine-resistant malignant B-1 cells by altering levels of bax/ bcl-2 ratio and BSAP which play different roles in cell cycle regulation and apoptosis induction.	fludarabine	73-84	BCL2-associated X protein	Mus musculus	137-140
9361016-5	1997	This correlated with their high Bax expression level and insensitivity to the caspase inhibitor, zVAD-fmk, a functional hallmark of Bax-like activity.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	97-105	BCL2-associated X protein	Mus musculus	132-135
9314540-6	1997	Wild-type granule cells in 5 mM K+ increased cleavage of DEVD-aminomethylcoumarin (DEVD-AMC), a fluorogenic substrate for caspases 2, 3, and 7; in contrast, Bax-deficient granule cells did not cleave DEVD-AMC.	devd-aminomethylcoumarin	57-81	BCL2-associated X protein	Mus musculus	157-160
9403711-5	1997	During cyclophosphamide-induced follicle dystrophy and alopecia, massive keratinocyte apoptosis occurred in the entire proximal hair bulb, except in the dermal papilla, despite a strong up-regulation of Bax and p75NTR immunoreactivity.	Cyclophosphamide	7-23	BCL2-associated X protein	Mus musculus	203-206
9314540-6	1997	Wild-type granule cells in 5 mM K+ increased cleavage of DEVD-aminomethylcoumarin (DEVD-AMC), a fluorogenic substrate for caspases 2, 3, and 7; in contrast, Bax-deficient granule cells did not cleave DEVD-AMC.	acetyl-aspartyl-glutamyl-valyl-aspartyl-amino-4-methylcoumarin	200-208	BCL2-associated X protein	Mus musculus	157-160
9314540-4	1997	Protein synthesis also decreased rapidly in both wild-type and Bax-deficient granule cells to 50% of control within 12 h after switching to 5 mM potassium.	Potassium	145-154	BCL2-associated X protein	Mus musculus	63-66
9333015-5	1997	Moreover, butyrate induced p53-independent apoptosis, which was, as well as p53-mediated apoptosis, associated with a dose-dependent increase in Bax and c-Myc protein.	Butyrates	10-18	BCL2-associated X protein	Mus musculus	145-148
9333015-8	1997	This was reflected in an enhanced decrease in c-Myc and Bax protein in response to mitomycin C with low concentrations of butyrate.	Mitomycin	83-94	BCL2-associated X protein	Mus musculus	56-59
9333015-8	1997	This was reflected in an enhanced decrease in c-Myc and Bax protein in response to mitomycin C with low concentrations of butyrate.	Butyrates	122-130	BCL2-associated X protein	Mus musculus	56-59
9230108-5	1997	GSH in cells overexpressing bax was reduced by approximately 36%.	Glutathione	0-3	BCL2-associated X protein	Mus musculus	28-31
9230198-5	1997	Dissociation of p53 proteins from degrading T antigens followed by a phenobarbital and c-myc-dependent, 15-fold induction of Bax protein, known to activate the apoptotic pathway downstream of p53, occurred in association with this phenomenon.	Phenobarbital	69-82	BCL2-associated X protein	Mus musculus	125-128
9230108-7	1997	Following IL-3 withdrawal, a condition known to cause apoptosis in these cells, a rapid loss of intracellular GSH occurred in control and bax transfectants, which preceded the onset of apoptosis.	Glutathione	110-113	BCL2-associated X protein	Mus musculus	138-141
9230198-6	1997	The effects of phenobarbital and c-myc in increasing Bax on shifting the temperature from 33 degrees C to 39 degrees C were additive, with both having similar degrees of influence on the protein level.	Phenobarbital	15-28	BCL2-associated X protein	Mus musculus	53-56
9096145-4	1997	bcl-x-/-/bax-/- mice demonstrate greatly reduced levels of apoptosis both in vivo and in vitro compared with the CNS of Bcl-xL-deficient mice, as assessed by histology and terminal deoxytransferase-mediated deoxyuridine triphosphate nick end-labeling.	deoxyuridine triphosphate	207-232	BCL2-associated X protein	Mus musculus	9-12
9230198-7	1997	Interestingly, subsequent introduction of an activated c-H-ras oncogene into the c-myc-transfected CHST8 cells resulted not only in escape from the growth arrest at 39 degrees C but also in complete inhibition of the phenobarbital-inducible apoptosis along with de novo induction of the Bax antagonist, Bcl-2.	Phenobarbital	217-230	BCL2-associated X protein	Mus musculus	287-290
9230198-8	1997	These findings strongly suggest that the phenobarbital-inducible apoptosis is mediated by Bax.	Phenobarbital	41-54	BCL2-associated X protein	Mus musculus	90-93
9177459-0	1997	Effects of dehydroepiandrosterone and calorie restriction on the Bcl-2/Bax-mediated apoptotic pathway in p53-deficient mice.	Dehydroepiandrosterone	11-33	BCL2-associated X protein	Mus musculus	71-74
9177459-1	1997	Modulation of apoptosis through altered expression of Bcl-2 and/or Bax may be a mechanism by which dehydroepiandrosterone (DHEA) administration and calorie restriction (CR) exert their chemopreventive effects in p53-deficient (p53-/-) mice.	Dehydroepiandrosterone	99-121	BCL2-associated X protein	Mus musculus	67-70
9177459-1	1997	Modulation of apoptosis through altered expression of Bcl-2 and/or Bax may be a mechanism by which dehydroepiandrosterone (DHEA) administration and calorie restriction (CR) exert their chemopreventive effects in p53-deficient (p53-/-) mice.	Dehydroepiandrosterone	123-127	BCL2-associated X protein	Mus musculus	67-70
9208127-0	1997	Attenuation of p53 expression and Bax down-regulation during phorbol ester mediated inhibition of apoptosis.	Phorbol Esters	61-74	BCL2-associated X protein	Mus musculus	34-37
9208127-17	1997	As well as affecting p53, TPA elicited a rapid decline of the steady state level of Bax within 30 min.	Tetradecanoylphorbol Acetate	26-29	BCL2-associated X protein	Mus musculus	84-87
9108035-4	1997	Induction of apoptosis in murine thymocytes by dexamethasone or gamma-irradiation shifts the subcellular locations of Bax and Bcl-X(L) from soluble to membrane-bound forms.	Dexamethasone	47-60	BCL2-associated X protein	Mus musculus	118-121
9108035-6	1997	Inhibition of apoptosis with cycloheximide inhibits the movement of Bax and Bcl-X(L) in thymocytes from the cytosol into membranes induced by dexamethasone treatment.	Cycloheximide	29-42	BCL2-associated X protein	Mus musculus	68-71
9108035-6	1997	Inhibition of apoptosis with cycloheximide inhibits the movement of Bax and Bcl-X(L) in thymocytes from the cytosol into membranes induced by dexamethasone treatment.	Dexamethasone	142-155	BCL2-associated X protein	Mus musculus	68-71
9223064-0	1997	Bax accelerates staurosporine-induced but suppresses nigericin-induced neuronal cell death.	Staurosporine	16-29	BCL2-associated X protein	Mus musculus	0-3
9223064-0	1997	Bax accelerates staurosporine-induced but suppresses nigericin-induced neuronal cell death.	Nigericin	53-62	BCL2-associated X protein	Mus musculus	0-3
9223064-4	1997	As expected, over-expression of Bax in MN9D cells accelerated staurosporine-induced cell death as measured by the MTT reduction assay (62.3% survival in MN9D/Neo vs 27.0% survival in MN9D/Bax).	Staurosporine	62-75	BCL2-associated X protein	Mus musculus	32-35
9223064-4	1997	As expected, over-expression of Bax in MN9D cells accelerated staurosporine-induced cell death as measured by the MTT reduction assay (62.3% survival in MN9D/Neo vs 27.0% survival in MN9D/Bax).	Staurosporine	62-75	BCL2-associated X protein	Mus musculus	188-191
9223064-4	1997	As expected, over-expression of Bax in MN9D cells accelerated staurosporine-induced cell death as measured by the MTT reduction assay (62.3% survival in MN9D/Neo vs 27.0% survival in MN9D/Bax).	monooxyethylene trimethylolpropane tristearate	114-117	BCL2-associated X protein	Mus musculus	32-35
9223064-5	1997	Surprizingly, both nigericin-induced cell death and its accompanying DNA fragmentation were largely attenuated in MN9D/Bax cells (22.0% survival in MN9D/Neo vs 86.7% survival in MN9D/Bax).	Nigericin	19-28	BCL2-associated X protein	Mus musculus	119-122
9223064-5	1997	Surprizingly, both nigericin-induced cell death and its accompanying DNA fragmentation were largely attenuated in MN9D/Bax cells (22.0% survival in MN9D/Neo vs 86.7% survival in MN9D/Bax).	Nigericin	19-28	BCL2-associated X protein	Mus musculus	183-186
9223064-7	1997	Cleavage of poly(ADP-ribose)polymerase caused by nigericin was greatly attenuated in MN9D/Bax cells suggesting that, like Bcl-2, Bax suppresses nigericin-induced cell death by inhibiting the activation of cysteine proteases.	Nigericin	49-58	BCL2-associated X protein	Mus musculus	90-93
9223064-7	1997	Cleavage of poly(ADP-ribose)polymerase caused by nigericin was greatly attenuated in MN9D/Bax cells suggesting that, like Bcl-2, Bax suppresses nigericin-induced cell death by inhibiting the activation of cysteine proteases.	Nigericin	49-58	BCL2-associated X protein	Mus musculus	129-132
9223064-7	1997	Cleavage of poly(ADP-ribose)polymerase caused by nigericin was greatly attenuated in MN9D/Bax cells suggesting that, like Bcl-2, Bax suppresses nigericin-induced cell death by inhibiting the activation of cysteine proteases.	Nigericin	144-153	BCL2-associated X protein	Mus musculus	90-93
9223064-7	1997	Cleavage of poly(ADP-ribose)polymerase caused by nigericin was greatly attenuated in MN9D/Bax cells suggesting that, like Bcl-2, Bax suppresses nigericin-induced cell death by inhibiting the activation of cysteine proteases.	Nigericin	144-153	BCL2-associated X protein	Mus musculus	129-132
8702745-11	1996	Moreover, GSNO induced increases in the steady-state levels of Bax protein in parental and Bcl-2-transfected cells.	S-Nitrosoglutathione	10-14	BCL2-associated X protein	Mus musculus	63-66
11725138-8	1997	In comparison, there was an elevated expression of IFN-gamma mRNA without apparent change in bax, p53 or GAPDH mRNA after 24 h. After treatment with DZA, there was an elevated expression of NF-kappaB DNA binding activity, which became more pronounced at 24 h. Simultaneously, there was an apparent disappearance of AP-1 activity.	3-deazaadenosine	149-152	BCL2-associated X protein	Mus musculus	93-96
7675327-0	1995	Up-regulation of bax and down-regulation of bcl-2 is associated with kainate-induced apoptosis in mouse brain.	Kainic Acid	69-76	BCL2-associated X protein	Mus musculus	17-20
8647960-6	1996	Furthermore, we transfected bax-alpha into breast cancer cell lines under the control of a tetracycline-dependent expression system.	Tetracycline	91-103	BCL2-associated X protein	Mus musculus	28-31
8929984-0	1996	Increase in bax expression in substantia nigra following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment of mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	57-101	BCL2-associated X protein	Mus musculus	12-15
8929984-0	1996	Increase in bax expression in substantia nigra following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment of mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	103-107	BCL2-associated X protein	Mus musculus	12-15
8929984-3	1996	Intraperitoneal MPTP injections in mice resulted in a significant increase in bax mRNA by about two- and three-fold after 3 and 6 days, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	16-20	BCL2-associated X protein	Mus musculus	78-81
8929984-5	1996	Our results indicate a pathophysiological significance of bax, which promotes programmed cell death, in MPTP neurotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	104-108	BCL2-associated X protein	Mus musculus	58-61
33821300-6	2021	DEX also markedly attenuated the increases in malondialdehyde 5 (MDA 5) and inositol-dependent enzyme a (IRE-a), attenuated the decrease in superoxide dismutase 1(SOD-1), reversed the low expression of B-cell lymphoma-2 (Bcl-2), and the high expressions of Bax and Caspase-3.	Dexmedetomidine	0-3	BCL2-associated X protein	Mus musculus	257-260
33104985-6	2021	Compared with the control group, the expressions of key regulators of oocyte apoptosis (bax, caspase-3) and autophagy (lc3, beclin, ATG12) pathway were increased in the HCPT-treated group.	10-hydroxycamptothecin	169-173	BCL2-associated X protein	Mus musculus	88-91
33811687-7	2021	We further investigated the transcriptome changes in the colon of hCYP1A mice treated with PhIP and identified that PhIP treatment increased the expression of Bax, Btg2, Ccng1, Cdkn1a, and Trp53inp1 and decreased the expression of Igf1 and Ccnd1.	2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine	116-120	BCL2-associated X protein	Mus musculus	159-162
33812255-7	2021	GM upregulated the expression levels of NOX4, cleaved Caspase-3 and p53 and the BAX/BCL2 ratio in vivo to stimulate oxidative stress and apoptosis.	Gentamicins	0-2	BCL2-associated X protein	Mus musculus	80-83
33782744-10	2021	At the same time, it was observed that DEX improved the Bcl-2/Bax ratio.	Dexmedetomidine	39-42	BCL2-associated X protein	Mus musculus	62-65
33767628-5	2021	The results clearly showed that DSS exposure caused excessive ER stress evidenced by a markedly increase of GRP78 and CHOP expression, and then activated the ER stress sensors PERK, IRE1, ATF6 and their respective signaling pathways, followed by upregulated caspases12 and lowered Bcl-2/Bax ratio.	Dextran Sulfate	32-35	BCL2-associated X protein	Mus musculus	287-290
33973356-13	2021	Ethanol promoted Bax expression and cytochrome C release and inhibited Bcl-2 and ATP expression.	Ethanol	0-7	BCL2-associated X protein	Mus musculus	17-20
32797474-13	2020	Correspondingly, the level of Bcl-2 was enhanced while the levels of Bax and Cleaved Caspase-3 were descended by miR-16-5p mimic, which were reversed by CXCL10 over-expression in HG-treated beta-TC-tet cells.	beta-tc-tet	190-201	BCL2-associated X protein	Mus musculus	69-72
26628978-7	2015	Decreased expression of Bad and Bax and increased expression of Bcl-2 was found after etoposide treatment in WISP-1 overexpressed cells.	Etoposide	86-95	BCL2-associated X protein	Mus musculus	32-35
25517918-9	2015	Moreover, esculetin treatment resulted in the collapse of mitochondrial membrane potential in vitro and in vivo accompanied by increased Bax expression and decreased Bcl-2 expression at both transcriptional and translational levels.	esculetin	10-19	BCL2-associated X protein	Mus musculus	137-140
34737012-18	2022	PB pretreatment also downregulated the apoptotic factors caspase-3, caspase-9, and apoptotic protein Bax, and it upregulated apoptotic protein Bcl-2.	physalin B	0-2	BCL2-associated X protein	Mus musculus	101-104
25887954-8	2015	DOB also up-regulated TNF-alpha expression, decreased Bcl-2 levels, promoted Bax translocation to mitochondria, mitochondrial membrane potential loss and cytochrome c release as well as IkappaBalpha, p38 MAPK, JNK and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation in LPS-treated cardiomyocytes.	Dobutamine	0-3	BCL2-associated X protein	Mus musculus	77-80
34877763-8	2022	In addition, DFC can induce the release of Cyt c, promote the collapse of mitochondrial membrane potential and increase the Bax/Bcl-2 ratio in RAW264.7 cells.	difenoconazole	13-16	BCL2-associated X protein	Mus musculus	124-127
34954267-4	2022	MATERIALS AND METHODS: The effect of cucurbitacin B on the growth of HCT116 and CT-26 was detected by CCK8; apoptosis was determined by flow cytometry and colony formation; the expression of apoptosis-related protein Bax, Bcl-2 and Cleaved-caspase-3 were examined by western Blot.	cucurbitacin B	37-51	BCL2-associated X protein	Mus musculus	217-220
34964693-7	2022	The PEG-EV-DOX administration in vivo reduced NF-kappaB activation and increased BAX expression, suggesting better prognosis of EV-based therapy than liposomal DOX treatment.	peg-ev	4-10	BCL2-associated X protein	Mus musculus	81-84
34964693-7	2022	The PEG-EV-DOX administration in vivo reduced NF-kappaB activation and increased BAX expression, suggesting better prognosis of EV-based therapy than liposomal DOX treatment.	Doxorubicin	11-14	BCL2-associated X protein	Mus musculus	81-84
34964693-7	2022	The PEG-EV-DOX administration in vivo reduced NF-kappaB activation and increased BAX expression, suggesting better prognosis of EV-based therapy than liposomal DOX treatment.	Doxorubicin	160-163	BCL2-associated X protein	Mus musculus	81-84
34763041-10	2022	Meanwhile, increased expression of the apoptosis-related proteins, caspase-3 and Bax, in cholestatic mice was reversed by CBBP treatment.	phosphon	122-126	BCL2-associated X protein	Mus musculus	81-84
34085179-15	2022	UA treatment prominently decreased cell viability, promoted apoptotic cells, enhanced Bax levels, declined Bcl-2 level as well as decreased insulin release in Min6 cells.	Uric Acid	0-2	BCL2-associated X protein	Mus musculus	86-89
34547420-13	2022	Moreover, BZBS treatment were associated with a declines in P53, caspase-3, Bax expressions and an increase in Sirt6, p-HO-1, p-NRF2, PGC-1alpha, and Bcl-2 expressions in the brains of this rapid aging mouse.	bzbs	10-14	BCL2-associated X protein	Mus musculus	76-79
34883100-10	2022	The gene expression of G-CSF, Bcl-2-associated X protein (BAX), and Bcl2 indicated the role of melatonin in G-CSF regulation and downstream pro-survival pathways along with anti-apoptotic activity.	Melatonin	95-104	BCL2-associated X protein	Mus musculus	30-56
34883100-10	2022	The gene expression of G-CSF, Bcl-2-associated X protein (BAX), and Bcl2 indicated the role of melatonin in G-CSF regulation and downstream pro-survival pathways along with anti-apoptotic activity.	Melatonin	95-104	BCL2-associated X protein	Mus musculus	58-61
34890760-5	2022	We found that NaB restored bodyweight and attenuated P-53, Bcl-2-associated X protein (BAX), and caspase cascades in the brains of HFD-fed mice.	nab	14-17	BCL2-associated X protein	Mus musculus	59-85
34363866-10	2022	Importantly, O-1602 treatment reversed Abeta1-42-induced GPR55 down-regulation, decreased pro-inflammatory cytokines, and the level of malondialdehyde (MDA), increased the levels of glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT), as well as suppressed apoptosis as indicated by decreased TUNEL-positive cells, and increased the ratio of Bcl-2/Bax.	O-1602	13-19	BCL2-associated X protein	Mus musculus	362-365
34480999-13	2022	The results demonstrated that HC067047 treatment decreased the protein levels of proapoptotic proteins such as Bax and caspase-3 in the hippocampus of SCP mice.	HC-067047	30-38	BCL2-associated X protein	Mus musculus	111-114
34480999-13	2022	The results demonstrated that HC067047 treatment decreased the protein levels of proapoptotic proteins such as Bax and caspase-3 in the hippocampus of SCP mice.	Scopolamine	151-154	BCL2-associated X protein	Mus musculus	111-114
34906654-7	2022	Additionally, acrylamide treatment significantly inhibited luteal angiogenesis and induced the apoptosis of ovarian cells by up-regulation of P53 and Bax protein and down-regulation of Bcl-2 protein.	Acrylamide	14-24	BCL2-associated X protein	Mus musculus	150-153
34890760-5	2022	We found that NaB restored bodyweight and attenuated P-53, Bcl-2-associated X protein (BAX), and caspase cascades in the brains of HFD-fed mice.	nab	14-17	BCL2-associated X protein	Mus musculus	87-90
34864627-10	2022	Moreover, we observed that RA induced G1/S cell cycle arrest and apoptosis in the PDAC cells through regulating the expression of P21, P27, CDK2, Cyclin E, Bax, and Bcl-2, it inhibited the PDAC cell migration and invasion via E-cadherin and MMP-9.	rosmarinic acid	27-29	BCL2-associated X protein	Mus musculus	156-159
34859534-11	2022	Most importantly, G-Rg1 suppressed LPS-mediated induction of proapoptotic Bax, activated Akt, induced GSK-3beta phosphorylation, and balanced mitochondrial calcium levels.	ginsenoside Rg1	18-23	BCL2-associated X protein	Mus musculus	74-77
34785775-9	2022	These in vitro results were confirmed by in mouse xenograft model, combined treatment with ODN and oxaliplatin significantly reduced tumor size and induced Bax upregulation.	odn	91-94	BCL2-associated X protein	Mus musculus	156-159
34785775-9	2022	These in vitro results were confirmed by in mouse xenograft model, combined treatment with ODN and oxaliplatin significantly reduced tumor size and induced Bax upregulation.	Oxaliplatin	99-110	BCL2-associated X protein	Mus musculus	156-159
34920313-10	2022	Hyperoside also significantly inhibited the translation and expression of apoptotic genes (caspase3, casepase9, Bax, Bcl-2) and the production of apoptotic bodies induced by ZEA in the spleen.	hyperoside	0-10	BCL2-associated X protein	Mus musculus	112-115
34967303-11	2021	In vitro, compared with the HG group, MC apoptosis reduced dramatically with Thd treatment along with upregulation of Bcl-2 and downregulation of Bax.	Thalidomide	77-80	BCL2-associated X protein	Mus musculus	146-149
34265765-11	2022	RMZ showed an antiapoptotic effect via reduction of Bax and increased the expression of Bcl-2 in Western blot analysis.	rhamnazin	0-3	BCL2-associated X protein	Mus musculus	52-55
34873220-8	2021	Although TAC upregulated the Bcl-2 family proapoptotic (Bax and Bak) and anti-apoptotic (Bcl-2 and Bcl-xL) molecules in non-transgenic mice, TAC-induced upregulation of Bax and Bak was alleviated and that of Bcl-2 was enhanced in Lats2 +/- mice.	tac	9-12	BCL2-associated X protein	Mus musculus	56-59
34962339-10	2022	Gingerol increased Bcl-2, BDNF, and TrkB levels and reduced Bax and cleaved caspase 3 levels after hypoxia/reoxygenation.	gingerol	0-8	BCL2-associated X protein	Mus musculus	60-63
34933001-11	2022	omega3-PUFA supplementation had neuroprotective effects on the retinas of Opa1enu/+ and wild-type mice via blockade of microglia and astrocytes activation and suppression of Bax and caspase-3.	omega3-pufa supplementation	0-27	BCL2-associated X protein	Mus musculus	174-177
34893683-8	2021	Administration of Na-AuPT (40 mg   kg-1   d-1, ip) in nude mice bearing A549 or SMMC7721 xenografts significantly inhibited the tumor growth in vivo, accompanied by increased levels of total ubiquitinated proteins, cleaved caspase 3 and Bax protein in tumor tissue.	na-aupt	18-25	BCL2-associated X protein	Mus musculus	237-240
34948107-9	2021	H2 treatment also decreased AD-related biomarkers, such as Apo-E, Abeta-40, p-tau, and Bax and OS markers such as ROS, NO, Ca2+, and MDA in both serum and brain.	Deuterium	0-2	BCL2-associated X protein	Mus musculus	87-90
34873220-8	2021	Although TAC upregulated the Bcl-2 family proapoptotic (Bax and Bak) and anti-apoptotic (Bcl-2 and Bcl-xL) molecules in non-transgenic mice, TAC-induced upregulation of Bax and Bak was alleviated and that of Bcl-2 was enhanced in Lats2 +/- mice.	tac	141-144	BCL2-associated X protein	Mus musculus	56-59
34873220-8	2021	Although TAC upregulated the Bcl-2 family proapoptotic (Bax and Bak) and anti-apoptotic (Bcl-2 and Bcl-xL) molecules in non-transgenic mice, TAC-induced upregulation of Bax and Bak was alleviated and that of Bcl-2 was enhanced in Lats2 +/- mice.	tac	141-144	BCL2-associated X protein	Mus musculus	169-172
34863080-6	2021	Puerarin induced the mitochondrial-dependent apoptosis of PCCs by causing a Bcl-2/Bax imbalance.	pccs	58-62	BCL2-associated X protein	Mus musculus	82-85
34863080-6	2021	Puerarin induced the mitochondrial-dependent apoptosis of PCCs by causing a Bcl-2/Bax imbalance.	puerarin	0-8	BCL2-associated X protein	Mus musculus	82-85
34907739-9	2021	Furthermore, in Ehrlich solid tumor mice, rosmarinic acid, and/or Paclitaxel significantly suppressed tumor growth with an increase in apoptotic markers P53 and Caspase-3 levels, and suppressed the Bcl2/Bax ratio.	rosmarinic acid	42-57	BCL2-associated X protein	Mus musculus	203-206
34853445-5	2021	In vitro, we found that DAPA inhibited the expression of cleaved caspase 3, Bax, C/EBP homologous protein (CHOP), and glucose-regulated protein78 (GRP78) and upregulated the cardiomyoprotective protein Bcl-2 in angiotensin II (Ang II)-treated cardiomyocytes.	dapagliflozin	24-28	BCL2-associated X protein	Mus musculus	76-79
34348577-3	2021	The results indicated that, N2O exposure elevated TXNIP/NLRP3 expression in vivo and in vitro, led to declined learning and memory capabilities in mice, reduced apoptosis rate in hippocampal neuron and Nissl bodies, elevated inflammatory factors TNF-alpha, IL-1beta and IL-6 levels, as well as cleaved caspase-3 and Bax expressions, and reduced Bcl-2 expression.	Nitrous Oxide	28-31	BCL2-associated X protein	Mus musculus	316-319
34515620-12	2021	Lycorine exerted an anti-apoptotic effect as evidenced by upregulating Bcl-2 and downregulating Bax.	lycorine	0-8	BCL2-associated X protein	Mus musculus	96-99
34331232-8	2021	The expression of FAS, FASL, Bax, and Caspase-3 in decidual cells of the uterus in the PFOA treatment groups significantly increased in a dose-dependent manner.	perfluorooctanoic acid	87-91	BCL2-associated X protein	Mus musculus	29-32
34192626-4	2021	Cellular experiments show that Dox-loaded self-assembled messenger RNA nanospheres (mRNA-NSs@Dox) can reduce the viability of 4 T1 breast cancer cells by significantly upregulating Bax protein, thereby inducing the activation of Caspase 3 in 4 T1 cells.	Doxorubicin	31-34	BCL2-associated X protein	Mus musculus	181-184
34192626-4	2021	Cellular experiments show that Dox-loaded self-assembled messenger RNA nanospheres (mRNA-NSs@Dox) can reduce the viability of 4 T1 breast cancer cells by significantly upregulating Bax protein, thereby inducing the activation of Caspase 3 in 4 T1 cells.	Doxorubicin	93-96	BCL2-associated X protein	Mus musculus	181-184
34907739-9	2021	Furthermore, in Ehrlich solid tumor mice, rosmarinic acid, and/or Paclitaxel significantly suppressed tumor growth with an increase in apoptotic markers P53 and Caspase-3 levels, and suppressed the Bcl2/Bax ratio.	Paclitaxel	66-76	BCL2-associated X protein	Mus musculus	203-206
34400214-7	2021	Furthermore, increased levels of cleaved caspase 3, cleaved caspase 7, cleaved caspase 9, cleaved poly (ADP-ribose) polymerase (PARP) and Bax and reduced levels of Bcl2 in LPS-treated mice and HK-2 cells were reversed after Ala administration.	alamandine	224-227	BCL2-associated X protein	Mus musculus	138-141
34778972-13	2021	Viphyllin (100 mg/kg) was found to be neuroprotective by reducing the Scop-induced upregulation of p-JNK and p-p38 MAPK proteins, Bax/Bcl-2 ratio, and caspase activation in the brain.	viphyllin	0-9	BCL2-associated X protein	Mus musculus	130-133
34778972-13	2021	Viphyllin (100 mg/kg) was found to be neuroprotective by reducing the Scop-induced upregulation of p-JNK and p-p38 MAPK proteins, Bax/Bcl-2 ratio, and caspase activation in the brain.	Scopolamine	70-74	BCL2-associated X protein	Mus musculus	130-133
34643246-12	2021	Furthermore, the expression levels of Bax and cleaved caspase-3 in the NBP + edaravone group were decreased significantly compared with the MCAO group, while the expression levels of Bcl-2 and mitochondrial cytochrome c were increased.	Edaravone	77-86	BCL2-associated X protein	Mus musculus	38-41
34749210-8	2021	Further studies revealed that ADTM significantly inhibited the CCl4-induced upregulation of Bax/Bcl-2, increased the CCl4-induced decrease of AKT phosphorylation and inhibited the expression level of NF-kappaB p65 in CCl4-intoxicated mice.	adtm	30-34	BCL2-associated X protein	Mus musculus	92-95
34699866-6	2021	Mechanistically, the ponatinib/gossypol combination significantly increased apoptotic markers p53, Bax, and caspase-9 while decreasing anti-apoptotic marker Bcl-2.	ponatinib	21-30	BCL2-associated X protein	Mus musculus	99-102
34699866-6	2021	Mechanistically, the ponatinib/gossypol combination significantly increased apoptotic markers p53, Bax, and caspase-9 while decreasing anti-apoptotic marker Bcl-2.	Gossypol	31-39	BCL2-associated X protein	Mus musculus	99-102
34899328-14	2021	Geniposide increased the protein expression of B-cell lymphoma-2 (Bcl-2) and downregulated the protein expression of Bcl-2 Associated X (Bax), cleaved-Caspase 3, and cleaved-Caspase 9.	geniposide	0-10	BCL2-associated X protein	Mus musculus	117-135
34956620-8	2021	In HK-2 cells, fructose promoted the secretion of TNF-alpha, IL-1beta and IL-6 and increased the levels of RAGE, p-IkappaBalpha, p-NF-kappaB, bax, caspase-3 and caspase-9, but decreased the levels of Bcl-2.	Fructose	15-23	BCL2-associated X protein	Mus musculus	142-145
34956620-9	2021	Moreover, RAGE siRNA could attenuate increased levels of p-IkappaBalpha, p-NF-kappaB, bax, caspase-3 and caspase-9 while restore decreased levels of Bcl-2 in fructose-treated HK-2 cells.	Fructose	158-166	BCL2-associated X protein	Mus musculus	86-89
34899328-14	2021	Geniposide increased the protein expression of B-cell lymphoma-2 (Bcl-2) and downregulated the protein expression of Bcl-2 Associated X (Bax), cleaved-Caspase 3, and cleaved-Caspase 9.	geniposide	0-10	BCL2-associated X protein	Mus musculus	137-140
34669944-12	2021	Consistent with increasing expressions of Bax, cleaved-caspase-9/-3, and a decrease of Bcl-2 level, typical apoptotic ultrastructure, and apoptosis-positive cells were also observed in the selenium-deficient placenta of mice.	Selenium	189-197	BCL2-associated X protein	Mus musculus	42-45
34830376-8	2021	Moreover, the accumulation of mitochondria was significantly reduced in AZOX treated primary neurons, indicative of mitochondrial deactivation and induction of apoptosis, which was quantified by Bcl2/Bax ratio and caspase 3 cleavage assay.	azox	72-76	BCL2-associated X protein	Mus musculus	200-203
34829088-4	2021	Moreover, H2O2-induced mitochondrial dysfunctions associated with apoptotic events, including loss of mitochondrial membrane potential (MMP), decreased Bcl-2/Bcl-2 associated x-protein (Bax) ratio, and cytosolic release of cytochrome c, were reduced in the presence of FST.	Hydrogen Peroxide	10-14	BCL2-associated X protein	Mus musculus	158-184
34829088-4	2021	Moreover, H2O2-induced mitochondrial dysfunctions associated with apoptotic events, including loss of mitochondrial membrane potential (MMP), decreased Bcl-2/Bcl-2 associated x-protein (Bax) ratio, and cytosolic release of cytochrome c, were reduced in the presence of FST.	Hydrogen Peroxide	10-14	BCL2-associated X protein	Mus musculus	186-189
34758863-4	2021	In this study, mitochondrial swelling and membrane defect mitochondria in granulosa cells were observed from PCOS patients and DHT-induced PCOS-like mice, and the cytochrome C level in the cytoplasm and the expression of BAX (BCL2-associated X protein) in mitochondria were significantly increased in GCs, with p-Akt decreased, showing mitochondrial membrane was damaged in GCs of PCOS.	Dihydrotestosterone	127-130	BCL2-associated X protein	Mus musculus	221-224
34758863-4	2021	In this study, mitochondrial swelling and membrane defect mitochondria in granulosa cells were observed from PCOS patients and DHT-induced PCOS-like mice, and the cytochrome C level in the cytoplasm and the expression of BAX (BCL2-associated X protein) in mitochondria were significantly increased in GCs, with p-Akt decreased, showing mitochondrial membrane was damaged in GCs of PCOS.	Dihydrotestosterone	127-130	BCL2-associated X protein	Mus musculus	226-251
34758863-6	2021	Furthermore, we found melatonin decreased the levels of cytochrome C and BAX in DHT-induced PCOS mice.	Melatonin	22-31	BCL2-associated X protein	Mus musculus	73-76
34758863-6	2021	Furthermore, we found melatonin decreased the levels of cytochrome C and BAX in DHT-induced PCOS mice.	Dihydrotestosterone	80-83	BCL2-associated X protein	Mus musculus	73-76
34725331-3	2021	Here we report the surprising finding that BAX/BAK DKO cells proliferate less than control cells expressing both BAX and BAK (or either BAX or BAK) when they are driven into tetraploidy by transient exposure to the microtubule inhibitor nocodazole.	Nocodazole	237-247	BCL2-associated X protein	Mus musculus	43-46
34725331-3	2021	Here we report the surprising finding that BAX/BAK DKO cells proliferate less than control cells expressing both BAX and BAK (or either BAX or BAK) when they are driven into tetraploidy by transient exposure to the microtubule inhibitor nocodazole.	Nocodazole	237-247	BCL2-associated X protein	Mus musculus	113-116
34725331-3	2021	Here we report the surprising finding that BAX/BAK DKO cells proliferate less than control cells expressing both BAX and BAK (or either BAX or BAK) when they are driven into tetraploidy by transient exposure to the microtubule inhibitor nocodazole.	Nocodazole	237-247	BCL2-associated X protein	Mus musculus	136-139
34146870-7	2021	The results on the mechanisms of liver toxicity indicated that butachlor induced overexpression of Apaf-1, Bax, Caspase-3, Caspase-9, Cyt-c, p53, Beclin-1, ATG-5, and LC3, whereas decreases the expression of Bcl-2 and p62 suggesting abnormal processes of apoptosis and autophagy.	butachlor	63-72	BCL2-associated X protein	Mus musculus	107-110
34628205-4	2021	Interestingly, topical application of OS-LL11 protected mouse skin against UVB irradiation damage by up-regulating the levels of superoxide dismutase, glutathione, and nitric oxide, but down-regulating the levels of H2O2, IL-1alpha, IL-1beta, IL-6, TNF-alpha, 8-OHdG, Bcl-2, and Bax, as well as the number of apoptotic bodies.	os-ll11	38-45	BCL2-associated X protein	Mus musculus	279-282
34649330-10	2021	These data show that P. sativum has a cardio-protective impact against DOX-induced cardiomyocyte damage in mice via boosting endogenous antioxidants, decreasing inflammation, and regulating BcL-2 and Bax apoptosis pathway, which might be related to the presence of flavonoid glycosides.	flavonoid glycosides	265-285	BCL2-associated X protein	Mus musculus	200-203
34844388-8	2021	Maternal swimming exercise inhibited Bax and cleaved caspase-3 expression and increased Bcl-2 expression in the valproic acid injected pups.	Valproic Acid	112-125	BCL2-associated X protein	Mus musculus	37-40
34560092-8	2021	We confirmed that 1,2-DCE induced increased apoptosis via mitochondrial pathway, both in vitro and in vivo, as evidenced by increased Caspase-3, cleaved Caspase-3, Cytochrome c and Bax expression, and decreased Bcl-2 expression.	ethylene dichloride	18-25	BCL2-associated X protein	Mus musculus	181-184
34448508-5	2021	Moreover, ARP treatment markedly inhibited UVA-induced apoptosis, cell cycle arrest and DNA fragmentation, while also significantly reversing UVA effects (elevated Bax levels, reduced Bcl-2 expression) by reducing Bax levels and increasing Bcl-2 expression.	arp	10-13	BCL2-associated X protein	Mus musculus	164-167
34448508-5	2021	Moreover, ARP treatment markedly inhibited UVA-induced apoptosis, cell cycle arrest and DNA fragmentation, while also significantly reversing UVA effects (elevated Bax levels, reduced Bcl-2 expression) by reducing Bax levels and increasing Bcl-2 expression.	arp	10-13	BCL2-associated X protein	Mus musculus	214-217
34746315-10	2021	Western blotting showed that hydrogen treatment reduced Bax and TNFalpha levels.	Hydrogen	29-37	BCL2-associated X protein	Mus musculus	56-59
34769159-6	2021	Further studies showed that AEMR inhibited cytochrome c release from mitochondria into the cytoplasm, and Bcl-2 suppression and Bax activation induced by H2O2.	aemr	28-32	BCL2-associated X protein	Mus musculus	128-131
34769159-6	2021	Further studies showed that AEMR inhibited cytochrome c release from mitochondria into the cytoplasm, and Bcl-2 suppression and Bax activation induced by H2O2.	Hydrogen Peroxide	154-158	BCL2-associated X protein	Mus musculus	128-131
34746315-13	2021	Hydrogen treatment also decreased Bax and TNFalpha levels and induced an anti-inflammatory response via regulation of IL-2 and IL-10.	Hydrogen	0-8	BCL2-associated X protein	Mus musculus	34-37
34829553-14	2021	Moreover, 17beta-estradiol administration rescued p53-associated apoptotic cell death in the SWI model by regulating the expression of Bcl-2 family proteins (Bax and Bcl-2) and caspase-3 activation.	Estradiol	10-26	BCL2-associated X protein	Mus musculus	158-161
34829755-5	2021	Treatment with EQ had evident anti-tumor effects on EAC as revealed by the remarkable decrease in the expression of the anti-apoptotic gene Bcl-2 and by a significant increase in the expression of apoptotic genes (BAX and caspase-3).	Ethoxyquin	15-17	BCL2-associated X protein	Mus musculus	214-217
34829755-5	2021	Treatment with EQ had evident anti-tumor effects on EAC as revealed by the remarkable decrease in the expression of the anti-apoptotic gene Bcl-2 and by a significant increase in the expression of apoptotic genes (BAX and caspase-3).	ethyl acetoacetate	52-55	BCL2-associated X protein	Mus musculus	214-217
34676557-6	2022	Copper-induced oxidative damage further decreased the phosphorylation of CREB, decreased expression of Bcl-2, enhanced expression of Bax, and accelerated the dissociation of keap1-Nrf2 complex, promoted the nuclear translocation of Nrf2, stimulate the expression of antioxidant molecules HO-1 and NQO1.	Copper	0-6	BCL2-associated X protein	Mus musculus	133-136
34676557-5	2022	Mechanistically, we found copper, on the one hand, prevented phosphorylation of cAMP response element binding protein (CREB) to decrease expression its downstream target protein Brain-derived neurotrophic factor (BDNF), and to decrease mitochondrial membrane potential and Bcl-2/Bax ratio; on the other hand, copper-induced reactive oxygen species (ROS), promoted lipid peroxidation, reduced antioxidant enzyme activity of GSH-Px.	Copper	26-32	BCL2-associated X protein	Mus musculus	279-282
34633804-10	2021	Moreover, GB treatment remarkably reduced the levels of RAGE and Bax and increased the level of Bcl-2 in AD model mice.	ginkgolide B	10-12	BCL2-associated X protein	Mus musculus	65-68
34746206-10	2021	Additionally, in the infected group, the mRNA expression of Bax and p53 was increasing and the Bcl-2 expression was decreasing, which was reversed by BA40 and PB6 treatment (P < 0.05).	ba40	150-154	BCL2-associated X protein	Mus musculus	60-63
34746206-10	2021	Additionally, in the infected group, the mRNA expression of Bax and p53 was increasing and the Bcl-2 expression was decreasing, which was reversed by BA40 and PB6 treatment (P < 0.05).	3-[(1e)-But-1-En-1-Yl]-1-(2,2-Diphosphonoethyl)pyridinium	159-162	BCL2-associated X protein	Mus musculus	60-63
34721041-11	2021	Results: Compared with the ATO group, the HES treatment groups reduced the levels of CK, LDH, cTnI, ROS, MDA, TNF-alpha, IL-6, Bax, Caspase-3, cleaved-Caspase-3 and Keap1 and enhanced the levels of SOD, GSH, CAT, Bcl-2, p62 and Nrf2.	Hesperidin	42-45	BCL2-associated X protein	Mus musculus	127-130
34174222-9	2021	RESULTS: The results showed that acteoside inhibited melanoma growth, alleviated inflammation levels in mice, attenuated ROS and apoptosis levels in the spleen, downregulated the levels of CD31, survivin, Ras, Raf1, p-STAT3, and Bcl-2, and upregulated the levels of ERbeta, Bax, cleaved caspase-3, and cleaved caspase-9.	acteoside	33-42	BCL2-associated X protein	Mus musculus	274-277
34721041-11	2021	Results: Compared with the ATO group, the HES treatment groups reduced the levels of CK, LDH, cTnI, ROS, MDA, TNF-alpha, IL-6, Bax, Caspase-3, cleaved-Caspase-3 and Keap1 and enhanced the levels of SOD, GSH, CAT, Bcl-2, p62 and Nrf2.	Arsenic Trioxide	27-30	BCL2-associated X protein	Mus musculus	127-130
34086879-9	2021	IAA exposure increased expression of the pro-apoptotic factors Bax and Aimf1, the anti-apoptotic factor Bcl2l10, the cell cycle regulators Ccna2, Ccnb1, Ccne1, and Cdk4, and estrogen receptor Esr1 compared to control.	Iodoacetic Acid	0-3	BCL2-associated X protein	Mus musculus	63-66
34675808-6	2021	In addition, kaempferol attenuated DEX-induced reduction of cyclin D1 and Bcl-2 expression and elevation of p53 and Bax expression.	kaempferol	13-23	BCL2-associated X protein	Mus musculus	116-119
34675808-6	2021	In addition, kaempferol attenuated DEX-induced reduction of cyclin D1 and Bcl-2 expression and elevation of p53 and Bax expression.	Dexamethasone	35-38	BCL2-associated X protein	Mus musculus	116-119
34271041-7	2021	PA024 decreased PHR death in rd1 mixed cultures; it reduced the amount of non-viable neurons, delayed the onset of PHR apoptosis, and decreased Bax mRNA levels.	pa024	0-5	BCL2-associated X protein	Mus musculus	144-147
34606561-15	2021	The disturbance of Pax3, P53 and Bax induced by diabetes was abolished in DMLn-3, DMHn-3 and DMn-6 groups.	Decahydro-2,6-naphthalenedicarboxylic Acid Dimethyl Ester	82-86	BCL2-associated X protein	Mus musculus	33-36
34464637-7	2021	The protective effect of MAME against iron-overload-induced apoptosis was confirmed by upregulation of protein levels of Bax, Caspase-3, and PARP.	mame	25-29	BCL2-associated X protein	Mus musculus	121-124
34634674-10	2021	Western blotting showed apparent changes in the expression levels of Bax and Bcl-2 proteins following iAs exposure, however the change was statistically insignificant.	4-Iodoacetamidosalicylic acid	102-105	BCL2-associated X protein	Mus musculus	69-72
34416629-14	2021	ABZ showed a considerable level of apoptotic activity as indicated by increased mRNA expression level of p53 and the increased Bax/BCL-2 ratio and active caspase-3.	Albendazole	0-3	BCL2-associated X protein	Mus musculus	127-130
34464637-7	2021	The protective effect of MAME against iron-overload-induced apoptosis was confirmed by upregulation of protein levels of Bax, Caspase-3, and PARP.	Iron	38-42	BCL2-associated X protein	Mus musculus	121-124
34333357-9	2021	Moreover, BA attenuated ATO-induced apoptosis by promoting the expression of Bcl-2 and suppressing the expression of Bax and caspase-3.	baicalin	10-12	BCL2-associated X protein	Mus musculus	117-120
34454721-12	2021	In brain tissue, resveratrol significantly attenuated thoracic blast exposure-induced generation of ROS and expressions of IRE-alpha and CHOP, lowered the expressions of Bax and p53, and maintained Bcl-2 expression (P < 0.05).	Resveratrol	17-28	BCL2-associated X protein	Mus musculus	170-173
34558146-7	2021	Furthermore, we analyzed that the molecular mechanical action of lycorine considerably repressed JAK1/STAT3 transactional activation and decrease its downstream molecules Bcl-2, and enhances the expressional activity of Bax, cytochrome c, caspase 3 and 9 in HT-3 cells.	lycorine	65-73	BCL2-associated X protein	Mus musculus	220-223
34333357-9	2021	Moreover, BA attenuated ATO-induced apoptosis by promoting the expression of Bcl-2 and suppressing the expression of Bax and caspase-3.	Arsenic Trioxide	24-27	BCL2-associated X protein	Mus musculus	117-120
34564943-4	2022	In addition, the apoptosis proteins (Bax and Bcl2) were altered in response to GFL treatment, and apoptosis cells were increased, indicating an anti-HCC effect.	gfl	79-82	BCL2-associated X protein	Mus musculus	37-40
34371252-14	2021	Furthermore, the changes of autophagy and apoptosis markers, such as LC3II, Beclin1, p62, Bcl-2, Bax and Cleaved-caspase-3 induced by ISO were resumed by PASE treatment.	Isoproterenol	134-137	BCL2-associated X protein	Mus musculus	97-100
34371252-14	2021	Furthermore, the changes of autophagy and apoptosis markers, such as LC3II, Beclin1, p62, Bcl-2, Bax and Cleaved-caspase-3 induced by ISO were resumed by PASE treatment.	pase	154-158	BCL2-associated X protein	Mus musculus	97-100
34627415-8	2021	The apoptosis of leukemia cells L1210 and K562 could be induced by ZL-n-91 (P<0.001), and the expression level of apoptosis related protein BAX significantly increased.	FFPM	67-74	BCL2-associated X protein	Mus musculus	140-143
34565275-6	2021	CsA increased caspase-3 activity, Bax, TOS, MDA, TAS, and MPO levels, and the administration of DAPA with CsA significantly reduced this increase in levels (p < 0.001, p < 0.001, p < 0.001, p < 0.001, p < 0.001, and p < 0.001, respectively).	Cyclosporine	0-3	BCL2-associated X protein	Mus musculus	34-37
34638536-10	2021	Western blot was performed to determine the levels of p-ERK1/2, Bcl-XL, Bax, and Hsp70 proteins upon DEX or DEX plus colostrum exposure.	Dexamethasone	101-104	BCL2-associated X protein	Mus musculus	72-75
34630081-9	2021	Also, GA protected against ANIT-induced mitochondrial apoptosis by regulating the expression of Bcl-2, Bax, cleaved caspase 3 and cleaved caspase 9.	Glycyrrhetinic Acid	6-8	BCL2-associated X protein	Mus musculus	103-106
34638536-10	2021	Western blot was performed to determine the levels of p-ERK1/2, Bcl-XL, Bax, and Hsp70 proteins upon DEX or DEX plus colostrum exposure.	Dexamethasone	108-111	BCL2-associated X protein	Mus musculus	72-75
34638536-12	2021	Cells, upon colostrum co-treated with DEX, exhibited higher levels of p-ERK1/2 and lower levels of Bcl-XL, Bax, and Hsp70.	Dexamethasone	38-41	BCL2-associated X protein	Mus musculus	107-110
34536204-0	2021	Selenomethionine Alleviates Intestinal Ischemia-Reperfusion Injury in Mice Through the Bax-Caspase Pathway.	Selenomethionine	0-16	BCL2-associated X protein	Mus musculus	87-90
34760256-9	2021	In addition, we observed NMCP-2 inhibited the activation of the mitochondrial apoptosis pathway and regulated the disordered expression of Bcl-2 and Bax in the myocardial tissues of DOX-treated mice.	Doxorubicin	182-185	BCL2-associated X protein	Mus musculus	149-152
34118224-4	2021	Besides, Scutellarin attenuated mouse serum concentrations of TNF-alpha and IL-6, heightened Bax expression and diminished B-cell lymphoma-2 (Bcl-2) level in CAC tissues of mice, through down-regulating Wnt/beta-catenin signaling cascade.	scutellarin	9-20	BCL2-associated X protein	Mus musculus	93-96
34595163-9	2021	Dictamnine caused increased oxidative stress and early hepatic apoptosis via up-regulation of glutathione S transferase a1 (GSTA1) and Bax/Bcl-2 ratio and down-regulation of the antioxidative enzymes superoxide dismutase (SOD), catalase, and glutathione peroxidase 1 (GPx-1).	dictamnine	0-10	BCL2-associated X protein	Mus musculus	135-138
34502488-8	2021	Further, we investigated the expression of pro- and anti-apoptotic cell death markers such as Bax, Bcl-2, Caspase-3, and Cox-2, which was significantly reduced in Abeta1-42 + Lut-treated mice brains compared to the brains of the Abeta-injected group.	Lutein	175-178	BCL2-associated X protein	Mus musculus	94-97
34165216-6	2021	DEHP could significantly decrease the cell viability percentage, reduce testosterone level, increase apoptosis, elevate Bax/ Bcl-2 ratio and enhance caspase-3 and -9 activity in the TM3 cells.	Diethylhexyl Phthalate	0-4	BCL2-associated X protein	Mus musculus	120-123
34373701-10	2021	The combination of bufalin and hydroxycampothecin also increased the expression of apoptosis-related proteins Bax, p53, PDCD4 and GSK-3beta, and decreased the expression of Bcl-XL and p-AKT compared with a single drug treatment.	bufalin	19-26	BCL2-associated X protein	Mus musculus	110-113
34571925-7	2021	Further, we also checked the pro- and anti-apoptotic proteins markers such as Bax, Bcl-2, and caspase-3, which were regulated in the cortex of ALA co-treated mouse brain.	alpha-Linolenic Acid	143-146	BCL2-associated X protein	Mus musculus	78-81
34371027-7	2021	Overall DHAc reversed behavioral anomalies in the scopolamine treated mice via oxidative stress quenching, enhancing antioxidative enzyme activity, enhancing BDNF and synaptophysin mRNA levels and reducing expression of apoptotic protein Bax.	5,6-dihydro-5-azacytidine	8-12	BCL2-associated X protein	Mus musculus	238-241
34159456-10	2021	In addition, Dex remarkably reduced the surgery-induced increased ratio of Bax/Bcl-2 and apoptotic neurons in the hippocampi of aged mice.	Dexmedetomidine	13-16	BCL2-associated X protein	Mus musculus	75-78
34371027-7	2021	Overall DHAc reversed behavioral anomalies in the scopolamine treated mice via oxidative stress quenching, enhancing antioxidative enzyme activity, enhancing BDNF and synaptophysin mRNA levels and reducing expression of apoptotic protein Bax.	Scopolamine	50-61	BCL2-associated X protein	Mus musculus	238-241
34438266-5	2021	Moreover, APSP downregulated Pb-induced Bax mRNA and protein expressions, suppressed activation of caspase-3, upregulated Bcl-2 protein expression, and prevented Pb-induced DNA damage.	Lead	29-31	BCL2-associated X protein	Mus musculus	40-43
34500626-6	2021	Administration of apigenin decreased the B-cell lymphoma 2-associated X/B-cell lymphoma 2 (Bax/Bcl-2) ratio and suppressed caspase-3 and poly ADP ribose polymerase cleavage.	Apigenin	18-26	BCL2-associated X protein	Mus musculus	91-94
34396458-7	2021	LYC also alleviated TiO2 NPs-induced germ cell apoptosis by inhibiting mitochondrial apoptotic pathway, as shown by the upregulation of Bcl-2, the downregulation of Bax, Cleaved Caspase 3, and Cleaved Caspase 9.	titanium dioxide	20-24	BCL2-associated X protein	Mus musculus	165-168
34376637-6	2021	We developed a mCherry-BCLXL fusion protein, which prevented BAX recruitment and activation to the mitochondria in tissue culture cells exposed to staurosporine.	Staurosporine	147-160	BCL2-associated X protein	Mus musculus	61-64
34439516-9	2021	Moreover, LUTN treatment considerably attenuates the AFB1-induced apoptosis in mouse liver, as demonstrated by declined apoptotic cells percentage, decreased Bax, Cyt-c, caspase-3 and caspase-9 transcription and protein with increased Bcl-2 expression.	Luteolin	10-14	BCL2-associated X protein	Mus musculus	158-161
34366426-8	2021	CONCLUSIONS The findings from this study showed that, compared with male mice, at 24 h after CCl4 toxicity, female mice showed more severe changes of hepatocyte necrosis and PAS-positivity, with significantly reduced expression of HSP27, HSP70, PCNA, and Bcl-2, and significantly increased expression of Bax, caspase-3, and CYP2E1.	Carbon Tetrachloride	93-97	BCL2-associated X protein	Mus musculus	304-307
34379013-9	2022	Furthermore, I3C combined with HCQ induced apoptosis by highly upregulating cleaved caspase-3 and Bax while downregulating Bcl-2 proteins expression in EAC cells in comparison with each drug alone.	Hydroxychloroquine	31-34	BCL2-associated X protein	Mus musculus	98-101
34223821-9	2021	Furthermore, dexamethasone stimulated pro-apoptotic signaling including superoxide production, caspase-8, -9, and -3 activities, NF- B, and Bax, but repressed the anti-apoptotic protein, Bcl-2.	Dexamethasone	13-26	BCL2-associated X protein	Mus musculus	140-143
34303733-4	2021	GC-2 cells were treated with PFOS (0, 50, 100 and 150microM) for 24 h or 48 h. Results demonstrated that PFOS dose-dependently inhibited cell viability, induced G0/G1 cell cycle arrest and triggered apoptosis, which might be partly explained by the decrease in cyclin D1, PCNA and Bcl-2 protein expression; increase in Bax protein expression; and activation of caspase-9, -3.	perfluorooctane sulfonic acid	29-33	BCL2-associated X protein	Mus musculus	319-322
34303733-4	2021	GC-2 cells were treated with PFOS (0, 50, 100 and 150microM) for 24 h or 48 h. Results demonstrated that PFOS dose-dependently inhibited cell viability, induced G0/G1 cell cycle arrest and triggered apoptosis, which might be partly explained by the decrease in cyclin D1, PCNA and Bcl-2 protein expression; increase in Bax protein expression; and activation of caspase-9, -3.	perfluorooctane sulfonic acid	105-109	BCL2-associated X protein	Mus musculus	319-322
34281337-5	2021	GLA reduced apoptosis, as indicated by decreases in the BAX/BCL2 expression level and apoptosis percentage.	gamma-Linolenic Acid	0-3	BCL2-associated X protein	Mus musculus	56-59
34356380-7	2021	Concurrently, light-induced oxidative stress markers, Nuclear factor erythroid 2-related factor 2 (Nrf2) and Heme Oxygenase 1 (HO-1), and mitochondrial apoptotic markers, B-cell lymphoma 2 apoptosis regulator (Bcl-2)-associated death promoter (Bad), and Bcl-2-associated X protein (Bax), were suppressed by 4-PBA administration.	4-phenylbutyric acid	307-312	BCL2-associated X protein	Mus musculus	254-280
34393792-10	2021	8-Gin also could lead to down-regulation of the activities of matrix metalloproteinases-9 (MMP-9), Caspase-9, and Bax protein, up-regulation of the activity of Bcl-2 protein, and alleviation of cardiomyocyte apoptosis.	8-gingerol	0-5	BCL2-associated X protein	Mus musculus	114-117
34356380-7	2021	Concurrently, light-induced oxidative stress markers, Nuclear factor erythroid 2-related factor 2 (Nrf2) and Heme Oxygenase 1 (HO-1), and mitochondrial apoptotic markers, B-cell lymphoma 2 apoptosis regulator (Bcl-2)-associated death promoter (Bad), and Bcl-2-associated X protein (Bax), were suppressed by 4-PBA administration.	4-phenylbutyric acid	307-312	BCL2-associated X protein	Mus musculus	282-285
34355084-5	2021	BSG treatment markedly activated P53/Bax/Bcl2/c-caspase 3 signalling for cell apoptosis and attenuated the expression of antiapoptotic survivin protein.	BSG	0-3	BCL2-associated X protein	Mus musculus	37-40
34299130-4	2021	CTPS significantly attenuated the apoptotic and necrotic population, as well as cell penetration in cisplatin-treated RAW264.7 cells, which ultimately inhibited the upregulation of Bcl-2-associated X protein (Bax), cytosolic cytochrome c, poly (adenosine diphosphateribose) polymerase (PARP) cleavage, and caspases-3, -8, and -9, and the downregulation of B cell lymphoma-2 (Bcl-2).	ctps	0-4	BCL2-associated X protein	Mus musculus	181-207
34299130-4	2021	CTPS significantly attenuated the apoptotic and necrotic population, as well as cell penetration in cisplatin-treated RAW264.7 cells, which ultimately inhibited the upregulation of Bcl-2-associated X protein (Bax), cytosolic cytochrome c, poly (adenosine diphosphateribose) polymerase (PARP) cleavage, and caspases-3, -8, and -9, and the downregulation of B cell lymphoma-2 (Bcl-2).	ctps	0-4	BCL2-associated X protein	Mus musculus	209-212
34299130-4	2021	CTPS significantly attenuated the apoptotic and necrotic population, as well as cell penetration in cisplatin-treated RAW264.7 cells, which ultimately inhibited the upregulation of Bcl-2-associated X protein (Bax), cytosolic cytochrome c, poly (adenosine diphosphateribose) polymerase (PARP) cleavage, and caspases-3, -8, and -9, and the downregulation of B cell lymphoma-2 (Bcl-2).	Cisplatin	100-109	BCL2-associated X protein	Mus musculus	181-207
34299130-4	2021	CTPS significantly attenuated the apoptotic and necrotic population, as well as cell penetration in cisplatin-treated RAW264.7 cells, which ultimately inhibited the upregulation of Bcl-2-associated X protein (Bax), cytosolic cytochrome c, poly (adenosine diphosphateribose) polymerase (PARP) cleavage, and caspases-3, -8, and -9, and the downregulation of B cell lymphoma-2 (Bcl-2).	Cisplatin	100-109	BCL2-associated X protein	Mus musculus	209-212
34080648-15	2021	Surgery-induced increases in neuronal loss and the Bax/Bcl-2 ratio in the hippocampus were significantly inhibited by pretreatment with GB.	ginkgolide B	136-138	BCL2-associated X protein	Mus musculus	51-54
34238204-11	2021	Further, miR-125b upregulation significantly decreased the protein levels of apoptosis-related makers c-caspase 3 and Bax, while increased Bcl-2 expression.	mir-125b	9-17	BCL2-associated X protein	Mus musculus	118-121
34356307-5	2021	Our results revealed the anxiolytic, antidepressant, and antinociceptive properties of DADS and GYY4137 during neuropathic pain by inhibiting microglial activation and the up-regulation of phosphoinositide 3-kinase/phosphorylated protein kinase B and BAX in the amygdala (AMG) and/or periaqueductal gray matter (PAG).	diallyl disulfide	87-91	BCL2-associated X protein	Mus musculus	251-254
34356307-5	2021	Our results revealed the anxiolytic, antidepressant, and antinociceptive properties of DADS and GYY4137 during neuropathic pain by inhibiting microglial activation and the up-regulation of phosphoinositide 3-kinase/phosphorylated protein kinase B and BAX in the amygdala (AMG) and/or periaqueductal gray matter (PAG).	GYY 4137	96-103	BCL2-associated X protein	Mus musculus	251-254
34105803-6	2021	In D-DT Tg irradiated mouse keratinocytes, the p53, PUMA, and Bax expression was lower than that in WT mice.	d-dt tg	3-10	BCL2-associated X protein	Mus musculus	62-65
34257696-12	2021	The numbers of TUNEL+ cells and the expression of Bax and caspase-3 proteins were significantly increased in the 5-FU + ETSJC groups when compared with the 5-FU group.	Fluorouracil	113-117	BCL2-associated X protein	Mus musculus	50-53
34257682-18	2021	The protein expression of NLRP3, ASC, Cle-caspase-1, IL-1beta, TXNIP, Cle-caspase-3, and Bax was downregulated in the LHF and perindopril treatment group, and Bcl-2 expression was upregulated.	Perindopril	126-137	BCL2-associated X protein	Mus musculus	89-92
34257696-12	2021	The numbers of TUNEL+ cells and the expression of Bax and caspase-3 proteins were significantly increased in the 5-FU + ETSJC groups when compared with the 5-FU group.	Fluorouracil	156-160	BCL2-associated X protein	Mus musculus	50-53
34203049-7	2021	Furthermore, IHC and western blot results suggested antioxidant (Keap-1/Nrf-2/HO-1), anti-inflammatory (TLR-4/NF-kB) and anti-apoptotic (Bcl-2/Bax/Caspase-3) effect of Bergenin.	bergenin	168-176	BCL2-associated X protein	Mus musculus	143-146
34205542-5	2021	In addition, IPEE regulated the expression levels of tau signaling, such as TNF-alpha, p-JNK, p-Akt, p-GSK3beta, p-tau, p-NF-kappaB, BAX and caspase 3.	ipee	13-17	BCL2-associated X protein	Mus musculus	133-136
34484665-7	2021	The protein expressions of cytosolic Bcl-2-associated x (Bax), Cyt-c, cleaved caspase-3, calmodulin (CaM), Ca2+/CaM-dependent protein kinases II (CaMKII) and phosphorylated CaMKII were increased significantly in cypermethrin-exposed TM4 cells.	cypermethrin	212-224	BCL2-associated X protein	Mus musculus	37-55
34484665-7	2021	The protein expressions of cytosolic Bcl-2-associated x (Bax), Cyt-c, cleaved caspase-3, calmodulin (CaM), Ca2+/CaM-dependent protein kinases II (CaMKII) and phosphorylated CaMKII were increased significantly in cypermethrin-exposed TM4 cells.	cypermethrin	212-224	BCL2-associated X protein	Mus musculus	57-60
34484662-9	2021	Simultaneously, the levels of proliferation marker (PCNA and Ki67) and apoptosis regulator (Bax and Caspase-3) showed clear increases in benzene-exposed group.	Benzene	137-144	BCL2-associated X protein	Mus musculus	92-95
34220528-6	2021	TMZ also reduced the levels of Bax and cleaved caspase-3 and promoted Bcl-2 expression.	Trimetazidine	0-3	BCL2-associated X protein	Mus musculus	31-34
34211563-8	2021	The levels of Bax/Bcl-2 protein ratio and caspase-3 increased in the DCD model while the HPTQ inhibited it.	hptq	89-93	BCL2-associated X protein	Mus musculus	14-17
34203930-5	2021	In addition, incubation with CVE significantly mitigated the increase in Bax and decrease in Bcl-2 induced by H2O2 treatment in HT22 cells.	Hydrogen Peroxide	110-114	BCL2-associated X protein	Mus musculus	73-76
34221003-10	2021	In the LPS-induced HT22 cells, hyperoside promotes cell survival; alleviates the level of IL-1beta, IL-6, IL-8, TNF-alpha, ROS, MDA, Bax, and caspase-3; and increases the expression of CAT, SOD, GSH, Bcl-2, BDNF, TrkB, and NGF.	hyperoside	31-41	BCL2-associated X protein	Mus musculus	133-136
34484660-14	2021	Licorice prevented the increase in immunoreactivity of testis for Bcl-2-associated X protein and cyclogenase-2 that were overexpressed in MTX-injected mice.	Methotrexate	138-141	BCL2-associated X protein	Mus musculus	66-92
34122726-7	2021	The antiapoptotic effect of melatonin on CI-AKI was revealed by decreasing the ratio of Bax/Bcl2 and the cleaved caspase3 level and by reducing the number of apoptosis-positive tubular cells.	Melatonin	28-37	BCL2-associated X protein	Mus musculus	88-91
34350246-14	2021	Western blot results indicated that iPSd-NSC transplantation significantly increased the expression level of B cell lymphoma/leukemia-2 (Bcl-2) (P<0.01) but decreased the expression levels of Bcl-2 associated X protein, cytochrome C, and cleaved caspase-3 (P<0.001).	ipsd	36-40	BCL2-associated X protein	Mus musculus	192-218
34068575-6	2021	Early apoptosis and Bax/Bcl-xL were lower with alpha-TCP 400 muM (2.4 +- 0.4% and 0.5-fold) and ZDF 200 muM (1.8 +- 0.4% and 0.3-fold) supplementation in comparison with the control (5.3 +- 1.4% and 1.0-fold) with normal characterization and functional activity.	alpha-Tocopherol	47-56	BCL2-associated X protein	Mus musculus	20-23
34069111-10	2021	Furthermore, nitazoxanide upregulated proapoptotic proteins (P53 and BAX) and caspases but downregulated BCL-2.	nitazoxanide	13-25	BCL2-associated X protein	Mus musculus	69-72
34068575-6	2021	Early apoptosis and Bax/Bcl-xL were lower with alpha-TCP 400 muM (2.4 +- 0.4% and 0.5-fold) and ZDF 200 muM (1.8 +- 0.4% and 0.3-fold) supplementation in comparison with the control (5.3 +- 1.4% and 1.0-fold) with normal characterization and functional activity.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	96-99	BCL2-associated X protein	Mus musculus	20-23
34542904-6	2021	IL-39 and H2O2 both significantly promoted the production of intracellular ROS, increased the level of intracellular CCL2, stimulated the apoptotic progress of cardiomyocytes, increased the mRNA and protein expression levels of Bax, caspase-3, and p-p38 MAPK, and decreased the mRNA and protein expression levels of Bcl-2.	Hydrogen Peroxide	10-14	BCL2-associated X protein	Mus musculus	228-231
34249264-8	2021	Results: When INS1 cells and diabetic mice were treated with quercetin, the levels of SOD2, CAT, and Sirt3 proteins were increased, the levels of cleaved Caspase-3 and the ratio of Bax to BCL-2 were decreased at different degrees, along with reduced blood glucose levels and elevated insulin levels in diabetic mice.	Quercetin	61-70	BCL2-associated X protein	Mus musculus	181-184
34719649-7	2021	Furthermore, our results showed that taurine decreased the expressions of cleaved caspase-3 and Bax/Bcl2, thereby inhibiting apoptosis.	Taurine	37-44	BCL2-associated X protein	Mus musculus	96-99
34542904-7	2021	ROS production, CCL2 level, cardiomyocyte apoptosis, and expression of Bax, caspase-3, and p-p38 MAPK were significantly amplified by the administration of IL-39 combined with H2O2, and these processes were significantly alleviated by an antioxidant Trolox.	Hydrogen Peroxide	176-180	BCL2-associated X protein	Mus musculus	71-74
34542904-7	2021	ROS production, CCL2 level, cardiomyocyte apoptosis, and expression of Bax, caspase-3, and p-p38 MAPK were significantly amplified by the administration of IL-39 combined with H2O2, and these processes were significantly alleviated by an antioxidant Trolox.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	250-256	BCL2-associated X protein	Mus musculus	71-74
34149855-10	2021	The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group.	Docetaxel	144-153	BCL2-associated X protein	Mus musculus	4-7
34149855-10	2021	The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group.	Docetaxel	48-57	BCL2-associated X protein	Mus musculus	4-7
34149855-10	2021	The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group.	Docetaxel	162-171	BCL2-associated X protein	Mus musculus	4-7
34149855-10	2021	The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group.	Docetaxel	66-75	BCL2-associated X protein	Mus musculus	4-7
35413363-6	2022	Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc).	Arsenic	29-31	BCL2-associated X protein	Mus musculus	184-187
34149855-10	2021	The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group.	Docetaxel	84-93	BCL2-associated X protein	Mus musculus	4-7
35405220-7	2022	Males also showed a broad range of anxiogenic responses to PS nanoparticles while hippocampal samples from treated females showed an increased expression of Bax and Nlrp3 genes, indicating a pro-apoptotic/proinflammatory effect of PS treatment.	Polystyrenes	59-61	BCL2-associated X protein	Mus musculus	157-160
35551953-10	2022	The CDAA-fed mice showed a significant inhibition of Akt phosphorylation, XIAP and Bcl2, whereas PTEN and bax expression were upregulated.	CDAA	4-8	BCL2-associated X protein	Mus musculus	106-109
35588859-6	2022	Moreover, microinjection of Abetao into the prefrontal cortex of mice increased the MDA level; while Bay 60-7550 reversed this effect and increased antioxidant and anti-apoptotic factors, i.e. increased trolox-equivalent-antioxidant capacity and Bcl-2/Bax ratio.	2-(3,4-dimethoxybenzyl)-7-(1-(1-hydroxyethyl)-4-phenylbutyl)-5-methylimidazo(5,1-f)(1,2,4)triazin-4 (3H)-one	101-112	BCL2-associated X protein	Mus musculus	252-255
35619282-12	2022	RESULTS: The expression level of caspase-3 and bax in liver decreased significantly after treatment with UDCA under HS conditions.	Ursodeoxycholic Acid	105-109	BCL2-associated X protein	Mus musculus	47-50
35623085-7	2022	In vitro, we found duloxetine notably inhibits the relative mRNA and protein expression levels of p53, Bax/Bcl2, caspase-3, and caspase-9 in DRG neurons, which may indicate duloxetine protected the DRG neuron by inhibiting p53-related pathways.	Duloxetine Hydrochloride	19-29	BCL2-associated X protein	Mus musculus	103-106
35286779-10	2022	Immunostaining of active caspase3 and BAX were intense in the endometrium of aging model compare to CN- and metformin-treated groups.	Metformin	108-117	BCL2-associated X protein	Mus musculus	38-41
35513128-8	2022	Further studies revealed that TAC-induced terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive nuclei and the protein levels of Bax/Bcl2 ratio and cleaved caspase 3 were substantially decreased by Daph treatment.	tac	30-33	BCL2-associated X protein	Mus musculus	153-156
35513128-8	2022	Further studies revealed that TAC-induced terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive nuclei and the protein levels of Bax/Bcl2 ratio and cleaved caspase 3 were substantially decreased by Daph treatment.	daphnetin	222-226	BCL2-associated X protein	Mus musculus	153-156
35338672-13	2022	Treatment with CP ameliorates the expression of Bax, Bcl-2 and caspase-3 in the brain tissue of glutamate induced brain injured mice.	Glutamic Acid	96-105	BCL2-associated X protein	Mus musculus	48-51
35617905-10	2022	Immunohistochemistry and RT-qPCR showed that the expression of Bax, caspase-3 and caspase-9 significantly increased in the MCZ- group.	mancozeb	123-126	BCL2-associated X protein	Mus musculus	63-66
35625905-10	2022	Additionally, meleagrin inhibited bleomycin-induced apoptosis by abating the activities of pro-apoptotic proteins Bax and caspase-3 while elevating Bcl2.	Bleomycin	34-43	BCL2-associated X protein	Mus musculus	114-117
35596056-12	2022	In addition, O-1602 treatment also significantly reduced Bax and increased Bcl-2 expression as well as decreased caspase-3 activity and TUNEL-positive cells in the hippocampus.	O-1602	13-19	BCL2-associated X protein	Mus musculus	57-60
35554836-8	2022	Treatment with BG significantly abrogated apoptosis and autophagy in lymphoid organs in diabetic mice by restoring the expression levels of LC3, Beclin-1, P62, Bcl-2, and Bax; decreasing inflammatory signals by downregulating the expression of MCP-1 and HSP-70; and promoting cell survival by enhancing the phosphorylation of AKT.	O(6)-benzylguanine	15-17	BCL2-associated X protein	Mus musculus	171-174
35600488-10	2022	Under oxygen glucose deprivation conditions that mimicked hypoxia and hypoglycemia in vitro, Maclpil siRNA silencing augmented macrophage apoptosis in conjunction with upregulation of proapoptotic Bax and caspase 3 expressions.	maclpil	93-100	BCL2-associated X protein	Mus musculus	197-200
35624799-4	2022	Immunoblotting results showed that GA (100 muM) caused cytotoxicity in murine renal glomerular mesangial cells (SV40 MES 13) and induced apoptosis via major modulators, decreasing Bcl-2 and increasing Bax, cytochrome c, and cleaved caspase-3/-9 expression.	glycolaldehyde	35-37	BCL2-associated X protein	Mus musculus	201-204
35514074-9	2022	Furthermore, FA markedly reversed the APAP-induced decline of mitochondria membrane potential, increased ratio of BAX/BCL2 and CASPASE 3 expression, and promoted autophagy flux of hepatocytes by upregulating AMPK phosphorylation, which were abrogated by a specific AMPK inhibitor, compound C. Overall, the hepatoprotective effect of FA on APAP-induced ALI might be associated with anti-oxidant and anti-apoptosis, which were at least partly attributed to AMPK-mediated protective autophagy.	Acetaminophen	38-42	BCL2-associated X protein	Mus musculus	114-117
35521965-9	2022	What"s more, the protein expressions of PCNA and Bcl-2 were up-regulated, the Bax expression was down-regulated after carnosol treatment.	carnosol	118-126	BCL2-associated X protein	Mus musculus	78-81
35507968-4	2022	METHODS: PCCL was orally administered at a dose of 20 mg kg-1 for 7 days and its protective effect on 5-FU-induced IM (5-FU, 50 mg kg-1 for 5 days) was evaluated by monitoring changes in body weight, degree of diarrhea, levels of tissue inflammatory factors (tumor necrosis factor alpha, interleukin 6, and interleukin 1beta levels), apoptosis rates, and the expression levels of caspase-3, Bax and Bcl-2.	pccl	9-13	BCL2-associated X protein	Mus musculus	391-394
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	137-140	BCL2-associated X protein	Mus musculus	42-45
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	177-180	BCL2-associated X protein	Mus musculus	42-45
35511600-6	2022	Dextran sodium sulfate (DSS) upregulated the mRNA levels of IL-6, IL-1beta, IL-17, IL-12, tumor necrosis factor-alpha, C-C chemokine receptor type 5 and Bax in splenic lymphocytes (SPLs) and colon tissues, while G3c/D665 treatment conversely inhibited the increase in mRNA levels of these genes.	dextran sodium sulfate	0-22	BCL2-associated X protein	Mus musculus	153-156
35511600-6	2022	Dextran sodium sulfate (DSS) upregulated the mRNA levels of IL-6, IL-1beta, IL-17, IL-12, tumor necrosis factor-alpha, C-C chemokine receptor type 5 and Bax in splenic lymphocytes (SPLs) and colon tissues, while G3c/D665 treatment conversely inhibited the increase in mRNA levels of these genes.	dss	24-27	BCL2-associated X protein	Mus musculus	153-156
35529482-10	2022	Dex inhibited MC3T3-E1 cell viability in a dose-dependent effect and induced apoptosis by increasing the expression levels of FOXO1, Bax, cleaved-Caspase-3, and cleaved-Caspase-9, while reducing the expression of Bcl-2.	Dexamethasone	0-3	BCL2-associated X protein	Mus musculus	133-136
35507968-6	2022	PCCL also reduced the levels of tissue inflammatory factors, the apoptosis rate, and the expression of caspase-3 and Bax, and increased Bcl-2 expression.	pccl	0-4	BCL2-associated X protein	Mus musculus	117-120
35493436-7	2022	In addition, co-administration with aCD47 effectively reduced the expression of Bax, collagen I, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in murine DCM.	acd47	36-41	BCL2-associated X protein	Mus musculus	80-83
35367536-4	2022	Moreover, melatonin administration protected kidney tissue by significantly upregulating the levels of PPARalpha reduced by cisplatin injection, resulting in increased FAO pathway-associated genes (PGC-1a, Acadm, Acat1, Acsm2, Acsm3, Bdh2, Echs and Pecr) as well as reducing protein levels of caspase-3, -9 and Bax.	Melatonin	10-19	BCL2-associated X protein	Mus musculus	311-314
35367536-4	2022	Moreover, melatonin administration protected kidney tissue by significantly upregulating the levels of PPARalpha reduced by cisplatin injection, resulting in increased FAO pathway-associated genes (PGC-1a, Acadm, Acat1, Acsm2, Acsm3, Bdh2, Echs and Pecr) as well as reducing protein levels of caspase-3, -9 and Bax.	Cisplatin	124-133	BCL2-associated X protein	Mus musculus	311-314
35367536-5	2022	Melatonin not only partially modulated FAO via PPARalpha signaling, but also decreased cisplatin-induced apoptosis by inhibiting the caspase-3, -9 and Bax pathways.	Melatonin	0-9	BCL2-associated X protein	Mus musculus	151-154
35367536-5	2022	Melatonin not only partially modulated FAO via PPARalpha signaling, but also decreased cisplatin-induced apoptosis by inhibiting the caspase-3, -9 and Bax pathways.	Cisplatin	87-96	BCL2-associated X protein	Mus musculus	151-154
35534220-9	2022	ATO significantly up-regulated the expression of BAX, PARP, and Caspase-3 and inhibited the expression of Bcl-2.	Atorvastatin	0-3	BCL2-associated X protein	Mus musculus	49-52
35191561-10	2022	Renal apoptosis, along with apoptotic markers, were enhanced by FA injection and suppressed by TMZ administration ( Caspase-3,  Bax, and  Bcl2 expression).	Temozolomide	95-98	BCL2-associated X protein	Mus musculus	128-131
35571896-8	2022	In addition, PF treatment inhibited the expression of the apoptotic protein Bax and restored the expression of tyrosine hydroxylase in the brains of the model mice.	peoniflorin	13-15	BCL2-associated X protein	Mus musculus	76-79
35369900-7	2022	Moreover, Ori regulated APAP-induced hepatocyte apoptosis and mitochondrial dysfunction by inhibiting cytochrome c mitochondrial translocation and c-jun N-terminal kinase phosphorylation, promoting Bcl-2 expression and reducing Bax and caspase-3 cleavage.	Acetaminophen	24-28	BCL2-associated X protein	Mus musculus	228-231
35545340-16	2022	Besides, the expression of miR-124a and Bax in the synovial tissue in miR-124a treatment group was significantly higher than those in the model group and NC group (P<0.01 or P<0.001), while the expressions of PIK3CA and Bcl-2 were decreased (P<0.05 or P<0.01 or P<0.001), and the ratio of Bcl-2 to Bax was significantly decreased (P<0.01 or P<0.001).	mir-124a	70-78	BCL2-associated X protein	Mus musculus	40-43
35545340-16	2022	Besides, the expression of miR-124a and Bax in the synovial tissue in miR-124a treatment group was significantly higher than those in the model group and NC group (P<0.01 or P<0.001), while the expressions of PIK3CA and Bcl-2 were decreased (P<0.05 or P<0.01 or P<0.001), and the ratio of Bcl-2 to Bax was significantly decreased (P<0.01 or P<0.001).	mir-124a	70-78	BCL2-associated X protein	Mus musculus	298-301
35471621-6	2022	In addition, H2O2 reduced mitochondrial membrane potential and caused downregulation of Bcl-2 and upregulation of Bax expression, although these were abrogated by CFE pretreatment.	Hydrogen Peroxide	13-17	BCL2-associated X protein	Mus musculus	114-117
35528515-6	2022	In addition, MgH2 decreased oxidative stress by eliminating intracellular ROS, inhibited apoptosis by regulating the expressions of cytochrome c, Bax, and Bcl-2, and suppressed barrier breakdown by up-regulating the expression of ZO-1 and occludin.	magnesium;hydride	13-17	BCL2-associated X protein	Mus musculus	146-149
35559264-7	2022	MCGP also enhanced the number of PCNA-positive hepatocytes, increased hepatic PCNA and Bcl-XL, and decreased BAX expression in APAP-/CCl4-intoxicated mice.	Acetaminophen	127-131	BCL2-associated X protein	Mus musculus	109-112
35278602-6	2022	The in vivo data demonstrated that mice given urethane alone had a significant increase in MDA, NO, NF-kappaB level, HIF1-alpha, and COX-2-positive expression in the lung tissue and serum VEGFR2, ALT, AST, urea, and creatinine accompanied with a significant decrease in GSH, SOD, caspase 9 in the lung tissue and serum BAX.	Urethane	46-54	BCL2-associated X protein	Mus musculus	319-322
35278602-7	2022	Co-treatment with BBR-COSNPs suppressed lung cancer growth and promoted apoptosis by modulating serum BAX and lung caspase 9 gene expressions.	bbr	18-21	BCL2-associated X protein	Mus musculus	102-105
35528513-7	2022	Our results showed that Dex (50 mug/kg) most significantly attenuated MPTP-induced motor dysfunction and restored TH-positive neurons in the SN, increased the expression of the antiapoptotic protein Bcl-2, and decreased the expression of apoptotic proteins cleaved casepase3, cleaved casepase9, and Bax.	Dexmedetomidine	24-27	BCL2-associated X protein	Mus musculus	299-302
35498148-7	2022	Genistein treatment reduced apoptosis by increasing Bcl2 protein expression and decreasing Bax and caspase 3 protein expression.	Genistein	0-9	BCL2-associated X protein	Mus musculus	91-94
35396933-0	2022	The pro-apoptotic Bax gene modifies susceptibility to craniofacial dysmorphology following gastrulation-stage alcohol exposure.	Alcohols	110-117	BCL2-associated X protein	Mus musculus	18-21
35396933-5	2022	The current study determines if mice lacking the Bax gene are less susceptible to the pathogenic effects of gastrulation-stage alcohol exposure.	Alcohols	127-134	BCL2-associated X protein	Mus musculus	49-52
35396933-9	2022	RESULTS: Full Bax deletion reduced embryonic apoptotic cell death and the incidence of fetal eye and face malformations, indicating that Bax normally facilitates the development of alcohol-induced defects.	Alcohols	181-188	BCL2-associated X protein	Mus musculus	14-17
35396933-9	2022	RESULTS: Full Bax deletion reduced embryonic apoptotic cell death and the incidence of fetal eye and face malformations, indicating that Bax normally facilitates the development of alcohol-induced defects.	Alcohols	181-188	BCL2-associated X protein	Mus musculus	137-140
35396933-11	2022	CONCLUSIONS: Overall, these experiments identify that Bax is a primary teratogenic mechanism of gastrulation-stage alcohol exposure.	Alcohols	115-122	BCL2-associated X protein	Mus musculus	54-57
35383529-11	2022	According to the findings, the SAH downregulated NOTCH1 signaling pathway, Jlk6 inhibited Notch1, Notch1 inactivation increased apoptotic protein expression and suppressed Bax, and cytochrome C. Fluoxetine reversed the effects of notch1 inhibition in SAH.	Fluoxetine	195-205	BCL2-associated X protein	Mus musculus	172-175
35457433-0	2022	Flurochloridone Induced Cell Apoptosis via ER Stress and eIF2alpha-ATF4/ATF6-CHOP-Bim/Bax Signaling Pathways in Mouse TM4 Sertoli Cells.	raiser	0-15	BCL2-associated X protein	Mus musculus	86-89
35332348-11	2022	Additionally, HES treatment up-regulated the expression of anti-apoptotic protein Bcl-2 and down-regulated the expression of pro-apoptotic proteins Bax and Caspase-3.	Hesperidin	14-17	BCL2-associated X protein	Mus musculus	148-151
34997458-11	2022	Rosuvastatin also downregulated pro-apoptotic proteins cleaved caspase-3, cytochrome C, p53 and Bax, and upregulated anti-apoptotic Bcl-2.	Rosuvastatin Calcium	0-12	BCL2-associated X protein	Mus musculus	96-99
35468679-14	2022	Western blot analysis displayed up-regulation of proapoptotic proteins (Bax, Cyt-c, p53) and down regulation of anti-apoptotic protein (Bcl2) in DL cells treated with ETME.	etme	167-171	BCL2-associated X protein	Mus musculus	72-75
34997458-12	2022	Rosuvastatin mitigates CME-induced cardiac injury by inhibiting Nox2-induced ROS overproduction and alleviating p53/Bax/Bcl-2-dependent cardiomyocyte apoptosis.	Rosuvastatin Calcium	0-12	BCL2-associated X protein	Mus musculus	116-119
35175747-9	2022	Further, the autophagy activator rapamycin (Rap) and the inhibitor 3-methylademine (3-MA) were introduced, which showed that the apoptosis rate and the ratio of Bax/Bcl-2 as well as the protein expression level of cleaved caspase-3 increased significantly with the pretreatment of Rap and decreased remarkably with the pretreatment of 3-MA.	3-methylademine	67-82	BCL2-associated X protein	Mus musculus	161-164
35094304-3	2022	Oxidative stress induced by H2O2 was significantly ameliorated by treatment with purpurin, based on changes in cell death, DNA fragmentation, formation of reactive oxygen species, and pro-apoptotic (Bax)/anti-apoptotic (Bcl-2) protein levels.	Hydrogen Peroxide	28-32	BCL2-associated X protein	Mus musculus	199-202
35235860-8	2022	RESULTS: Valsartan suppressed CRC cell-growth and synergistically enhanced the anti-tumor-activities of 5-FU by induction of apoptosis, BAX, BCL2, P53 and modulation of the cell cycle.	Valsartan	9-18	BCL2-associated X protein	Mus musculus	136-139
35235860-8	2022	RESULTS: Valsartan suppressed CRC cell-growth and synergistically enhanced the anti-tumor-activities of 5-FU by induction of apoptosis, BAX, BCL2, P53 and modulation of the cell cycle.	Fluorouracil	104-108	BCL2-associated X protein	Mus musculus	136-139
35344814-4	2022	Metformin upregulated BAX activation with facilitation of BIM, BAD and PUMA; downregulated Bcl-2 and Bcl-xl, but did not affect Mcl-1.	Metformin	0-9	BCL2-associated X protein	Mus musculus	22-25
35175747-9	2022	Further, the autophagy activator rapamycin (Rap) and the inhibitor 3-methylademine (3-MA) were introduced, which showed that the apoptosis rate and the ratio of Bax/Bcl-2 as well as the protein expression level of cleaved caspase-3 increased significantly with the pretreatment of Rap and decreased remarkably with the pretreatment of 3-MA.	3-methyladenine	84-88	BCL2-associated X protein	Mus musculus	161-164
35355866-9	2022	Furthermore, GSPE could attenuate mitochondrial-associated cell apoptosis via decreasing the Bax/Bcl-2 ratio.	gspe	13-17	BCL2-associated X protein	Mus musculus	93-96
35340413-17	2022	The expression of apoptotic proteins Bax and cleaved caspase-3 increased in the CoCl2 group, and that of the antiapoptotic protein Bcl-2 decreased.	cobaltous chloride	80-85	BCL2-associated X protein	Mus musculus	37-40
35340413-18	2022	The expression of apoptotic proteins Bax and cleaved caspase-3 reduced in the CoCl2+ML133 group, whereas that of the antiapoptotic protein Bcl-2 increased.	cobaltous chloride	78-83	BCL2-associated X protein	Mus musculus	37-40
35059715-6	2022	At the same time, the western blot evaluation revealed that Liriodendrin significantly inhibited the activation of Bcl-2/Bax/Caspase-3 and NF-kappaB signaling pathways.	liriodendrin	60-72	BCL2-associated X protein	Mus musculus	121-124
35326251-8	2022	In particular, the combination treatment of MFSCE and pyridoxal 5"-phosphate (PLP) showed greater suppression of Bax and cleaved caspase-3 protein expression compared to the MFSCE- or PLP-only treatment.	mfsce	44-49	BCL2-associated X protein	Mus musculus	113-116
35326251-8	2022	In particular, the combination treatment of MFSCE and pyridoxal 5"-phosphate (PLP) showed greater suppression of Bax and cleaved caspase-3 protein expression compared to the MFSCE- or PLP-only treatment.	Pyridoxal Phosphate	54-76	BCL2-associated X protein	Mus musculus	113-116
35326251-8	2022	In particular, the combination treatment of MFSCE and pyridoxal 5"-phosphate (PLP) showed greater suppression of Bax and cleaved caspase-3 protein expression compared to the MFSCE- or PLP-only treatment.	Pyridoxal Phosphate	78-81	BCL2-associated X protein	Mus musculus	113-116
35298966-6	2022	Additionally, BPA significantly increased Bax/Bcl-2 ratio, Caspase-3 expression and apoptosis rate.	bisphenol A	14-17	BCL2-associated X protein	Mus musculus	42-45
35422916-8	2022	Meanwhile, the unbalanced expressions of Bax and Bcl-xL in renal tubules were restored by artemether.	Artemether	90-100	BCL2-associated X protein	Mus musculus	41-44
35370749-7	2022	In LPS-induced ALI mice, FOL administration showed inhibition of IL-1beta, IL-6, and TNF-alpha in Bronchoalveolar lavage fluid (BALF) and decreased protein expression levels of PI3K, AKT, NF-kappaB p50, and NF-kappaB p65, and elevated protein expression levels of Bax and cleaved-caspase-3 significantly.	Folic Acid	25-28	BCL2-associated X protein	Mus musculus	264-267
35298966-7	2022	We found that RAPA ameliorated the cell viability, Bax/Bcl-2 ratio, and macrophage function damage induced by BPA.	bisphenol A	110-113	BCL2-associated X protein	Mus musculus	51-54
35434046-9	2022	Of note, dexmedetomidine suppressed LIR-induced lung tissue apoptosis by modulating apoptosis-associated protein such as Bax, Bcl-2, and cleaved caspase 3.	Dexmedetomidine	9-24	BCL2-associated X protein	Mus musculus	121-124
35167638-6	2022	Pb(Ac)2 exposure significantly increased cellular oxidative damage and the levels of pro-inflammatory cytokines (interleukin (IL)-1beta, IL-6 and tumor necrosis factor-alpha (TNF-alpha), ionized calcium binding adaptor molecule 1 (Iba1) and pro-apoptotic proteins (caspase 3, caspase 9 and Bax), while downregulating the expression of Bcl-2 in the brain.	pb(ac)2	0-7	BCL2-associated X protein	Mus musculus	290-293
35434046-9	2022	Of note, dexmedetomidine suppressed LIR-induced lung tissue apoptosis by modulating apoptosis-associated protein such as Bax, Bcl-2, and cleaved caspase 3.	lir	36-39	BCL2-associated X protein	Mus musculus	121-124
35244883-8	2022	Diacerein also counteracted acetaminophen-induced hepatocellular apoptosis by increasing Bcl-2 and decreasing Bax and caspase-3 expression levels.	diacerein	0-9	BCL2-associated X protein	Mus musculus	110-113
35281932-10	2022	Dapagliflozin reduced the level of ROS caused by high glucose, decreased the expression of cleaved-caspase3 and the ratio of BAX/Bcl-2.	dapagliflozin	0-13	BCL2-associated X protein	Mus musculus	125-128
33673794-6	2022	Besides, apigenin modulates 7 Gy radiation-induced apoptotic markers (p53, p21, Bax, caspase-3, -9) expression in the GI tissue of WBI mice.	Apigenin	9-17	BCL2-associated X protein	Mus musculus	80-83
35202175-4	2022	In addition, the key proteins involved in apoptosis, cleaved caspase-3 and -8, BAD, BAX, and phosphorylation of p53 and ERK1/2, were significantly increased in ZEN-exposed GC-1 spg cells for 24 h, and cytochrome c was released from mitochondria by ZEN.	Zearalenone	160-163	BCL2-associated X protein	Mus musculus	84-87
35356144-8	2022	Treadmill exercise suppressed ethanol with LPS and CCl4-mediated elevation of Bax expression and increased Bcl-2 expression suppressed by application of ethanol with LPS and CCl4.	Ethanol	30-37	BCL2-associated X protein	Mus musculus	78-81
35356144-8	2022	Treadmill exercise suppressed ethanol with LPS and CCl4-mediated elevation of Bax expression and increased Bcl-2 expression suppressed by application of ethanol with LPS and CCl4.	Ethanol	153-160	BCL2-associated X protein	Mus musculus	78-81
35191484-7	2022	Thus, aberrant DUX4 expression appeared to alter nucleocytoplasmic protein transport and generate double-strand DNA breaks in FSHD1 myotube nuclei, and the Bax/Bak pathway is required for DUX4-induced caspase activation but not gammaH2AX accumulation.	gammah2ax	228-237	BCL2-associated X protein	Mus musculus	156-159
35186190-3	2022	The T1DM mice results indicated that BefA significantly reduced blood glucose levels; exerted a protective effect on islet beta cell morphology; downregulated the expressions of TLR-4, p-NFkappaB/NFkappaB, and Bax/Bcl-2, and the secretion levels of IL-1beta and TNF-alpha; increased the expression of PDX-1 protein and insulin secretion in a concentration-dependent manner; and restored the disturbed microbial diversity to normal levels.	befa	37-41	BCL2-associated X protein	Mus musculus	210-213
35119561-4	2022	Mechanistically, a H2S concentration of 100-800 pm upregulates PARP1 and Bax expression in a dose-dependent manner in vivo and in vitro, and functional gain-and-loss experiments verified that an excessive amount of H2S plays a pro-apoptotic role in HT22 and MML1 cells via regulation of PARP1 and Bax in vitro.	Deuterium	19-22	BCL2-associated X protein	Mus musculus	73-76
35178161-9	2022	The activation of MPO/HOCl pathways facilitated apoptosis and ferroptosis through increasing the Bax/Bcl-2 ratio and expression of caspase-3 or inhibiting the expressions of GPX4 and NQO1 and thus leading to irreversible lipid peroxidation.	Hypochlorous Acid	22-26	BCL2-associated X protein	Mus musculus	97-100
35119561-0	2022	Excessive hydrogen sulfide causes lung and brain tissue damage by promoting PARP1/Bax and C9 and inhibiting LAMB1.	Hydrogen Sulfide	10-26	BCL2-associated X protein	Mus musculus	82-85
35119561-4	2022	Mechanistically, a H2S concentration of 100-800 pm upregulates PARP1 and Bax expression in a dose-dependent manner in vivo and in vitro, and functional gain-and-loss experiments verified that an excessive amount of H2S plays a pro-apoptotic role in HT22 and MML1 cells via regulation of PARP1 and Bax in vitro.	Deuterium	215-218	BCL2-associated X protein	Mus musculus	73-76
35119561-8	2022	In summary, 100-800 pm H2S causes the brain and lung tissue damage in ICR mice, the underlying mechanisms include H2S induced apoptosis and inflammation of mouse brain and lung cells by upregulation of PARP1/Bax and C9, respectively, and H2S might induce fibrosis of mouse brain and lung cells by downregulation of LAMB1.	Deuterium	23-26	BCL2-associated X protein	Mus musculus	208-211
35119561-8	2022	In summary, 100-800 pm H2S causes the brain and lung tissue damage in ICR mice, the underlying mechanisms include H2S induced apoptosis and inflammation of mouse brain and lung cells by upregulation of PARP1/Bax and C9, respectively, and H2S might induce fibrosis of mouse brain and lung cells by downregulation of LAMB1.	Deuterium	114-117	BCL2-associated X protein	Mus musculus	208-211
35129051-13	2022	Cell apoptosis was attenuated following CBT adding in ATDC5 cells exposed to LPS, accompanied by upregulated Bcl-2 expression and downregulated Bax and cleaved caspase 3 expression.	columbianetin	40-43	BCL2-associated X protein	Mus musculus	144-147
34653291-6	2022	Furthermore, these results suggest that pretreatment with FG-4592 significantly reduced the tubular cells apoptosis (decreased TUNEL-positive cells, Bax, caspase12 levels), attenuated mitochondrial damage (increased ATPbeta, PPARgamma, mitochondrial DNA copy number, and decreased cytoplasmic cytochrome C), and alleviated DNA damage after IRI.	roxadustat	58-65	BCL2-associated X protein	Mus musculus	149-152
34990787-6	2022	Moreover, BPS stimulation enhanced BAX expression and caspase-3 activity and inhibited BCL-2 expression.	bis(4-hydroxyphenyl)sulfone	10-13	BCL2-associated X protein	Mus musculus	35-38
34923584-6	2022	Finally, TUNEL staining and immunohistochemistry indicated that specnuezhenide prevented CCl4-induced hepatocytic apoptosis by up-regulating B-cell lymphoma 2 (Bcl-2) expression and downregulating Bcl-2-associated X (Bax) expression.	nuezhenide	64-78	BCL2-associated X protein	Mus musculus	197-215
34923584-6	2022	Finally, TUNEL staining and immunohistochemistry indicated that specnuezhenide prevented CCl4-induced hepatocytic apoptosis by up-regulating B-cell lymphoma 2 (Bcl-2) expression and downregulating Bcl-2-associated X (Bax) expression.	nuezhenide	64-78	BCL2-associated X protein	Mus musculus	217-220
35163399-5	2022	Meanwhile, LPC was shown to induce apoptosis, which is accompanied by an increase in apoptosis-related protein levels, such as cleaved caspase-3, cleaved caspase-8 and Bax, as well as a decrease in Bcl-2.	Lysophosphatidylcholines	11-14	BCL2-associated X protein	Mus musculus	168-171
35386464-6	2022	The Rh2@HMnO2-AM nanoparticles can effectively trigger immunogenic cell death (ICD), activate CD4+/CD8+ T cells in vivo, and upregulate BAX, BCL-2 and Caspase-3 in cellular level.	rh2	4-7	BCL2-associated X protein	Mus musculus	136-139
35386464-6	2022	The Rh2@HMnO2-AM nanoparticles can effectively trigger immunogenic cell death (ICD), activate CD4+/CD8+ T cells in vivo, and upregulate BAX, BCL-2 and Caspase-3 in cellular level.	hmno2-am	8-16	BCL2-associated X protein	Mus musculus	136-139
35126176-11	2021	Levosimendan also maintained mitochondrial membrane potential, decreased cleaved caspase-3 (P = 0.034), cleaved caspase-9 (P < 0.0001), Bax expression (P < 0.0001), and increased Bcl2 expression (P = 0.0036).	Simendan	0-12	BCL2-associated X protein	Mus musculus	136-139
35146419-7	2022	Additionally, ER stress induced neuronal apoptosis was attenuated by GSK2606414 treatment via inhibiting the PERK-eIF2alpha-ATF4-CHOP axis that not only curtailed the levels of apoptotic proteins like Bax and caspase 3 but also elevated the levels of anti-apoptotic Bcl-2.	7-methyl-5-(1-((3-(trifluoromethyl)phenyl)acetyl)-2,3-dihydro-1H-indol-5-yl)-7H-pyrrolo(2,3-d)pyrimidin-4-amine	69-79	BCL2-associated X protein	Mus musculus	201-204
35013891-5	2022	After different concentration of nano-TiO2 treatments, the cell viability, apoptosis, mitochondrial membrane potential (Deltapsim), BTB junction proteins (Claudin-11, ZO-1, beta-catenin), apoptosis-related proteins (Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3), and phosphorylated (p)-JNK protein were examined.	titanium dioxide	38-42	BCL2-associated X protein	Mus musculus	216-219
35164001-4	2022	Furthermore, alpha-cubebenoate treatment increased the number of apoptotic CT26 cells as compared with Vehicle-treated cells and increased Bax, Bcl-2, Cas-3, and Cleaved Cas-3 protein levels by activating the MAP kinase signaling pathway.	alpha-cubebenoate	13-30	BCL2-associated X protein	Mus musculus	139-142
35057828-6	2022	Melatonin increased Bcl2 and decreased Bax gene expression in PCOS and control oocytes compared to non-treated oocytes.	Melatonin	0-9	BCL2-associated X protein	Mus musculus	39-42
35013891-9	2022	The protein levels of Bax, cleaved caspase-9, and cleaved caspase-3 increased significantly from 150 mug/mL nano-TiO2 group, and the protein level of Bcl-2 decreased significantly from 100 mug/mL nano-TiO2 group.	titanium dioxide	201-205	BCL2-associated X protein	Mus musculus	22-25
35013891-9	2022	The protein levels of Bax, cleaved caspase-9, and cleaved caspase-3 increased significantly from 150 mug/mL nano-TiO2 group, and the protein level of Bcl-2 decreased significantly from 100 mug/mL nano-TiO2 group.	titanium dioxide	113-117	BCL2-associated X protein	Mus musculus	22-25
34983307-11	2022	Furthermore, miR-373-3p overexpression elevated Bax and caspase 3 expressions and attenuated Bcl2"s level.	mir-373-3p	13-23	BCL2-associated X protein	Mus musculus	48-51
35069207-4	2021	The results show that administration of quercetin attenuated the level of podocyte apoptosis by decreasing the expression of pro-apoptotic protein Bax, cleaved caspase 3 and increasing the expression of anti-apoptotic protein Bcl-2 in the db/db mice and HG-induced MPs.	Quercetin	40-49	BCL2-associated X protein	Mus musculus	147-150
34292250-6	2022	The Bcl-2/Bax ratio and the number of Schwann cell nucleus in the proximal nerve stumps in the EMC group were greater than those in the P-EMC group.	Ethylmercuric Chloride	95-98	BCL2-associated X protein	Mus musculus	10-13
34261915-6	2022	Furthermore, atractylenolide III also significantly inhibited the tumor growth of HCT-116 tumor xenografts bearing in nude mice through inducing apoptosis by upregulation of the expressions of Bax, cleaved caspase-3 and p53 but downregulation of the expressions of Bcl-2 in HCT-116 tumor tissues in vivo.	atractylenolide III	13-32	BCL2-associated X protein	Mus musculus	193-196
35101250-11	2022	The results demonstrated that EGb protection can effectively diminish H2O2-induced apoptosis by inhibiting p53 acetylation, reducing the ratio of Bax/Bcl-2 and suppressing the expression of specific cleavage of Caspase-9 and Caspase-3.	Hydrogen Peroxide	70-74	BCL2-associated X protein	Mus musculus	146-149
34265832-7	2022	RESULTS: CS promoted AEC apoptosis, increased DAPK1 and P53 expression and induced the binding of DAPK1 and P53; inhibition of DAPK1 or P53 reduced CS induced AEC apoptosis, suppressed the expression of Bax, increased Bcl-2 level and stabilized MMP; AEC apoptosis and the level of P53 were both increased after overexpressing of DAPK1.	Cesium	9-11	BCL2-associated X protein	Mus musculus	203-206
34265832-7	2022	RESULTS: CS promoted AEC apoptosis, increased DAPK1 and P53 expression and induced the binding of DAPK1 and P53; inhibition of DAPK1 or P53 reduced CS induced AEC apoptosis, suppressed the expression of Bax, increased Bcl-2 level and stabilized MMP; AEC apoptosis and the level of P53 were both increased after overexpressing of DAPK1.	Cesium	148-150	BCL2-associated X protein	Mus musculus	203-206
35154540-10	2022	Results: Real-time PCR revealed that AZ31 (40%) concentration increased the apoptotic genes such as NF-kappaB, caspase-3, Bax and Bax/Bcl-2 ratio as compared to the control group.	AZ31	37-41	BCL2-associated X protein	Mus musculus	122-125
35237418-5	2022	ZOL caused apoptosis via phosphorylation of c-Jun N-terminal kinase, increased ratio of Bax to Bcl-2, disruption of mitochondrial membrane potential, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase.	tiletamine, zolazepam drug combination	0-3	BCL2-associated X protein	Mus musculus	88-91
35154540-10	2022	Results: Real-time PCR revealed that AZ31 (40%) concentration increased the apoptotic genes such as NF-kappaB, caspase-3, Bax and Bax/Bcl-2 ratio as compared to the control group.	AZ31	37-41	BCL2-associated X protein	Mus musculus	130-133
35154540-12	2022	Conclusions: To conclude, it can be stated that AZ31 induces apoptosis via alteration in genes including nuclear factor kappa-B (NF-kappaB), caspase-3, Bax and Bax/Bcl-2 ratio and improved the hematological, hepatic and non-hepatic parameters.	AZ31	48-52	BCL2-associated X protein	Mus musculus	152-155
35154540-12	2022	Conclusions: To conclude, it can be stated that AZ31 induces apoptosis via alteration in genes including nuclear factor kappa-B (NF-kappaB), caspase-3, Bax and Bax/Bcl-2 ratio and improved the hematological, hepatic and non-hepatic parameters.	AZ31	48-52	BCL2-associated X protein	Mus musculus	160-163
35356725-7	2022	LCBP significantly regulated the expression of antioxidant and inflammatory proteins, Bcl-2 /Bax apoptosis proteins, and the PKCalpha -NOx2 / Nox4 pathway proteins, and activated the expression of AMPK-PGC1alpha -NRF1-TFAM proteins in skeletal muscle mitochondria.	lcbp	0-4	BCL2-associated X protein	Mus musculus	93-96
33752931-5	2021	In response H2O2, miR-96 inhibitor could significantly promote cell viability and reduce cell apoptosis of CMs, and inhibit the expression of Cleaved caspase-3 and Bax, while promote Bcl-2 expression.	Hydrogen Peroxide	12-16	BCL2-associated X protein	Mus musculus	164-167
34955852-7	2021	Meanwhile, MaR1 administration obviously diminished pro-inflammatory cytokines (TNF-alpha, IL-6, IL-1beta, and MCP-1), downregulated BAX and cleaved caspase-3 expression, and upregulated BCL-2 expression in the injured kidney tissues and TCMK-1 cells.	7,14-dihydroxydocosa-4,8,10,12,16,19-hexaenoic acid	11-15	BCL2-associated X protein	Mus musculus	133-136
33786616-6	2021	DHM also inhibited cell apoptosis induced by OGD/R, and decreased the protein expression levels of Bax and caspase-3, and increased the expression levels of Bcl-2.	dihydromyricetin	0-3	BCL2-associated X protein	Mus musculus	99-102
33646450-0	2021	PPAR-delta activation reduces cisplatin-induced apoptosis via inhibiting p53/Bax/caspase-3 pathway without modulating autophagy in murine renal proximal tubular cells.	Cisplatin	30-39	BCL2-associated X protein	Mus musculus	77-80
33646450-5	2021	Cisplatin-induced cell damages were evaluated by TUNEL assay and immunoblot analyses for p53, 14-3-3, Bax, Bcl2, cytochrome C, and activated caspases.	Cisplatin	0-9	BCL2-associated X protein	Mus musculus	102-105
33646450-7	2021	RESULTS: GW0742 suppressed cisplatin-induced apoptosis of mProx cells by reducing the activation of caspase-3 via attenuating the phosphorylation of p53 and 14-3-3, mitochondrial Bax accumulation, cytochrome C release from mitochondria to the cytosol and ensuing cytosolic caspase-9 activation.	GW0742	9-15	BCL2-associated X protein	Mus musculus	179-182
33646450-7	2021	RESULTS: GW0742 suppressed cisplatin-induced apoptosis of mProx cells by reducing the activation of caspase-3 via attenuating the phosphorylation of p53 and 14-3-3, mitochondrial Bax accumulation, cytochrome C release from mitochondria to the cytosol and ensuing cytosolic caspase-9 activation.	Cisplatin	27-36	BCL2-associated X protein	Mus musculus	179-182
33677255-5	2021	The changes of cleaved-caspase 3, cleaved-caspase 8, Bax, Bcl2 in mouse kidney and NRK-52E cells treated by LPS were reversed by GA administration.	ginkgolide A	129-131	BCL2-associated X protein	Mus musculus	53-56
34059044-6	2021	Furthermore, silibinin strongly induced apoptosis and autophagy by up-regulating the expression of Bax, Caspase-3, Atg5, Atg7 and BECN1 and down-regulating Bcl-2.	Silybin	13-22	BCL2-associated X protein	Mus musculus	99-102
32840726-9	2021	Bax/Bcl2 ratio was decreased in the presence of high Zn.	Zinc	53-55	BCL2-associated X protein	Mus musculus	0-3
34058674-9	2021	Additionally, Rb1 significantly reversed the DON-induced excessive splenic apoptosis via modulating the mitochondria-mediated apoptosis pathway in mice, depicting the decreased percentage of splenocyte apoptotic cells by 26.65%, down-regulated the mRNA abundance of Bax, caspase-3, caspase-9, and protein expression of Bax, cleaved caspase-3, and Cyt-c.	deoxynivalenol	45-48	BCL2-associated X protein	Mus musculus	266-269
34047315-6	2021	It was found that isoquercitrin ameliorated the animal behaviors against MPTP-induced neurotoxicity, mitigated the loss of dopamine neurons induced by MPTP, increased tyrosine hydroxylase and dopamine transporter expression, reduced the pro-apoptotic signaling molecule bax expression and inhibited MPTP-triggered oxidative stress.	isoquercitrin	18-31	BCL2-associated X protein	Mus musculus	270-273
34051206-8	2021	TUNEL staining and western blot revealed that anemoside B4 suppressed cell apoptosis, along with decreased Bax, leaved caspase-3, cleaved PARP, but increased Bcl-2.	anemoside B4	46-58	BCL2-associated X protein	Mus musculus	107-110
34058674-9	2021	Additionally, Rb1 significantly reversed the DON-induced excessive splenic apoptosis via modulating the mitochondria-mediated apoptosis pathway in mice, depicting the decreased percentage of splenocyte apoptotic cells by 26.65%, down-regulated the mRNA abundance of Bax, caspase-3, caspase-9, and protein expression of Bax, cleaved caspase-3, and Cyt-c.	deoxynivalenol	45-48	BCL2-associated X protein	Mus musculus	319-322
33652185-8	2021	In vitro, the mimic of miRNA-450 b-3p reversed the decrease of viability and the increase of apoptosis rate and significantly antagonized the expression enhancements of the MTCH2, BID, BAX, Cytochrome C, Caspase-9, Caspase-3 induced by SiNPs, while inhibitor of miRNA-450 b-3p further promoted the effects induced by SiNPs.	mirna-450 b-3p	23-37	BCL2-associated X protein	Mus musculus	185-188
34044723-8	2021	Differential regulations of Bcl2, Bax and NF-kappaB with reduced serum TNF-alpha level indicated anti-apoptotic and anti-inflammatory roles of Q-3-R.	Rutin	143-148	BCL2-associated X protein	Mus musculus	34-37
34002388-8	2021	BPS also significantly upregulated cleaved caspase-8, cleaved caspase-9, cleaved caspase-3, Fas, and FasL and significantly downregulated the Bcl-2/Bax ratio.	bis(4-hydroxyphenyl)sulfone	0-3	BCL2-associated X protein	Mus musculus	148-151
33713693-11	2021	GluA1 silencing aggravated ethanol-induced changes in cell viability and apoptosis and the expression of BDNF, BAX and cleaved caspase-3, and GluA1 overexpression attenuated these changes.	Ethanol	27-34	BCL2-associated X protein	Mus musculus	111-114
33978226-10	2021	The inhibition of PKM2 by shikonin notably suppressed the expression of HIF-1alpha and apoptosis-related factors such as BNIP3, Bax, and Caspase-3, while the inhibition of PKM2 by shikonin significantly improved the histopathological symptoms of LPS-induced AKI.	shikonin	26-34	BCL2-associated X protein	Mus musculus	128-131
33713693-10	2021	Ethanol exposure decreased cell viability and the expression of BDNF and increased the cell apoptosis rate and the expression of BAX, cleaved caspase-3, IL-1beta and IL-6.	Ethanol	0-7	BCL2-associated X protein	Mus musculus	129-132
33411269-8	2021	In addition, Bcl-2 was reduced and Bax/Bcl-2 was elevated in mouse testes exposed to 500 mg/kg/day DEHP.	Diethylhexyl Phthalate	99-103	BCL2-associated X protein	Mus musculus	35-38
33957170-6	2021	Glabridin substantially prevented methotrexate-induced down-regulation of Nrf2, & activation of NF-kappaB, and caused up-regulation of BAX at different dose levels.	glabridin	0-9	BCL2-associated X protein	Mus musculus	135-138
34012924-6	2021	Our results indicate that in vitro, MET increased the efficacy of TMZ on TMZ-sensitive and on TMZ-resistant cells by deregulating the balance between pro-survival (bcl2) and pro-apoptotic (bax/bad) Bcl-family members and promoting early apoptosis in both Gli36DeltaEGFR-1 and Gli36DeltaEGFR-2 cells.	Temozolomide	66-69	BCL2-associated X protein	Mus musculus	189-192
33347706-12	2021	RT-PCR study proved the enhanced expression of pro-apoptotic protein (p53, Bax, caspase-3 and -9) in the dieckol treated animals.	dieckol	105-112	BCL2-associated X protein	Mus musculus	75-78
33955683-7	2021	In addition, anlotinib induced apoptosis of these cells along with down-regulated expression level of Bcl-2 whereas up-regulated Bax and cleaved caspase-3 expression.	anlotinib	13-22	BCL2-associated X protein	Mus musculus	129-132
33711377-5	2021	The results showed that oxidative stress levels increased with increasing DINP exposure concentrations, which triggered apoptosis (Bcl-2 levels decreased, Bax levels increased), resulting in nerve cell damage and a decline in the learning and memory abilities of mice.	diisononyl phthalate	74-78	BCL2-associated X protein	Mus musculus	155-158
33030694-6	2021	In comparison, Cys-SLN (5 muM) is more effective than Cys-CS-NC (10 muM) groups to improve the expression of antioxidant genes (SOD, CAT, GPx) or anti-apoptotic (BCL-2) gene and decreased apoptosis (BAX and caspase-3) or intra-/extracellular ROS levels.	Cystamine	15-18	BCL2-associated X protein	Mus musculus	199-202
33638773-7	2021	In miR-506-3p mimic group or siRNA-CCL2 group, the expression of CCL2, TLR4, NF-kappaB (p65) and Bcl-2 decreased obviously, while that of Bax increased, cell proliferation decreased, G1 phase prolonged, G2 & S phases shortened, and apoptosis rate increased significantly (all P < 0.05), whereas the opposite trends were found in miR-506-3p inhibitor group (all P < 0.05).	mir-506-3p	3-13	BCL2-associated X protein	Mus musculus	138-141
33909081-0	2021	Xanthohumol ameliorates memory impairment and reduces the deposition of beta-amyloid in APP/PS1 mice via regulating the mTOR/LC3II and Bax/Bcl-2 signalling pathways.	xanthohumol	0-11	BCL2-associated X protein	Mus musculus	135-138
33925146-5	2021	MPTP and NE52-QQ57 co-treatment in mice significantly decreased pro-apoptotic marker Bax protein levels and increased anti-apoptotic marker Bcl-2 protein levels in the SNpc and striatum.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	BCL2-associated X protein	Mus musculus	85-88
33909081-10	2021	CONCLUSIONS: Xanthohumol effectively ameliorates memory impairment of APP/PS1 mice by activating mTOR/LC3 and Bax/Bcl-2 signalling pathways, which provides new insight into the neuroprotective effects of Xanthohumol.	xanthohumol	13-24	BCL2-associated X protein	Mus musculus	110-113
33919028-6	2021	CdCl2 increased the mRNA of IL-1beta, TNF-alpha, p53, and BAX while reduced that of Bcl-2 and induced tubular lesions and apoptosis of germinal cells.	Cadmium Chloride	0-5	BCL2-associated X protein	Mus musculus	58-61
33460759-15	2021	The above effects of SC-FL are closely related to up-regulation of GFRa1, RET, PI3K, p-AKT, and bcl-2 and down-regulation of BAD and BAX proteins and mRNA expression.	sc-fl	21-26	BCL2-associated X protein	Mus musculus	133-136
33880124-9	2021	The results showed that paeoniflorin increased alkaline phosphatase (ALP) activity and upregulated the expression of osteocalcin and beclin-1 but reduced the levels of Bax and C-terminal telopeptide of type I collagen (CTX-1).	peoniflorin	24-36	BCL2-associated X protein	Mus musculus	168-171
33864821-8	2021	Moreover, Proto reduced cisplatin-induced apoptosis in the liver through decreasing caspase-3, annexin-V, and BAX.	Cisplatin	24-33	BCL2-associated X protein	Mus musculus	110-113
33871176-9	2021	In addition, PFOA-treated oocytes exhibited a significantly higher percentage of P-H2AX, defective beta-tubulin, abnormal chromosome alignment, lower expression of the anti-apoptotic gene Bcl-2, and higher expression of the apoptotic genes caspase3 and Bax.	perfluorooctanoic acid	13-17	BCL2-associated X protein	Mus musculus	253-256
33471160-15	2021	A significantly higher gene expression for Bax and Bax/Bcl2 ratio was seen after 5-FU treatment.	Fluorouracil	81-85	BCL2-associated X protein	Mus musculus	43-46
33825597-6	2021	The results showed that cell apoptosis, lung structural damage, and the activity of MDA, as well as the expression of apoptosis-related proteins Bax, total caspase-3, and cleaved caspase-3 were increased in CS-treated mice.	Cesium	207-209	BCL2-associated X protein	Mus musculus	145-148
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	45-61	BCL2-associated X protein	Mus musculus	214-217
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	63-66	BCL2-associated X protein	Mus musculus	214-217
33485069-13	2021	Western blotting showed that policosanol significantly reduced the protein expression of TGF-beta2, cleaved caspese-9, cleaved caspase-3, and Bax, and increased that of Bcl2.	policosanol	29-40	BCL2-associated X protein	Mus musculus	142-145
33471160-15	2021	A significantly higher gene expression for Bax and Bax/Bcl2 ratio was seen after 5-FU treatment.	Fluorouracil	81-85	BCL2-associated X protein	Mus musculus	51-54
33404076-9	2021	Lastly, nicorandil efficiently decreased expression of the proapoptotic protein (Bax) and caspase 3.	Nicorandil	8-18	BCL2-associated X protein	Mus musculus	81-84
33582480-3	2021	Therefore, the present study was set out to investigate the effect of bone marrow mesenchymal stem cells derived exosomes (BMSCs-Exo) and miR-150-5p in MI via regulating B-cell lymphoma-associated X (Bax).	mir-150-5p	138-148	BCL2-associated X protein	Mus musculus	170-198
33582480-3	2021	Therefore, the present study was set out to investigate the effect of bone marrow mesenchymal stem cells derived exosomes (BMSCs-Exo) and miR-150-5p in MI via regulating B-cell lymphoma-associated X (Bax).	mir-150-5p	138-148	BCL2-associated X protein	Mus musculus	200-203
33582480-8	2021	The targeting relationship between miR-150-5p and Bax was verified.	mir-150-5p	35-45	BCL2-associated X protein	Mus musculus	50-53
33582480-12	2021	miR-150-5p was found to target Bax.	mir-150-5p	0-10	BCL2-associated X protein	Mus musculus	31-34
33582480-13	2021	CONCLUSION: On all accounts, the present study provides evidence that BMSCs-derived exosomal miR-150-5p attenuates apoptosis of cardiomyocytes and improves cardiac function of MI mice via targeting Bax.	mir-150-5p	93-103	BCL2-associated X protein	Mus musculus	198-201
33724692-5	2021	In vitro, T3 pretreatment decreased cell apoptosis rate, inhibited caspase-3 activity and decreased the Bax/Bcl-2 ration induced by H/R injury.	Triiodothyronine	10-12	BCL2-associated X protein	Mus musculus	104-107
33433546-4	2021	In one set of experiments, the primary cultured mouse ovarian GCs were co-treated with ZEA and Scu for 24 h. The results showed that Scu significantly alleviated ZEA-induced cell damage, restored cell cycle arrest, and inhibited apoptosis by reducing the ratio of cleaved-caspase-3, cleaved-PARP, and Bax/Bcl-2.	Zearalenone	87-90	BCL2-associated X protein	Mus musculus	301-304
33217075-5	2021	In addition, xanthomicrol reduced the expression of TNFalpha, VEGF, MMP9, and Ki67, while upregulating the expression of apoptotic markers such as Bax, caspase3, and caspase9.	xanthomicrol	13-25	BCL2-associated X protein	Mus musculus	147-150
33754447-9	2021	Mechanically, CoQ10 statistically decreased the levels of Bcl-2 and cytochrome C in mitochondria and upregulated the levels of Bax, cleaved caspase 3, and cytochrome C in the cytoplasm.	coenzyme Q10	14-19	BCL2-associated X protein	Mus musculus	127-130
33655821-7	2021	Moreover, in I/R group, the number of apoptotic cells in lung tissue was higher than that in sham group, and p53, Caspase-3 and Bax expression was up-regulated; however, following treatment with Y-27632 (10, 20 and 30 mg/kg), these changes were reversed.	Y 27632	195-202	BCL2-associated X protein	Mus musculus	128-131
32647341-8	2021	Furthermore, ZNS administration significantly inhibited the Bax and caspase-3 activity, upregulated Bcl-2 activity, and decreased the proportion of TUNEL-positive cells in heart tissues.	Zonisamide	13-16	BCL2-associated X protein	Mus musculus	60-63
33497687-9	2021	Arsenic increased proinflammatory cytokine (tumor necrosis factor-alpha and interleukin-1beta) levels, enhanced caspase-3 and Bax expression, and reduced Bcl-2 expression.	Arsenic	0-7	BCL2-associated X protein	Mus musculus	126-129
32691366-5	2021	Tumor formation, TUNEL detection and immunohistochemical results of Ki67, BAX, Bcl-2 and Caspase-3 in nude mice showed that paeonol could inhibit T24 cell proliferation and induce apoptosis in vivo, thus inhibiting tumor growth.	paeonol	124-131	BCL2-associated X protein	Mus musculus	74-77
33664566-8	2021	In addition, TUNEL staining and Bcl-2/Bax pathway confirmed that taxifolin significantly inhibited hepatocyte apoptosis.	taxifolin	65-74	BCL2-associated X protein	Mus musculus	38-41
33605486-0	2021	Endogenous production of n-3 PUFAs protects mice from CCl4 -induced liver fibrosis by regulating mTOR and Bcl-2/Bax signaling pathways.	Fatty Acids, Omega-3	25-34	BCL2-associated X protein	Mus musculus	112-115
33605486-19	2021	Moreover, mfat-1 transgenic mice showed significant reduction of proteins which are involved in mTOR and Bcl-2/Bax signaling pathways.Collectively, these results suggest that n-3 PUFAs elevation strongly prevents CCl4 -induced hepatic damage by directly inhibiting the activation of HSCs and regulating the basal activity of mTOR and Bcl-2/Bax signaling pathways.	Fatty Acids, Omega-3	175-184	BCL2-associated X protein	Mus musculus	111-114
33605486-19	2021	Moreover, mfat-1 transgenic mice showed significant reduction of proteins which are involved in mTOR and Bcl-2/Bax signaling pathways.Collectively, these results suggest that n-3 PUFAs elevation strongly prevents CCl4 -induced hepatic damage by directly inhibiting the activation of HSCs and regulating the basal activity of mTOR and Bcl-2/Bax signaling pathways.	Fatty Acids, Omega-3	175-184	BCL2-associated X protein	Mus musculus	340-343
33738683-5	2022	However, zinc sulfate led to the attenuation of deleterious effects, including increases in apoptosis, caspase-3 activity, Bax, GRP78, and CHOP expression, and decreases in cell viability and Bcl-2 protein expression in cells treated with HS or thapsigargin (an ER stress activator).	Zinc Sulfate	9-21	BCL2-associated X protein	Mus musculus	123-126
33395603-9	2021	HJT inhibited H2O2-induced cell apoptosis by significantly decreasing the levels of cleaved caspase 3 and increasing the Bcl-2/Bax ratio.	Hydrogen Peroxide	14-18	BCL2-associated X protein	Mus musculus	127-130
33394285-7	2021	Additionally, CUS significantly increased the mRNA expression of Bax (pro-apoptosis marker), but not Bcl-2 (anti-apoptosis marker) in the hippocampus.	cus	14-17	BCL2-associated X protein	Mus musculus	65-68
33394285-9	2021	Ursolic acid, but not fluoxetine, prevented CUS-induced increase in the expression of Bax, but both ursolic acid and fluoxetine prevented CUS-induced reduction on Bcl-2/Bax ratio.	ursolic acid	0-12	BCL2-associated X protein	Mus musculus	86-89
33394285-9	2021	Ursolic acid, but not fluoxetine, prevented CUS-induced increase in the expression of Bax, but both ursolic acid and fluoxetine prevented CUS-induced reduction on Bcl-2/Bax ratio.	cus	44-47	BCL2-associated X protein	Mus musculus	86-89
33394285-9	2021	Ursolic acid, but not fluoxetine, prevented CUS-induced increase in the expression of Bax, but both ursolic acid and fluoxetine prevented CUS-induced reduction on Bcl-2/Bax ratio.	ursolic acid	100-112	BCL2-associated X protein	Mus musculus	169-172
33394285-9	2021	Ursolic acid, but not fluoxetine, prevented CUS-induced increase in the expression of Bax, but both ursolic acid and fluoxetine prevented CUS-induced reduction on Bcl-2/Bax ratio.	Fluoxetine	117-127	BCL2-associated X protein	Mus musculus	169-172
33394285-9	2021	Ursolic acid, but not fluoxetine, prevented CUS-induced increase in the expression of Bax, but both ursolic acid and fluoxetine prevented CUS-induced reduction on Bcl-2/Bax ratio.	cus	138-141	BCL2-associated X protein	Mus musculus	169-172
33394285-11	2021	Our study unveils the ability of ursolic acid to prevent the depressive-like behavior induced by stress and the modulation of Bcl-2/Bax expression could be associated with this response.	ursolic acid	33-45	BCL2-associated X protein	Mus musculus	132-135
33433546-4	2021	In one set of experiments, the primary cultured mouse ovarian GCs were co-treated with ZEA and Scu for 24 h. The results showed that Scu significantly alleviated ZEA-induced cell damage, restored cell cycle arrest, and inhibited apoptosis by reducing the ratio of cleaved-caspase-3, cleaved-PARP, and Bax/Bcl-2.	scutellarin	133-136	BCL2-associated X protein	Mus musculus	301-304
33058431-0	2021	Chlorogenic acid induces 4T1 breast cancer tumor"s apoptosis via p53, Bax, Bcl-2, and caspase-3 signaling pathways in BALB/c mice.	Chlorogenic Acid	0-16	BCL2-associated X protein	Mus musculus	70-73
33568941-15	2021	Mechanism investigation showed that TW-37 and ABT-263 synergistically induced apoptosis via the mitochondrial pathway and relied on the activation of Bax and caspases.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	46-49	BCL2-associated X protein	Mus musculus	150-153
33603823-7	2021	Furthermore, topical application of geniposide reduced the expressions of 8-OHdG and Bax and increased the expression of occludin in the dorsal skin lesions of DEP-stimulated mice.	geniposide	36-46	BCL2-associated X protein	Mus musculus	85-88
33352442-5	2021	In addition, we found that emodin inhibited apoptosis and demonstrated an anti-fibrotic effect by down-regulating the pro-apoptotic protein Bax and up-regulating the anti-apoptotic protein Bcl-2.	Emodin	27-33	BCL2-associated X protein	Mus musculus	140-143
33586527-0	2022	Radix Tetrastigma Inhibits the Non-Small Cell Lung Cancer via Bax/Bcl-2/Caspase-9/Caspase-3 Pathway.	tetrastigma	6-17	BCL2-associated X protein	Mus musculus	62-65
33528726-7	2021	CQMUH-011 was seen to induce apoptosis in activated microglia by regulating the expression of Bax and Bcl-2.	cqmuh-011	0-9	BCL2-associated X protein	Mus musculus	94-97
32856486-7	2021	RESULTS: After mice injected by cisplatin, the levels of Cr, BUN, urine cystatin C, urine NGAL and urine ACR were increased and GFR was decreased with the elevation of renal tubular injury scores, the upregulation of the expressions of MDM2, N1ICD, Hes1 and Cleaved caspase-3, as well as the enhancement of cell apoptosis accompanying decreased ratio of Bcl-2/Bax.	Cisplatin	32-41	BCL2-associated X protein	Mus musculus	360-363
33509759-9	2021	BPA exposure at 50 mumol/L and 200 mumol/L produced opposite effects on the protein expressions of Bcl-2 (P < 0.01), Bax (P < 0.05) and p53 (P < 0.05) in mouse ovarian preantral follicular granulosa cells.	bisphenol A	0-3	BCL2-associated X protein	Mus musculus	117-120
33508982-7	2021	Meanwhile, Iso decreased the OGD-induced apoptosis with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2, which was reversed by ML385.	Isoflurane	11-14	BCL2-associated X protein	Mus musculus	80-83
33496895-8	2021	PRO ameliorated the abnormal histopathology, reduced cell apoptosis and the levels of AST, ALT, Bnip3, Cleaved Caspase-3, and Bax, but upregulated the Bcl-2 level in the liver tissues of I/R mice.	Propofol	0-3	BCL2-associated X protein	Mus musculus	126-129
33302237-6	2021	For this purpose, we used a bi-transgenic mouse line (iBax) in which AHN increase was induced by deletion of the pro-apoptotic gene Bax from the neural progenitors following the tamoxifen-dependent action of CreERT2 recombinases.	Tamoxifen	178-187	BCL2-associated X protein	Mus musculus	55-58
33678633-12	2021	Compared to the MFN-M group, cell apoptosis and the protein level of Bax in the MFN+LY294002 group were significantly increased; the Bcl-2 protein expression was significantly decreased (all P<0.05).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	84-92	BCL2-associated X protein	Mus musculus	69-72
33494783-12	2021	Western blot showed that application of Pt-MWNTS can significantly upregulate the expression level of Bax, Bim, Bid, Caspase-3 and Caspase-9 while downregulate the expression level of Bcl-2, compared with free cisplatin.	Platinum	40-42	BCL2-associated X protein	Mus musculus	102-105
33575163-13	2021	Compared with the LPS group, APS pretreatment could inhibit the expression of inflammatory factors including TNF-alpha, IL-1 beta, IL-6, and IL-8 (all P < 0.05), reducing the number of apoptotic cells (P < 0.05), suppressing the expression of caspase-3, caspase-9, and Bax, but upregulating the expression levels of Bcl-2.	aps	29-32	BCL2-associated X protein	Mus musculus	269-272
33491773-7	2021	Additionally, mechanistic studies showed that PPCCA down-regulated the expression of Caspase-3, Bax and cytochrome P450 2E1 (CYP2E1) proteins in the liver and up-regulated the expression of Bcl-2.	ppcca	46-51	BCL2-associated X protein	Mus musculus	96-99
33467546-9	2021	Finally, empagliflozin increased the Bcl2/Bax ratio and inhibited CASPASE-8 cleavage, reducing liver cell apoptosis.	empagliflozin	9-22	BCL2-associated X protein	Mus musculus	42-45
33410857-8	2021	Furthermore, supplementation with aloin inhibited hepatocyte apoptosis caused by Bcl-2 up-regulation and cleaved caspase-3 and Bax down-regulation.	alloin	34-39	BCL2-associated X protein	Mus musculus	127-130
33275989-5	2021	KEY FINDINGS: Compared with those in the control group, the apoptosis rate and expression levels of Bax and Fas increased in the CoCl2-induced hypoxia model group.	cobaltous chloride	129-134	BCL2-associated X protein	Mus musculus	100-103
33536915-7	2020	Additionally, OEA markedly reduced the expression levels of Bax, Bcl-2 and cleaved caspase-3 to suppress hepatocyte apoptosis.	oleoylethanolamide	14-17	BCL2-associated X protein	Mus musculus	60-63
33426650-5	2021	Additionally, elevated cleaved caspase-3 and Bax protein levels and reduced Bcl-2 protein levels in response to hypoxia-ischemia were diminished after melatonin treatment.	Melatonin	151-160	BCL2-associated X protein	Mus musculus	45-48
33159990-8	2021	Subsequently, our results showed that increased expression level of BAX protein, reduced expression of BCL-2 protein, ATG12 and LC3 protein expression increased in ovaries after Gly treatment.	glyphosate	178-181	BCL2-associated X protein	Mus musculus	68-71
33428678-7	2021	It also significantly reduced the renal transcript levels of Kim-1, MIP-1/CCL3, TNF-alpha, and Bax in CP-N mice.	cp-n	102-106	BCL2-associated X protein	Mus musculus	95-98
33430854-12	2021	RESULTS: Fucoidan inhibited the proliferation and angiogenesis of NSCLC cells via the mTOR pathway and promoted their apoptosis by increasing the Bax/Bcl-2 ratio.	fucoidan	9-17	BCL2-associated X protein	Mus musculus	146-149
33430871-9	2021	Western-blot, immunohistochemical analysis and qPCR suggested that gastroprotective properties of lactate were mediated by its modulatory effects on the expression of the apoptosis regulator gene Bax, the apoptotic executive protein gene Casp3, and genes critical for gastric mucosal integrity, including those encoding tight junction proteins Occludin, Claudin-1, Claudin-5, and that for lactate receptor GPR81.	Lactic Acid	98-105	BCL2-associated X protein	Mus musculus	196-199
33430871-10	2021	CONCLUSION: Lactate mitigates ethanol-induced GMI by curtailing local gastric inflammatory response, down-regulating the expression of the apoptosis regulator and executor genes Bax and Casp3, and up-regulating the expression of genes encoding tight junction proteins Occludin, Claudin-1, and Claudin-5 and the lactate receptor GPR81.	Lactic Acid	12-19	BCL2-associated X protein	Mus musculus	178-181
33430871-10	2021	CONCLUSION: Lactate mitigates ethanol-induced GMI by curtailing local gastric inflammatory response, down-regulating the expression of the apoptosis regulator and executor genes Bax and Casp3, and up-regulating the expression of genes encoding tight junction proteins Occludin, Claudin-1, and Claudin-5 and the lactate receptor GPR81.	Ethanol	30-37	BCL2-associated X protein	Mus musculus	178-181
33407504-13	2021	MiR-139-3p mimic and shPCAT6 inhibited the cell cycle progression of PA cells, decreased the weight and volume of the xenotransplanted tumor, and reduced the levels of Bcl-2 and BRD4 while enhancing the levels of Bax, miR-139-3p, and Cleaved caspase-3.	mir-139-3p	0-10	BCL2-associated X protein	Mus musculus	213-216
33569454-7	2021	In the H2O2-induced 661W cell model, H2O2 increased cellular apoptosis rates, the expression levels of Bcl-2-associated X-protein (BAX) and cleaved caspase 3, reactive oxygen species (ROS) production, and malondialdehyde content, while decreasing the cell viability, and Bcl-2, superoxide dismutase, catalase, and glutathione peroxidase activity.	Hydrogen Peroxide	7-11	BCL2-associated X protein	Mus musculus	103-129
33490128-7	2020	Quercetin supplementation also inhibited the activities of caspases-9 and-3, and the expression of p53 and Bax mRNAs.	Quercetin	0-9	BCL2-associated X protein	Mus musculus	107-110
33188406-11	2021	Moreover, combined BSp and GTPs induced apoptosis by regulating Bcl-2-associated X protein and B-cell lymphoma 2 (P < 0.05).	bsp	19-22	BCL2-associated X protein	Mus musculus	64-90
33188406-11	2021	Moreover, combined BSp and GTPs induced apoptosis by regulating Bcl-2-associated X protein and B-cell lymphoma 2 (P < 0.05).	Guanosine Triphosphate	27-31	BCL2-associated X protein	Mus musculus	64-90
33569454-7	2021	In the H2O2-induced 661W cell model, H2O2 increased cellular apoptosis rates, the expression levels of Bcl-2-associated X-protein (BAX) and cleaved caspase 3, reactive oxygen species (ROS) production, and malondialdehyde content, while decreasing the cell viability, and Bcl-2, superoxide dismutase, catalase, and glutathione peroxidase activity.	Hydrogen Peroxide	7-11	BCL2-associated X protein	Mus musculus	131-134
33569454-7	2021	In the H2O2-induced 661W cell model, H2O2 increased cellular apoptosis rates, the expression levels of Bcl-2-associated X-protein (BAX) and cleaved caspase 3, reactive oxygen species (ROS) production, and malondialdehyde content, while decreasing the cell viability, and Bcl-2, superoxide dismutase, catalase, and glutathione peroxidase activity.	Hydrogen Peroxide	37-41	BCL2-associated X protein	Mus musculus	103-129
33569454-7	2021	In the H2O2-induced 661W cell model, H2O2 increased cellular apoptosis rates, the expression levels of Bcl-2-associated X-protein (BAX) and cleaved caspase 3, reactive oxygen species (ROS) production, and malondialdehyde content, while decreasing the cell viability, and Bcl-2, superoxide dismutase, catalase, and glutathione peroxidase activity.	Hydrogen Peroxide	37-41	BCL2-associated X protein	Mus musculus	131-134
33577037-13	2021	In addition, compared with ITGB3-siRNA group, SB203580 + ITGB3-siRNA group showed significantly upregulated mRNA and protein expressions of Bax, downregulated mRNA and protein expressions of p38MAPK/p-p38MAPK, GSK-3beta/p-GSK-3beta, Cx43/p-Cx43 and Bcl-2, as well as decreased cell proliferation and increased cell apoptosis (all p<0.05).	SB 203580	46-54	BCL2-associated X protein	Mus musculus	140-143
32942336-8	2021	High glucose led to suppressed viability, enhanced apoptosis, reduced Bcl-2 expression, elevated Bax expression and cleavage of Caspase-3/-9 in GC-1 spg cells, and these effects were abrogated by Clusterin overexpression.	Glucose	5-12	BCL2-associated X protein	Mus musculus	97-100
32303879-11	2021	Montelukast mitigated THIM-induced social deficit probably through alpha7nAChRs upregulation, NF-kappaB p65, Bax, and brain injury markers downregulation, thus suppressing THIM-induced neuronal toxicity and inflammation.	montelukast	0-11	BCL2-associated X protein	Mus musculus	109-112
33154094-9	2021	The molecular events associated with the protective effect of quercetin and myricetin were related to the elevated expression of photoreceptor-specific proteins, rhodopsin and cone opsins, decreased expression of the specific inflammatory markers, and the shift of the equilibrium between BAX/BCL-2 towards an anti-apoptotic profile.	Quercetin	62-71	BCL2-associated X protein	Mus musculus	289-292
33357780-13	2021	RESULTS: In vivo, fasudil treatment ameliorated DOX-induced immunofluorescence reaction of DNA damage-related factors (8-OHdG), decreased the expression of Bax, Caspase-3, p16, p21 and p53, and increased the expression of protein of Bcl-2, Bmi-1 and Sirt-1.	fasudil	18-25	BCL2-associated X protein	Mus musculus	156-159
33969676-7	2021	The results showed that the administration of Fasudil improved learning and memory ability, elevated the concentration of antioxidative substances and decreased lipid peroxides, as well as inhibited neuronal apoptosis by increasing the expression of B-cell lymphoma-2 (Bcl-2) (p < 0.05), reducing Bcl-2 Associated X (Bax) (p < 0.05) and cleaved caspase-3 (p < 0.05) of APP/PS1 mice.	fasudil	46-53	BCL2-associated X protein	Mus musculus	297-315
33969676-7	2021	The results showed that the administration of Fasudil improved learning and memory ability, elevated the concentration of antioxidative substances and decreased lipid peroxides, as well as inhibited neuronal apoptosis by increasing the expression of B-cell lymphoma-2 (Bcl-2) (p < 0.05), reducing Bcl-2 Associated X (Bax) (p < 0.05) and cleaved caspase-3 (p < 0.05) of APP/PS1 mice.	fasudil	46-53	BCL2-associated X protein	Mus musculus	317-320
33154094-9	2021	The molecular events associated with the protective effect of quercetin and myricetin were related to the elevated expression of photoreceptor-specific proteins, rhodopsin and cone opsins, decreased expression of the specific inflammatory markers, and the shift of the equilibrium between BAX/BCL-2 towards an anti-apoptotic profile.	myricetin	76-85	BCL2-associated X protein	Mus musculus	289-292
33424608-8	2020	In vivo, IQC administration strikingly reduced cisplatin-induced nephrotoxicity as evidenced by the improvement in renal function (serum creatinine and blood urea nitrogen), kidney histology (PAS staining), apoptotic molecules (cleaved caspase-3, caspase-8, Bax and Bcl-2), inflammatory cytokines (IL-1beta, IL-6, TNF-alpha, and COX-2), oxidative stress (MDA and total glutathione) and p-ERK.	isoquercitrin	9-12	BCL2-associated X protein	Mus musculus	258-261
33342312-0	2022	Nephroprotection through Modifying the Apoptotic TNF-alpha/ERK1/2/Bax Signaling Pathway and Oxidative Stress by Long-term Sodium Hydrosulfide Administration in Ovalbumin-induced Chronic Asthma.	sodium bisulfide	122-141	BCL2-associated X protein	Mus musculus	66-69
33342312-10	2022	The MDA levels and expressions of p-ERK1/2 and Bax were decreased and SOD activity and expressions of Bcl-2 and p-Akt were significantly increased in kidney tissues by NaHS administration.	sodium bisulfide	168-172	BCL2-associated X protein	Mus musculus	47-50
33380391-4	2020	The effect of 3-MA treatment for 24 h on LPS-induced apoptosis of mDPC-23 cells was evaluated by detecting the expressions of apoptosis-related proteins caspase-3 and Bax using Western blotting.	3-methyladenine	14-18	BCL2-associated X protein	Mus musculus	167-170
33380391-7	2020	Treatment with 3-MA markedly lowered caspase-3 and Bax protein expressions in LPS-stimulated cells (P < 0.05).	3-methyladenine	15-19	BCL2-associated X protein	Mus musculus	51-54
33323915-17	2020	The paclitaxel effects were accompanied by inhibition of the inflammatory cytokines, MCP-1, TNF-alpha, TNF-R2, and TLR4, as well as attenuation of the apoptosis markers, Bax, Bcl-2, and Caspase-3.	Paclitaxel	4-14	BCL2-associated X protein	Mus musculus	170-173
32958254-8	2020	The anti-apoptotic activity of ADP355 was indicated by reduction in TUNEL-positive cells and cleaved caspase-3 expression, along with decreased BCL2-associated X protein/B cell lymphoma 2 (BAX/BCL2) levels in heart tissues.	asparaginyl-isoleucyl-prolyl-norvalyl-leucyl-tyrosyl-seryl-phenylalanyl-alanyl-serinamide	31-37	BCL2-associated X protein	Mus musculus	189-192
33103444-5	2020	Compound C, a selective AMPK inhibitor, suppressed cisplatin-induced AMPK activation, p53 phosphorylation, Bax induction and caspase 3 activation.	Cisplatin	51-60	BCL2-associated X protein	Mus musculus	107-110
33363155-7	2020	These findings suggest that inhibition of PDE4D enhances signaling through the cAMP-PKA-SIRT1-Akt -Bcl-2/Bax pathway and thereby may provide therapeutic benefit in neurocognitive disorders.	Cyclic AMP	79-83	BCL2-associated X protein	Mus musculus	105-108
33344474-8	2020	Mice in the heparin intervention group showed decreased levels of EH4, neutrophil gelatinase-associated lipocalin (NAGL), kidney injury molecule-1 (KIM-1), tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-6 in the blood serum, longer average 72-h survival rate, significantly decreased kidney tissue edema, and a clearer glomerular structure coupled with decreased protein and mRNA expression levels of kidney apoptosis-related proteins (cleaved Caspase-3/Caspase-3 and Bax/Bcl-2) compared with those in the sepsis group at 6 h after CLP (P < 0.05).	Heparin	12-19	BCL2-associated X protein	Mus musculus	483-486
32645141-9	2020	Further, roflumilast reversed the decreased ratio of Bcl-2/Bax and the increased expression of PDE4B and PDE4D in the cerebral cortex and hippocampus of AD mice.	Roflumilast	9-20	BCL2-associated X protein	Mus musculus	59-62
33103444-6	2020	Furthermore, silencing AMPK expression by siRNA attenuated cisplatin-induced p53 phosphorylation, Bax induction, and caspase 3 activation.	Cisplatin	59-68	BCL2-associated X protein	Mus musculus	98-101
33103444-8	2020	Taken together, these results suggest that AMPK-p53-Bax signaling pathway plays a crucial role in cisplatin-induced tubular epithelial cell apoptosis.	Cisplatin	98-107	BCL2-associated X protein	Mus musculus	52-55
33045563-8	2020	Moreover, in the renal tissues of LIGHT KO mice, cisplatin-induced mitochondrion injury and the levels of the pro-apoptotic molecules Bax, Cytochrome C (Cyt C), cleaved caspase-3, and cleaved caspase-9 were dramatically increased; in contrast, the expression of anti-apoptotic molecule Bcl-2 was markedly reduced, compared to those in WT mice, suggesting that LIGHT deficiency accelerated cisplatin-induced mitochondrial apoptosis of renal tubular cells in these mice.	Cisplatin	49-58	BCL2-associated X protein	Mus musculus	134-137
32412432-4	2020	Perindopril remarkably ameliorated cisplatin-induced perturbations in renal histology, renal levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-10, apoptosis-regulating protein expressions (Bax and Bcl2), and partially normalized Bax to Bcl2 ratio and active caspase 3 protein expression.	Perindopril	0-11	BCL2-associated X protein	Mus musculus	208-211
32412432-4	2020	Perindopril remarkably ameliorated cisplatin-induced perturbations in renal histology, renal levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-10, apoptosis-regulating protein expressions (Bax and Bcl2), and partially normalized Bax to Bcl2 ratio and active caspase 3 protein expression.	Perindopril	0-11	BCL2-associated X protein	Mus musculus	248-251
32412432-4	2020	Perindopril remarkably ameliorated cisplatin-induced perturbations in renal histology, renal levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-10, apoptosis-regulating protein expressions (Bax and Bcl2), and partially normalized Bax to Bcl2 ratio and active caspase 3 protein expression.	Cisplatin	35-44	BCL2-associated X protein	Mus musculus	208-211
32412432-4	2020	Perindopril remarkably ameliorated cisplatin-induced perturbations in renal histology, renal levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-10, apoptosis-regulating protein expressions (Bax and Bcl2), and partially normalized Bax to Bcl2 ratio and active caspase 3 protein expression.	Cisplatin	35-44	BCL2-associated X protein	Mus musculus	248-251
32266641-8	2020	Additionally, cis-[RuCl(BzCN)(phen)(dppb)]PF6 increased the gene expression of Bax, Casp3, and Tp53 in S180 cells.	cis-[rucl(bzcn)(phen)(dppb)]pf6	14-45	BCL2-associated X protein	Mus musculus	79-82
32920884-8	2020	In contrast, the expression of apoptotic markers including caspase 3, caspase 9 and Bax was increased in the presence of MK801.	Dizocilpine Maleate	121-126	BCL2-associated X protein	Mus musculus	84-87
32768686-13	2020	Irisin significantly increased the proliferation of osteocytes, protected them from apoptosis, and maintained cellular activity by regulating the expression of Bax, Bcl-2, and osteoprotegerin/receptor activator of nuclear factor (NF)-kB-ligand (OPG/Rankl).	irisin	0-6	BCL2-associated X protein	Mus musculus	160-163
32962483-9	2020	Moreover, YHPG significantly down-regulated the mRNA and protein expression of Bax and caspase-3 in lung tissues of mice infected with IFV, and up-regulated the expression of Bcl-2.	yhpg	10-14	BCL2-associated X protein	Mus musculus	79-82
33183976-8	2020	Moreover, taraxasterol treatment remarkably ameliorated apoptosis in the kidney by decreasing Bax expression and conserving Bcl2.	taraxasterol	10-22	BCL2-associated X protein	Mus musculus	94-97
31967706-9	2020	Also, Irb mitigated APAP-induced inflammation in liver tissues via decreasing the expression of hepatic NF-kappaB, phosphorylated NF-kappaB and TNF-alpha, and attenuated hepatic apoptosis via decreasing Bax/Bcl-2 ratio and caspase 3 expression and activation.	irb	6-9	BCL2-associated X protein	Mus musculus	203-206
31967706-9	2020	Also, Irb mitigated APAP-induced inflammation in liver tissues via decreasing the expression of hepatic NF-kappaB, phosphorylated NF-kappaB and TNF-alpha, and attenuated hepatic apoptosis via decreasing Bax/Bcl-2 ratio and caspase 3 expression and activation.	Acetaminophen	20-24	BCL2-associated X protein	Mus musculus	203-206
32892382-6	2020	But, shikonin treatment significantly reduced the expression levels of TNF-alpha, IFN-gamma and Bax.	shikonin	5-13	BCL2-associated X protein	Mus musculus	96-99
32970507-11	2020	RESULTS: Decreased cleaved caspase-3 (1.30 +- 0.09) and Bax/Bcl2 ratio (1.32 +- 0.11) were observed in BV2 cells induced by d-gal + PTM (50 mug/mL).	Galactose	124-129	BCL2-associated X protein	Mus musculus	56-59
33256231-7	2020	Apoptosis by CRS exposure was induced by Bcl-2 and Bax expression regulation and was suppressed by reducing caspase-3 and poly (ADP-ribose) polymerase expression after treatment with the ML extract.	3-cresol	13-16	BCL2-associated X protein	Mus musculus	51-54
33215568-5	2020	The expression of the Bcl-2 gene was upregulated and the expression of Bax, caspase-3, and PARP gene were downregulated when L-arginine was added to the cultured cells.	Arginine	125-135	BCL2-associated X protein	Mus musculus	71-74
33197894-9	2020	We also found that geniposide significantly reduced vascular permeability and cellular apoptosis of the kidney, with increase of Bcl-2 and decrease of Bax and cleaved caspase-3.	geniposide	19-29	BCL2-associated X protein	Mus musculus	151-154
33200710-9	2020	Several mechanisms for the anticancer effects of DMAKO-20 have been identified in B16/F10 melanoma cells, including apoptosis, upregulation of mitochondrial apoptotic Bax proteins and downregulation of anti-apoptotic Bcl-2.	dmako-20	49-57	BCL2-associated X protein	Mus musculus	167-170
32561283-6	2020	Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax.	Fluorouracil	47-51	BCL2-associated X protein	Mus musculus	270-273
32561283-6	2020	Further mechanistic studies indicated that the 5-Fu + SATP group showed a decrease in hepatotoxicity caused by 5-Fu via a reduction in the levels of interleukin-1beta (IL-1beta), an increase in the expression of Bcl-2 and decreases in the expression of p-p38, p-JNK and Bax.	satp	54-58	BCL2-associated X protein	Mus musculus	270-273
33177860-14	2020	Conclusion: Our results demonstrated that MG might protect RAW264.7 cells from S. aureus-induced apoptosis and autophagy via inhibiting JNK/Bax-dependent signal pathway.	mangiferin	42-44	BCL2-associated X protein	Mus musculus	140-143
32964418-7	2020	ATRA mitigated gene expression of markers for damage-associated molecular pattern (DAMP, HMGB1), apoptosis (caspase-3 and Bax), activated microglia (TSPO), and reactive astrogliosis (GFAP, SerpinA3N) at 7 dpi and a subset of markers at 30 dpi (GFAP, TSPO).	Tretinoin	0-4	BCL2-associated X protein	Mus musculus	122-125
32838983-0	2020	Corrigendum to "Mangiferin attenuates MPTP induced dopaminergic neurodegeneration and improves motor impairment, redox balance and Bcl-2/Bax expression in experimental Parkinson"s disease mice" [Chem.	mangiferin	16-26	BCL2-associated X protein	Mus musculus	137-140
32926492-4	2020	Moreover, icariin induced cell apoptosis via a mitochondria-mediated pathway, as indicated by upregulated ratio of Bax/Bcl-2 and ROS induction.	icariin	10-17	BCL2-associated X protein	Mus musculus	115-118
32910486-7	2020	Furthermore, SAL was found to be able to inhibit PA-induced apoptosis that down-regulates cleaved caspase-3 and Bax expressions, while up-regulating Bcl-2 expression and up-regulates the Bcl-2/Bax ratio in glucosamine induced insulin resistance model.	rhodioloside	13-16	BCL2-associated X protein	Mus musculus	112-115
32918989-8	2020	Furthermore, ASX markedly upregulated the expression of Bcl-2 and downregulated the expressions of Fas, FasL, RIPK1, FADD, Bax, Cytochrome C, Caspase-9, Cleaved Caspase-8, Cleaved Caspase-3, RIPK3, MLKL and FLIP in the testis tissues compared with the NF group.	astaxanthine	13-16	BCL2-associated X protein	Mus musculus	123-126
33006132-12	2020	Moreover, downregulation of miR-204-5p inhibited sevoflurane-induced apoptosis and promoted cell proliferation by upregulating the proteins of Bcl-2 and downregulating the expressions of Bax and active caspase-3 in HT22 cells.	Sevoflurane	49-60	BCL2-associated X protein	Mus musculus	187-190
32519758-7	2020	NaAsO2 exposure was associated with marked increases in renal inflammatory marker (interleukin-1beta and tumor necrosis factor-alpha) and apoptosis indicators including Bax and caspase-3 levels contaminant with a marked decrease in Bcl-2, an anti-apoptotic protein, in the NaAsO2- treated group compared with the control group.	sodium arsenite	0-6	BCL2-associated X protein	Mus musculus	169-172
32910486-7	2020	Furthermore, SAL was found to be able to inhibit PA-induced apoptosis that down-regulates cleaved caspase-3 and Bax expressions, while up-regulating Bcl-2 expression and up-regulates the Bcl-2/Bax ratio in glucosamine induced insulin resistance model.	rhodioloside	13-16	BCL2-associated X protein	Mus musculus	193-196
32910486-7	2020	Furthermore, SAL was found to be able to inhibit PA-induced apoptosis that down-regulates cleaved caspase-3 and Bax expressions, while up-regulating Bcl-2 expression and up-regulates the Bcl-2/Bax ratio in glucosamine induced insulin resistance model.	Palmitates	49-51	BCL2-associated X protein	Mus musculus	112-115
32910486-7	2020	Furthermore, SAL was found to be able to inhibit PA-induced apoptosis that down-regulates cleaved caspase-3 and Bax expressions, while up-regulating Bcl-2 expression and up-regulates the Bcl-2/Bax ratio in glucosamine induced insulin resistance model.	Palmitates	49-51	BCL2-associated X protein	Mus musculus	193-196
33100110-8	2022	Moreover, MOR treatment caused a significant increase in bcl-2 expression, and obvious decreases in the expression levels of bax, cleaved caspase-3, and cleaved caspase-9 expression.	morroniside	10-13	BCL2-associated X protein	Mus musculus	125-128
32909914-4	2020	The protein levels of cleaved Caspase-8, cleaved Caspase-3, and Bax markedly increased in the DEHP-treated cells, whereas there was a significant decrease in the Bcl-2 protein level, implying that DEHP could induce apoptosis of mouse HT22 cells.	Diethylhexyl Phthalate	94-98	BCL2-associated X protein	Mus musculus	64-67
32761924-4	2020	Moreover, melatonin therapy suppressed PA-induced apoptosis by modulating apoptosis-associated proteins such as Bcl2, Bax, C-Caspase3, C-Caspase12, and CHOP in type B spermatogonial stem cells.	Melatonin	10-19	BCL2-associated X protein	Mus musculus	118-121
32761924-4	2020	Moreover, melatonin therapy suppressed PA-induced apoptosis by modulating apoptosis-associated proteins such as Bcl2, Bax, C-Caspase3, C-Caspase12, and CHOP in type B spermatogonial stem cells.	Palmitic Acid	39-41	BCL2-associated X protein	Mus musculus	118-121
33107017-8	2021	In addition, Bcl-2 expression was downregulated, and Bax expression was upregulated in Pb-treated group in comparison with the control and Pb + quercetin groups.	Lead	87-89	BCL2-associated X protein	Mus musculus	53-56
33023026-7	2020	In glaucomatous retina, ubiquinol supplementation significantly promoted RGC survival, blocked BAX activation and increased TFAM and OXPHOS complex II protein expression.	ubiquinol	24-33	BCL2-associated X protein	Mus musculus	95-98
33076507-8	2020	Adding eucalyptol to glucose- or Abeta-loaded RPE cells, and diabetic mouse eyes reciprocally reversed induction/activation of apoptosis-related bcl-2, bax, cytochrome C/Apaf-1 and caspases.	Eucalyptol	7-17	BCL2-associated X protein	Mus musculus	152-155
33059700-8	2020	We also found that Gly reversed D-gal-induced neuroapoptosis by significantly reducing the protein expression levels of proapoptotic markers (Bax, cytochrome c, cleaved caspase-3, and cleaved PARP-1) and increasing the protein expression level of the antiapoptotic protein Bcl-2.	Glycine	19-22	BCL2-associated X protein	Mus musculus	142-145
33059700-8	2020	We also found that Gly reversed D-gal-induced neuroapoptosis by significantly reducing the protein expression levels of proapoptotic markers (Bax, cytochrome c, cleaved caspase-3, and cleaved PARP-1) and increasing the protein expression level of the antiapoptotic protein Bcl-2.	Galactose	32-37	BCL2-associated X protein	Mus musculus	142-145
32673631-6	2020	Administration of ASX to mice receiving La2O3 NPs also resulted in decreased expression of iNOS, IL-1beta, TNF-alpha, COX-2, Bax and Caspase-3 and in increased expression of BDNF, NGF and Bcl-2 observed in response to La2O3 NPs.	astaxanthine	18-21	BCL2-associated X protein	Mus musculus	125-128
32495646-8	2020	The BCL-2/Bax ratio significantly increased in the MPTP + EE compared to the MPTP + SC group.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	51-55	BCL2-associated X protein	Mus musculus	10-13
32495646-8	2020	The BCL-2/Bax ratio significantly increased in the MPTP + EE compared to the MPTP + SC group.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	77-81	BCL2-associated X protein	Mus musculus	10-13
32495646-8	2020	The BCL-2/Bax ratio significantly increased in the MPTP + EE compared to the MPTP + SC group.	Scandium	84-86	BCL2-associated X protein	Mus musculus	10-13
32673631-6	2020	Administration of ASX to mice receiving La2O3 NPs also resulted in decreased expression of iNOS, IL-1beta, TNF-alpha, COX-2, Bax and Caspase-3 and in increased expression of BDNF, NGF and Bcl-2 observed in response to La2O3 NPs.	lanthanum oxide	40-45	BCL2-associated X protein	Mus musculus	125-128
32659346-2	2020	Studies from our laboratory show that the intrinsic pathway proapoptotic proteins BAX and caspase-3 (CASP3) lie upstream of mitochondrial production of oxidative stress-inducing reactive species (RS) such as reactive oxygen and reactive nitrogen species (ROS and RNS) in apoptotic and nonapoptotic neurons in cell culture.	Nitrogen	237-245	BCL2-associated X protein	Mus musculus	82-85
32808351-8	2020	Inhibition of mTOR/FOXO1 by rapamycin/AS1842856 decreased the ratio of Bcl-2/Bax and exacerbated TJ protein loss.	Sirolimus	28-37	BCL2-associated X protein	Mus musculus	77-80
32808351-8	2020	Inhibition of mTOR/FOXO1 by rapamycin/AS1842856 decreased the ratio of Bcl-2/Bax and exacerbated TJ protein loss.	5-amino-7-(cyclohexylamino)-1-ethyl-6-fluoro-4-oxo-1,4-dihydroquinoline-3-carboxylic acid	38-47	BCL2-associated X protein	Mus musculus	77-80
32659346-2	2020	Studies from our laboratory show that the intrinsic pathway proapoptotic proteins BAX and caspase-3 (CASP3) lie upstream of mitochondrial production of oxidative stress-inducing reactive species (RS) such as reactive oxygen and reactive nitrogen species (ROS and RNS) in apoptotic and nonapoptotic neurons in cell culture.	ros	255-258	BCL2-associated X protein	Mus musculus	82-85
32659346-2	2020	Studies from our laboratory show that the intrinsic pathway proapoptotic proteins BAX and caspase-3 (CASP3) lie upstream of mitochondrial production of oxidative stress-inducing reactive species (RS) such as reactive oxygen and reactive nitrogen species (ROS and RNS) in apoptotic and nonapoptotic neurons in cell culture.	Radon	263-266	BCL2-associated X protein	Mus musculus	82-85
32705396-7	2020	Additionally, the Bax/Bcl-2 ratio and the levels of cleaved caspase-3 and p53 were markedly lower in the cells cultured in thrombin + melatonin-CM than in the cells cultured in thrombin-CM.	Melatonin	134-143	BCL2-associated X protein	Mus musculus	18-21
32578916-8	2020	Vin administration ameliorated liver injury as indicated by decreased liver injury parameters; serum aminotransferases, ALK-P, GGT, and bilirubin, restored the anti-oxidant status by decrease MDA and NOx , and increased GSH and SOD, inhibited inflammation (IL-6, TNF-alpha, NFkappaB-p65, and iNOS) and apoptosis (Annexin-V, Bax, and Caspase-3) parameters.	vinpocetine	0-3	BCL2-associated X protein	Mus musculus	324-327
33342809-0	2020	Chlorogenic acid inhibits growth of 4T1 breast cancer cells through involvement in Bax/Bcl2 pathway.	Chlorogenic Acid	0-16	BCL2-associated X protein	Mus musculus	83-86
33342809-10	2020	Immunocytochemistry results showed the upregulation of Bax and also the downregulation of Bcl-2 in 4T1 cells treated with chlorogenic acid (P < 0.001).	Chlorogenic Acid	122-138	BCL2-associated X protein	Mus musculus	55-58
33024575-0	2020	Apoptotic stress induces Bax-dependent, caspase-independent redistribution of LINC complex nesprins.	linc	78-82	BCL2-associated X protein	Mus musculus	25-28
32990238-11	2020	In both I-10 and TCAM cells, shikonin treatment significantly down- regulated the expressions of Bax, Bcl-2, cleaved caspase-3, PKM2, GLUT1 and HK2, and up-regulated the expression of autophagy-related protein LC3B (P < 0.05).	shikonin	29-37	BCL2-associated X protein	Mus musculus	97-100
32945516-9	2020	ATX significantly suppressed the LPS-induced increased production of TNF-alpha and IL-6 and suppressed the protein expression levels of BNP, Bax and Bcl-2 to normal levels.	astaxanthine	0-3	BCL2-associated X protein	Mus musculus	141-144
33024575-0	2020	Apoptotic stress induces Bax-dependent, caspase-independent redistribution of LINC complex nesprins.	nesprins	91-99	BCL2-associated X protein	Mus musculus	25-28
33024575-4	2020	We show here that the apoptotic stimuli cisplatin and staurosporine induce a Bax/Bak-dependent degradation and subcellular redistribution of nesprin-1 and nesprin-2 but not nesprin-3, of the linker of nucleoskeleton and cytoskeleton (LINC) complex.	Cisplatin	40-49	BCL2-associated X protein	Mus musculus	77-80
33024575-4	2020	We show here that the apoptotic stimuli cisplatin and staurosporine induce a Bax/Bak-dependent degradation and subcellular redistribution of nesprin-1 and nesprin-2 but not nesprin-3, of the linker of nucleoskeleton and cytoskeleton (LINC) complex.	Staurosporine	54-67	BCL2-associated X protein	Mus musculus	77-80
32589884-11	2020	Meanwhile, 6H2L remarkably up-regulated Bax while suppressing Bcl-2 in tumors.	6h2l	11-15	BCL2-associated X protein	Mus musculus	40-43
31792773-7	2020	Compared with the control group, the protein expression levels of Cav1.2, CaM, and Bax significantly increased, and those of CaMKII and Bcl-2 significantly decreased, the ratio of Bax/Bcl-2 also significantly increased, and the number of apoptotic kidney cells significantly increased in the high/low-fluoride group and in the high/low-fluoride + agonist group.	Fluorides	301-309	BCL2-associated X protein	Mus musculus	180-183
31792773-7	2020	Compared with the control group, the protein expression levels of Cav1.2, CaM, and Bax significantly increased, and those of CaMKII and Bcl-2 significantly decreased, the ratio of Bax/Bcl-2 also significantly increased, and the number of apoptotic kidney cells significantly increased in the high/low-fluoride group and in the high/low-fluoride + agonist group.	Fluorides	336-344	BCL2-associated X protein	Mus musculus	180-183
32390525-7	2020	Apoptotic signaling, measured by Bcl-2/Bax ratio, was significantly increased in the saline group but was mitigated with Na2S.	sodium sulfide	121-125	BCL2-associated X protein	Mus musculus	39-42
32882870-12	2020	FKB+doxorubicin-mediated dysregulated Bax/Bcl-2, Beclin-1/Bcl-2 ratios suggested apoptosis, autophagy induction in AGS cells.	flavokawain B	0-3	BCL2-associated X protein	Mus musculus	38-41
32882870-12	2020	FKB+doxorubicin-mediated dysregulated Bax/Bcl-2, Beclin-1/Bcl-2 ratios suggested apoptosis, autophagy induction in AGS cells.	Doxorubicin	4-15	BCL2-associated X protein	Mus musculus	38-41
32911587-0	2020	Effect of L-carnitine on the expression of the apoptotic genes Bcl-2 and Bax.	Carnitine	10-21	BCL2-associated X protein	Mus musculus	73-76
32911587-4	2020	In this study, we examined the levels of expression of Bcl-2 and Bax in mice treated with formalin and L-carnitine.	Formaldehyde	90-98	BCL2-associated X protein	Mus musculus	65-68
32911587-4	2020	In this study, we examined the levels of expression of Bcl-2 and Bax in mice treated with formalin and L-carnitine.	Carnitine	103-114	BCL2-associated X protein	Mus musculus	65-68
32911587-9	2020	RESULTS: The expression of Bax was significantly higher in the formalin-treated mice than in the mice of the control group, while the expression of Bcl-2 was significantly lower in the formalin-treated mice than in the control mice.	Formaldehyde	63-71	BCL2-associated X protein	Mus musculus	27-30
32911587-10	2020	Additionally, relative to control mice, Bcl-2 expression increased and Bax expression decreased in the mice administered both formalin and L-carnitine.	Formaldehyde	126-134	BCL2-associated X protein	Mus musculus	71-74
32911587-10	2020	Additionally, relative to control mice, Bcl-2 expression increased and Bax expression decreased in the mice administered both formalin and L-carnitine.	Carnitine	139-150	BCL2-associated X protein	Mus musculus	71-74
32911587-11	2020	CONCLUSION: In this study, L-carnitine was shown to augment Bcl-2 expression and to reduce Bax expression, indicating that this compound may inhibit apoptosis.	Carnitine	27-38	BCL2-associated X protein	Mus musculus	91-94
32918616-6	2020	Gossypol significantly induced apoptosis, decreased Bcl2 expression, and increased the protein levels of Bax and the cleaved caspase 3.	Gossypol	0-8	BCL2-associated X protein	Mus musculus	105-108
32656716-12	2020	Moreover, licoricidin decreased the TUNEL positive neurons, downregulated the expression of Cyt-C, cleaved-Caspase-3, cleaved-Caspase-9 and Bax and upregulated the Bcl-2, attenuated cellular apoptosis.	licoricidin	10-21	BCL2-associated X protein	Mus musculus	140-143
33070826-44	2020	45, and the ratio of Bax/Bcl-2 decreased after treatment with myricetin of 100, 200 and 400 mg/kg, which were 2.	myricetin	62-71	BCL2-associated X protein	Mus musculus	21-24
33377708-8	2020	CONCLUSIONS: Bushen Huoxue Recipe can reduce cyclophosphamide-induced apoptosis of testicular spermatogenic cells in mice, which may be associated with its ability of regulating the expressions of Bax and Bcl-2 mRNA and proteins in the testis tissue.	huoxue	20-26	BCL2-associated X protein	Mus musculus	197-200
33377708-8	2020	CONCLUSIONS: Bushen Huoxue Recipe can reduce cyclophosphamide-induced apoptosis of testicular spermatogenic cells in mice, which may be associated with its ability of regulating the expressions of Bax and Bcl-2 mRNA and proteins in the testis tissue.	Cyclophosphamide	45-61	BCL2-associated X protein	Mus musculus	197-200
32868905-9	2021	DL0410 administration upregulated Bcl-2, increased the Bcl-2/Bax ratio and the level of caspase 3 and PARP-1, alleviating neuronal apoptosis.	DL0410	0-6	BCL2-associated X protein	Mus musculus	61-64
31884568-7	2020	Moreover, sevoflurane anaesthesia increased the number of TUNEL-positive cells and the levels of Bax, cleaved caspase 3 and cleaved PARP and reduced Bcl-2 levels in the hippocampus and temporal lobe.	sevoflurane	10-21	BCL2-associated X protein	Mus musculus	97-100
31786295-4	2020	Moreover, DEX-induced increase of Bax, cytochrome c and caspase-3, as well as decrease of Bcl-2, Wnt3, beta-catenin and c-Myc protein expression in MC3T3-E1 cells were also reversed.	Dexamethasone	10-13	BCL2-associated X protein	Mus musculus	34-37
32454054-6	2020	It was found that STZ treatment induced apoptotic and pyroptotic cell death in the hippocampus as evidenced by increases of cleaved caspase 3 positive hippocampal neurons, TUNEL-positive cells, protein levels of p53, Bax, Puma, and the cleaved GSDMD N-terminal fragment, all of which were decreased in NLRP3 deficient mice.	Streptozocin	18-21	BCL2-associated X protein	Mus musculus	217-220
32439493-9	2020	Inhibition of miR-142-5p decreased cytoplasmic Cytochrome C and increased mitochondrial Cytochrome C, reduced cleaved-caspase3 and Bax levels, and elevated Bcl2 in vivo and in vitro.	mir-142-5p	14-24	BCL2-associated X protein	Mus musculus	131-134
31972207-8	2020	Additionally, curcumin reduced the LPS-induced increase in Bax, cleaved-caspase3/caspase 3, p-IkBalpha/IkBalpha, p-p65/p65, p-JNK/JNK, and p-c-JUN/c-JUN protein expression, and increased Bcl2 protein expression in NRK cells.	Curcumin	14-22	BCL2-associated X protein	Mus musculus	59-62
32220594-9	2020	In 5 mM LC-treated group, Bax was down-regulated (P < 0.05) while Bcl-2 was up-regulated (P < 0.001) compared to the untreated group.	Carnitine	8-10	BCL2-associated X protein	Mus musculus	26-29
32048261-13	2020	Bax Bcl-2-associated X protein, Bcl2 B-cell lymphoma 2, MMF Mycophenolate mofetil, Con A Concanavalin A, GSH reduced glutathione, HO-1 Heme oxygenase-1, IL-1beta Interleukin-1beta, IFN-gamma Interferon-gamma, MDA Malondialdehyde, NF-kappaB Nuclear Factor Kappa B, Nrf2 Nuclear factor erythroid 2-related factor 2, NO Nitric Oxide, SOD Superoxide Dismutase, TLR4 Toll-like receptor 4, TNF-alpha tumor necrosis factor-alpha.	Glutathione	117-128	BCL2-associated X protein	Mus musculus	0-3
32048261-13	2020	Bax Bcl-2-associated X protein, Bcl2 B-cell lymphoma 2, MMF Mycophenolate mofetil, Con A Concanavalin A, GSH reduced glutathione, HO-1 Heme oxygenase-1, IL-1beta Interleukin-1beta, IFN-gamma Interferon-gamma, MDA Malondialdehyde, NF-kappaB Nuclear Factor Kappa B, Nrf2 Nuclear factor erythroid 2-related factor 2, NO Nitric Oxide, SOD Superoxide Dismutase, TLR4 Toll-like receptor 4, TNF-alpha tumor necrosis factor-alpha.	Glutathione	117-128	BCL2-associated X protein	Mus musculus	4-30
32080901-0	2020	Targeting MDR-1 gene expression, BAX/BCL2, caspase-3 and Ki-67 by nano-encapsulated imatinib and hesperidin to enhance anticancer activity and ameliorate cardiotoxicity.	Imatinib Mesylate	84-92	BCL2-associated X protein	Mus musculus	33-36
32048261-10	2020	Also, MMF administration significantly decreased Con A-induced increase in the immune-expression of pro-apoptotic Bcl-2-associated X protein (Bax) and markedly increased Con A-induced decrease in the anti-apoptotic B-cell lymphoma 2 protein (Bcl2).	mycophenolate mofetil	6-9	BCL2-associated X protein	Mus musculus	114-140
32048261-10	2020	Also, MMF administration significantly decreased Con A-induced increase in the immune-expression of pro-apoptotic Bcl-2-associated X protein (Bax) and markedly increased Con A-induced decrease in the anti-apoptotic B-cell lymphoma 2 protein (Bcl2).	mycophenolate mofetil	6-9	BCL2-associated X protein	Mus musculus	142-145
32686739-10	2020	Similar to E2, the complex I inhibitor Rotenone decreased osteoclastogenesis by promoting osteoclast progenitor apoptosis via Bak/Bax.	Rotenone	39-47	BCL2-associated X protein	Mus musculus	130-133
32268165-5	2020	DMAMCL treatment also induces apoptosis via the intrinsic apoptotic pathway in HCC cells, which could be blocked by the pan-caspase inhibitor zVAD-fmk and silencing of Bax/Bak or overexpression of Bcl-2.	dimethylaminomicheliolide	0-6	BCL2-associated X protein	Mus musculus	168-171
32733943-5	2020	The outcomes represented that Polyphyllin I promoted A375 cell apoptosis via upregulating Bax level and cleaved caspase-3 level and downregulating Bcl-2 level, inhibited the growth of A375 cells at the G0/G1 phase, and enhanced cell autophagy via regulating the levels of Beclin 1, LC3II, and p62.	polyphyllin I	30-43	BCL2-associated X protein	Mus musculus	90-93
32754039-0	2020	Verification of Resveratrol Inhibits Intestinal Aging by Downregulating ATF4/Chop/Bcl-2/Bax Signaling Pathway: Based on Network Pharmacology and Animal Experiment.	Resveratrol	16-27	BCL2-associated X protein	Mus musculus	88-91
32709024-7	2020	Quercetin can protect against dexamethasone-induced muscle atrophy by regulating the Bax/Bcl-2 ratio at the protein level and abnormal DeltaPsim, which leads to the suppression of apoptosis.	Dexamethasone	30-43	BCL2-associated X protein	Mus musculus	85-88
32679837-8	2020	Further, a significant elevation in mRNA expression and immunostaining for caspase 3 and BAX was detected in mice group treated with DOXY-PNPs.	doxy-pnps	133-142	BCL2-associated X protein	Mus musculus	89-92
32471877-6	2020	We further show that mice that lack the activity-dependent Bax/Bak pathway or caspase-9 similarly exhibit defects in elimination of ipsilateral CS projections, suggesting that the activity-dependent Bax/Bak-caspase-9 pathway is essential for the removal of ipsilateral CS projections.	Cesium	144-146	BCL2-associated X protein	Mus musculus	59-62
32471877-6	2020	We further show that mice that lack the activity-dependent Bax/Bak pathway or caspase-9 similarly exhibit defects in elimination of ipsilateral CS projections, suggesting that the activity-dependent Bax/Bak-caspase-9 pathway is essential for the removal of ipsilateral CS projections.	Cesium	144-146	BCL2-associated X protein	Mus musculus	199-202
32471877-6	2020	We further show that mice that lack the activity-dependent Bax/Bak pathway or caspase-9 similarly exhibit defects in elimination of ipsilateral CS projections, suggesting that the activity-dependent Bax/Bak-caspase-9 pathway is essential for the removal of ipsilateral CS projections.	Cesium	269-271	BCL2-associated X protein	Mus musculus	59-62
32471877-6	2020	We further show that mice that lack the activity-dependent Bax/Bak pathway or caspase-9 similarly exhibit defects in elimination of ipsilateral CS projections, suggesting that the activity-dependent Bax/Bak-caspase-9 pathway is essential for the removal of ipsilateral CS projections.	Cesium	269-271	BCL2-associated X protein	Mus musculus	199-202
32709024-7	2020	Quercetin can protect against dexamethasone-induced muscle atrophy by regulating the Bax/Bcl-2 ratio at the protein level and abnormal DeltaPsim, which leads to the suppression of apoptosis.	Quercetin	0-9	BCL2-associated X protein	Mus musculus	85-88
32952128-5	2020	Also, CuSO4 induced apoptosis, which was accompanied by decreasing Bcl-2, Bcl-xL mRNA expression levels and protein expression levels, and increasing Bax, Bak, cleaved-caspase-3, cleaved-caspase-9 mRNA, and protein expression levels, and Bax/Bcl-2 ratio.	Copper Sulfate	6-11	BCL2-associated X protein	Mus musculus	150-153
32952128-5	2020	Also, CuSO4 induced apoptosis, which was accompanied by decreasing Bcl-2, Bcl-xL mRNA expression levels and protein expression levels, and increasing Bax, Bak, cleaved-caspase-3, cleaved-caspase-9 mRNA, and protein expression levels, and Bax/Bcl-2 ratio.	Copper Sulfate	6-11	BCL2-associated X protein	Mus musculus	238-241
32754039-13	2020	Decreased ATF4, Chop, Bax but increased Bcl-2 proteins and mRNAs expression were determined after resveratrol treatment compared with the control group; lower ATF4, Chop, Bax but higher Bcl-2 proteins and mRNAs expression were found in KD mice than that in WT mice.	Resveratrol	98-109	BCL2-associated X protein	Mus musculus	22-25
32754039-13	2020	Decreased ATF4, Chop, Bax but increased Bcl-2 proteins and mRNAs expression were determined after resveratrol treatment compared with the control group; lower ATF4, Chop, Bax but higher Bcl-2 proteins and mRNAs expression were found in KD mice than that in WT mice.	Resveratrol	98-109	BCL2-associated X protein	Mus musculus	171-174
32754039-14	2020	Additionally, lower relative proteins and mRNAs expression of ATF4, Chop, Bax and higher relative expression of Bcl-2 in KD mice than that in WT mice after resveratrol treatment.	Resveratrol	156-167	BCL2-associated X protein	Mus musculus	74-77
32754039-15	2020	These findings demonstrated that resveratrol substantially inhibited intestinal aging via downregulating ATF4/Chop/Bcl-2/Bax signaling pathway.	Resveratrol	33-44	BCL2-associated X protein	Mus musculus	121-124
31642999-14	2020	The 630-nm laser mediated by hematoporphyrin derivatives can significantly inhibit the growth of human lung adenocarcinoma xenograft tumor in nude mice, the mechanism of which is related to the inhibition of tumor angiogenesis by down-regulating VEGF and HIF-1alpha gene expression, and the promotion of tumor apoptosis by up-regulating Bax, Caspase-3, and down-regulating Bcl-2 gene expression.	Hematoporphyrins	29-44	BCL2-associated X protein	Mus musculus	337-340
32750754-9	2020	Compared with the control group, the miR-124-3p mimic group and si-MEKK3 group had greater cell apoptosis rates and Bax levels, weaker cell proliferation and invasion abilities, slower cell cycle progression, and lower PCNA and Bcl-2 levels (all p < 0.050).	mir-124-3p	37-47	BCL2-associated X protein	Mus musculus	116-119
32443253-8	2020	In addition, arsenite exposure resulted in the up-regulation of ER stress indicator GRP78 and ER stress-related proteins including p-PERK, ATF4, CHOP, calpain2 and cleaved caspases-12, accompanied by the down-regulation of Bcl-2 and up-regulation of Bax and cleaved caspase-3.	arsenite	13-21	BCL2-associated X protein	Mus musculus	250-253
32344356-4	2020	RESULTS: Our findings confirmed that cafestol preconditioning groups could reduce the levels of ALT and AST, alleviate liver pathological damage, suppress the release of inflammation mediators, inhibit the production of pro-apoptosis protein including caspase-3, caspase-9 and Bax, decrease the expression of autophagy-linked protein including Beclin-1 and LC3, increase anti-apoptosis protein Bcl-2, and restrain the activation of ERK and PPARgamma.	cafestol	37-45	BCL2-associated X protein	Mus musculus	277-280
32907306-6	2020	The results found that NMDA can increase the oxidative stress of HT22 cells in a dose-dependent manner, downregulate the expression of miR-382-3p, upregulate the expression of mRNA and protein abundance of ROCK1 and RhoC, increase the expression levels of proapoptotic proteins Bax, Caspase-3, and Caspase-9, increase the apoptosis of HT22 cells, and reduce the activity and survival rate of HT22 cells.	N-Methylaspartate	23-27	BCL2-associated X protein	Mus musculus	278-281
32907306-7	2020	Compared with the NMDA-induced group, the miR-382-3p mimic-transfected HT22 cells increased the expression of miR- 382-3p, reduced the expression of the mRNA and protein abundance of ROCK1 and RhoC, inhibited the expression of proapoptotic proteins Bax, Caspase-3, and Caspase-9, reduced the apoptosis of HT22 cells, and increased the activity and survival rate of HT22 cells.	N-Methylaspartate	18-22	BCL2-associated X protein	Mus musculus	249-252
32617047-9	2020	Consistent with the in vitro data, ginsenoside Mc1 upregulated the levels of catalase and SOD2 and decreased the Bax:B-cell lymphoma-extra large ratio and caspase-3 activity in the heart tissues of HFD-induced obese mice, resulting in reduced collagen deposition.	ginsenoside mc1	35-50	BCL2-associated X protein	Mus musculus	113-116
32714403-0	2020	Antidiabetic Effects of Arginyl-Fructosyl-Glucose, a Nonsaponin Fraction from Ginseng Processing in Streptozotocin-Induced Type 2 Diabetic Mice through Regulating the PI3K/AKT/GSK-3beta and Bcl-2/Bax Signaling Pathways.	Glucose	42-49	BCL2-associated X protein	Mus musculus	196-199
32361189-10	2020	Moreover, the decreased expression of Bcl-xl and Bcl-2 and the increased expression of Bax protein were also blocked by hydrogen treatment.	Hydrogen	120-128	BCL2-associated X protein	Mus musculus	87-90
33308376-9	2020	Expression of p53 and Bax in islet grafts was upregulated in the recipients treated with octreotide one day after islet transplantation, and the octreotide-treated group produced significantly less Bax than the control group on days 3 and 7 following transplantation.	Octreotide	89-99	BCL2-associated X protein	Mus musculus	22-25
33308376-9	2020	Expression of p53 and Bax in islet grafts was upregulated in the recipients treated with octreotide one day after islet transplantation, and the octreotide-treated group produced significantly less Bax than the control group on days 3 and 7 following transplantation.	Octreotide	145-155	BCL2-associated X protein	Mus musculus	22-25
33308376-9	2020	Expression of p53 and Bax in islet grafts was upregulated in the recipients treated with octreotide one day after islet transplantation, and the octreotide-treated group produced significantly less Bax than the control group on days 3 and 7 following transplantation.	Octreotide	145-155	BCL2-associated X protein	Mus musculus	198-201
32438504-9	2020	Further, [6]-gingerol improved ISO-induced morphological pathologies, reduced the expression of TNF-alpha, IL-6, c-fos, c-jun, Bax, Caspase-3, TLR4, NF-kappaB, p38, p-p38, ERK1/2, p-ERK1/2, JNK, and p-JNK, and increased Bcl-2 protein expression.	gingerol	9-21	BCL2-associated X protein	Mus musculus	127-130
32087283-7	2020	In addition, DHT modulated the expression of Abeta, the apoptotic proteins caspase-3, Bcl-2, and Bax, and synaptophysin, as well as neuronal damage in LPS-treated mouse brains.	Dihydrotestosterone	13-16	BCL2-associated X protein	Mus musculus	97-100
31950223-5	2020	Furthermore, pantoprazole mostly normalized cisplatin-induced distortion of renal levels of inflammatory cytokines (tumor necrosis factor-alpha, interleukin-6, interleukin-10) and renal content of apoptosis regulating protein expressions (Bax, Bcl2, and active caspase 3).	pantoprazole	13-25	BCL2-associated X protein	Mus musculus	239-242
32714426-0	2020	Icaritin Improves Memory and Learning Ability by Decreasing BACE-1 Expression and the Bax/Bcl-2 Ratio in Senescence-Accelerated Mouse Prone 8 (SAMP8) Mice.	icaritin	0-8	BCL2-associated X protein	Mus musculus	86-89
31950223-5	2020	Furthermore, pantoprazole mostly normalized cisplatin-induced distortion of renal levels of inflammatory cytokines (tumor necrosis factor-alpha, interleukin-6, interleukin-10) and renal content of apoptosis regulating protein expressions (Bax, Bcl2, and active caspase 3).	Cisplatin	44-53	BCL2-associated X protein	Mus musculus	239-242
31950223-8	2020	The protective mechanism of pantoprazole could be through diminution of cisplatin-induced inflammation, oxidative stress, and their subsequent apoptotic renal cell death via abatement of apoptosis regulating protein expressions (Bax, Bcl2, and active caspase3).	pantoprazole	28-40	BCL2-associated X protein	Mus musculus	229-232
32386222-8	2020	The CPO-A treatment attenuated or restored (P < 0.05) these changes and inhibited (P < 0.05) the MPTP-induced activation of P38 mitogen-activated protein kinase (P38MAPK) and P53, along with the downstream expression of BCL-2 associated X protein (BAX) in the SN.	cpo-a	4-9	BCL2-associated X protein	Mus musculus	220-246
32386222-8	2020	The CPO-A treatment attenuated or restored (P < 0.05) these changes and inhibited (P < 0.05) the MPTP-induced activation of P38 mitogen-activated protein kinase (P38MAPK) and P53, along with the downstream expression of BCL-2 associated X protein (BAX) in the SN.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	97-101	BCL2-associated X protein	Mus musculus	220-246
32386222-11	2020	CONCLUSION: CPO-A protected against MPP+-induced cytotoxicity in SH-SY5Y cells and MPTP-induced neurotoxicity in mice by regulating the P38MAPK/P53/BAX signaling.	cpo-a	12-17	BCL2-associated X protein	Mus musculus	148-151
32636604-9	2020	In addition, TMP rapidly increased the expression of Nrf2 and HO-1 and decreased BAX expression in mice retinas after NaIO3 injection.	tetramethylpyrazine	13-16	BCL2-associated X protein	Mus musculus	81-84
32636604-9	2020	In addition, TMP rapidly increased the expression of Nrf2 and HO-1 and decreased BAX expression in mice retinas after NaIO3 injection.	sodium iodate	118-123	BCL2-associated X protein	Mus musculus	81-84
32571324-8	2020	The data showed that ASP decreased damage to the mitochondrial outer membrane, improved the stabilization of the mitochondrial membrane, and corrected the abnormal levels of ROS and mitochondrial-associated apoptosis proteins, including the Bcl-2/Bax ratio and caspase-3 and caspase-9 expression, in BMNCs which were sorted from the bone marrow cells of AA mice.	Aspartic Acid	21-24	BCL2-associated X protein	Mus musculus	247-250
32625089-8	2020	Additionally, BA induced cell apoptosis via the mitochondria-mediated pathway, as evidenced by cellular induction of reactive oxygen species and upregulated expression of the Bax/Bcl-2 ratio.	baicalin	14-16	BCL2-associated X protein	Mus musculus	175-178
32545262-4	2020	Ursolic acid and 3-O-acetylursolic acid have shown similar GI50 on A375 cells (26 microM vs. 32 microM, respectively) significantly increased both early and late apoptotic populations, activated caspases 3/7 (48-72 h), and enhanced Bax whilst attenuating Bcl-2 expression.	ursolic acid	0-12	BCL2-associated X protein	Mus musculus	232-235
32560430-7	2020	GAS inhibited Pb-induced apoptosis of neurons in hippocampus tissue, as indicated by the decreased levels of pro-apoptotic proteins Bax and cleaved caspase-3.	Lead	14-16	BCL2-associated X protein	Mus musculus	132-135
32545262-4	2020	Ursolic acid and 3-O-acetylursolic acid have shown similar GI50 on A375 cells (26 microM vs. 32 microM, respectively) significantly increased both early and late apoptotic populations, activated caspases 3/7 (48-72 h), and enhanced Bax whilst attenuating Bcl-2 expression.	Acetylursolic acid	17-39	BCL2-associated X protein	Mus musculus	232-235
32427716-6	2020	Furthermore, ICA siginificantly increase the Bcl-2/Bax ratio by increasing the expression of anti-apoptotic protein Bcl-2, and decreasing the expression of pro-apoptotic protein Bax, and thus inhibit neurons apoptosis.	icariin	13-16	BCL2-associated X protein	Mus musculus	51-54
32587830-7	2020	Mechanistically, VC caused a significant increase in the levels of reactive oxygen species (ROS), which led to induced genotoxic (DNA damage) and metabolic (ATP depletion) stresses, inhibited Bcl-2 expression, and promoted Bax expression and caspase-3 cleavage.	Reactive Oxygen Species	67-90	BCL2-associated X protein	Mus musculus	223-226
32587830-7	2020	Mechanistically, VC caused a significant increase in the levels of reactive oxygen species (ROS), which led to induced genotoxic (DNA damage) and metabolic (ATP depletion) stresses, inhibited Bcl-2 expression, and promoted Bax expression and caspase-3 cleavage.	Reactive Oxygen Species	92-95	BCL2-associated X protein	Mus musculus	223-226
32172103-5	2020	Meanwhile, RT-PCR indicated that mercury-exposure significantly increased the expression of pro-apoptotic genes including Bax, JNK, ASK1, caspase3 and TNF-alpha, and significantly decreased the expression of the anti-apoptotic gene Bcl-2.	Mercury	33-40	BCL2-associated X protein	Mus musculus	122-125
32513923-4	2020	When these triple mutant lines were exposed to dexamethasone for 10 days, they arrested, but after dexamethasone was removed, they had 10-fold higher clone forming efficiency than Bax/Bak1 double knock-out cells.	Dexamethasone	47-60	BCL2-associated X protein	Mus musculus	180-183
32511663-5	2020	Upon selenium treatment, the bcl-2 levels were upregulated, while the levels of Bax and cyto-C were down-regulated.	Selenium	5-13	BCL2-associated X protein	Mus musculus	80-83
32427716-6	2020	Furthermore, ICA siginificantly increase the Bcl-2/Bax ratio by increasing the expression of anti-apoptotic protein Bcl-2, and decreasing the expression of pro-apoptotic protein Bax, and thus inhibit neurons apoptosis.	icariin	13-16	BCL2-associated X protein	Mus musculus	178-181
32503738-10	2020	Hence, SGY-P therapy exhibited a protective effect on pancreatic beta-cells by decreasing the expression of cleaved caspase-3, cleaved PARP and Bax, and increasing Bcl-2 by suppressing ER stress (Bip/XBP1/IRE1alpha/CHOP/Caspase-12) and autophagy (LC3/p62/Atg5) pathways.2/Atg5) pathways.	sgy-p	7-12	BCL2-associated X protein	Mus musculus	144-147
32500859-10	2020	In addition, apoptotic cells were visually decreased in the DSS+MRS (10) group, in which the pro-apoptotic molecules Bax and cleaved caspase-3 were reduced, whereas the level of Bcl-2 was increased.	Dextran Sulfate	60-63	BCL2-associated X protein	Mus musculus	117-120
31927655-11	2020	In addition, DEX dramatically prevented sepsis-induced pulmonary cell apoptosis in mice, as reflected by decreases in the number of TUNEL-positive cells, the protein expression of cleaved caspase-9 and cleaved caspase 3 and the Bax/Bcl-2 ratio.	Dexmedetomidine	13-16	BCL2-associated X protein	Mus musculus	228-231
32278510-0	2020	Protective effect of bleomycin on 5-azacitidine induced cytotoxicity and apoptosis in mice hematopoietic stem cells via Bcl-2/Bax and HMGB1 signaling pathway.	Bleomycin	21-30	BCL2-associated X protein	Mus musculus	126-129
32171145-0	2020	Low-dose naltrexone inhibits colorectal cancer progression and promotes apoptosis by increasing M1-type macrophages and activating the Bax/Bcl-2/caspase-3/PARP pathway.	Naltrexone	9-19	BCL2-associated X protein	Mus musculus	135-138
32307890-5	2020	Loganin also showed evident anti-oxidative stress, anti-apoptotic and anti-inflammatory effects on DM-induced reproductive damage by restoring glutathione (GSH) level and superoxide dismutase (SOD) activity, as well as reducing reactive oxygen species (ROS) level and Bax/Bcl-2 ratio in vivo and in vitro.	loganin	0-7	BCL2-associated X protein	Mus musculus	268-271
32278510-0	2020	Protective effect of bleomycin on 5-azacitidine induced cytotoxicity and apoptosis in mice hematopoietic stem cells via Bcl-2/Bax and HMGB1 signaling pathway.	Azacitidine	34-47	BCL2-associated X protein	Mus musculus	126-129
32278510-7	2020	5-AZA significantly downregulated high mobility group Box1 (HMGB1) and Bcl-2 gene expression but upregulated Bax gene expression, while BLM impeded the action of 5-AZA.	Azacitidine	0-5	BCL2-associated X protein	Mus musculus	109-112
32508567-5	2020	Furthermore, inhibition of TLR4 by TAK-242 administration significantly improved neurological function, decreased the level of Bax, and caused a significant reduction in the levels of M1-markers (iNOS and TNFalpha), while the expressions of M2-phenotype markers (Trem-2 and Arg-1) were increased both in vivo and in vitro.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	35-42	BCL2-associated X protein	Mus musculus	127-130
32448237-8	2020	RESULTS: Treatment with AME induced anti-tumor effects against EST as indicated by 1) notable reduction in tumor size; 2) elevation in tissue necrosis and apoptosis, as confirmed histologically; 3) increased DNA fragmentation; 4) decreased expression of the apoptotic genes (p53, Bax and caspase 3), and increased expression of the anti-apoptotic marker Bcl2; 5) significantly upregulated cell cycle regulatory genes Cdc2 and connexin26, and; 6) decreased TNFa levels in tumor tissues.	ame	24-27	BCL2-associated X protein	Mus musculus	280-283
32187955-12	2020	We also observed significantly reduced expression of cleaved Caspase-3 and Bax expression in spinal cord of MitoQ-treated mice with Vin stimulation.	mitoquinone	108-113	BCL2-associated X protein	Mus musculus	75-78
32534357-12	2020	Animal experiments confirmed that EPI significantly alleviated tumor growth in MKN-45 xenograft mice via p53/Bax pathway.	epiberberine	34-37	BCL2-associated X protein	Mus musculus	109-112
32534357-12	2020	Animal experiments confirmed that EPI significantly alleviated tumor growth in MKN-45 xenograft mice via p53/Bax pathway.	mkn-45	79-85	BCL2-associated X protein	Mus musculus	109-112
31918014-15	2020	Western blot analysis shows that 7-HC treatment decreases the level of the anti-apoptotic protein Bcl-2 and increases the level of the pro-apoptotic protein Bax.	7-hydroxycholesterol-3-stearate	33-37	BCL2-associated X protein	Mus musculus	157-160
32499705-9	2020	Compared to the ISO group, the TA group had reduced levels of TLR4, p38, p-p38, NF-kappaB (p65), p-NF-kappaB (p-p65), caspase-3, Bax, and Bcl-2, as well as CK, CK-MB, and LDH.	Tannins	31-33	BCL2-associated X protein	Mus musculus	129-132
32147428-7	2020	Furthermore, curcumin treatment following administration of the DHEA resulted in a significant decrease in BAX (p < 0.001) and levels of expression of Caspase3 (CASP3) protein, increased levels of B-cell lymphoma 2 (Bcl2) expression (p < 0.05), and moderated apoptosis in granulosa cells in comparison with the ones seen in the PCOS group.	Curcumin	13-21	BCL2-associated X protein	Mus musculus	107-110
32147428-7	2020	Furthermore, curcumin treatment following administration of the DHEA resulted in a significant decrease in BAX (p < 0.001) and levels of expression of Caspase3 (CASP3) protein, increased levels of B-cell lymphoma 2 (Bcl2) expression (p < 0.05), and moderated apoptosis in granulosa cells in comparison with the ones seen in the PCOS group.	Dehydroepiandrosterone	64-68	BCL2-associated X protein	Mus musculus	107-110
32385796-9	2021	Western blot demonstrated that the expression of Bax, LC3II, P62 and KIF3B proteins were elevated, and the expression of Bcl-2 and DIC proteins were reduced in the sevoflurane group.	Sevoflurane	164-175	BCL2-associated X protein	Mus musculus	49-52
30810974-11	2020	Moreover, BBP treatment remarkably suppressed the STAT3 phosphorylation and modulated the expression of critical target genes including Bcl-2, Bax, Cyclin D1, CDK4 and VEGF-A in HCC mice.	bbp	10-13	BCL2-associated X protein	Mus musculus	143-146
32333598-11	2020	The levels of p-JNK and cleaved caspase-3 levels were significantly reduced in astrocytes treated with MPP+ following pre-treatment with 2-aminoquinoline, which also reversed the increase in the Bax/Bcl-2 ratio.	mangion-purified polysaccharide (Candida albicans)	103-107	BCL2-associated X protein	Mus musculus	195-198
32143102-6	2020	Western blot analysis suggested chlorogenic acid could rescue the up-regulated apoptosis of GCs induced by ZEA via attenuating the protein expression of cleaved caspase-3, the ratio of Bax/Bcl-2 and cleaved-PARP.	Chlorogenic Acid	32-48	BCL2-associated X protein	Mus musculus	185-188
32068067-5	2020	PQQ and PQQE induced apoptosis involving increase of Bax, decrease of Bcl-2, release of mitochondrial cytochrome C into the cytosol, activation of caspase-3 and cleavage of PARP.	PQQ Cofactor	0-3	BCL2-associated X protein	Mus musculus	53-56
32333598-11	2020	The levels of p-JNK and cleaved caspase-3 levels were significantly reduced in astrocytes treated with MPP+ following pre-treatment with 2-aminoquinoline, which also reversed the increase in the Bax/Bcl-2 ratio.	2-AMINOQUINOLINE	137-153	BCL2-associated X protein	Mus musculus	195-198
32333598-12	2020	CONCLUSIONS In the mouse model of MPTP-induced PD, 2-aminoquinoline reduced motor deficiencies, inhibited MPP+ activated astrocyte apoptosis, and regulated the Bax/Bcl-2 ratio by targeting p-JNK.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	34-38	BCL2-associated X protein	Mus musculus	160-163
32333598-12	2020	CONCLUSIONS In the mouse model of MPTP-induced PD, 2-aminoquinoline reduced motor deficiencies, inhibited MPP+ activated astrocyte apoptosis, and regulated the Bax/Bcl-2 ratio by targeting p-JNK.	2-AMINOQUINOLINE	51-67	BCL2-associated X protein	Mus musculus	160-163
32368137-9	2020	Conclusion: All in all, miR-29b-3p can reverse the cisplatin resistance of A549/DDP cells by inhibiting the expression of COL1A1 gene and increasing the expression of PTEN and BAX.	Cisplatin	51-60	BCL2-associated X protein	Mus musculus	176-179
32368014-7	2020	Upregulated Bcl-2 and downregulated Bax were observed in propofol-treated HT-22 cells following metformin administration.	Propofol	57-65	BCL2-associated X protein	Mus musculus	36-39
32368014-7	2020	Upregulated Bcl-2 and downregulated Bax were observed in propofol-treated HT-22 cells following metformin administration.	Metformin	96-105	BCL2-associated X protein	Mus musculus	36-39
32306006-13	2020	In addition, the Fei-Liu-Ping ointment + cyclophosphamide group"s cell apoptosis increased significantly compared with saline group and there were significant differences on expressions of HIF-1alpha, Bcl-2, Bax, Caspase-3, IL-2 for this group compared with saline group.	Cyclophosphamide	41-57	BCL2-associated X protein	Mus musculus	208-211
31960547-8	2020	Important markers for cancer progression (Bcl-2, Bax, NF-kB, and intratumor antioxidants) demonstrated that liposomal simvastatin might sensitize C26 cells to liposomal 5-fluorouracil administration in both regimens tested.	Simvastatin	118-129	BCL2-associated X protein	Mus musculus	49-52
32268299-8	2020	In addition, western blot results (Bcl-2, Bax and Caspase-3, NLRP3, IL-18, IL-1beta) showed that spermidine and spermine prevented apoptosis and inflammation, and elevate the expression of neurotrophic factors, including NGF, PSD95and PSD93 and BDNF in neurons of SAMP8 mice.	Spermidine	97-107	BCL2-associated X protein	Mus musculus	42-45
32268299-8	2020	In addition, western blot results (Bcl-2, Bax and Caspase-3, NLRP3, IL-18, IL-1beta) showed that spermidine and spermine prevented apoptosis and inflammation, and elevate the expression of neurotrophic factors, including NGF, PSD95and PSD93 and BDNF in neurons of SAMP8 mice.	Spermine	112-120	BCL2-associated X protein	Mus musculus	42-45
31939088-10	2020	Mice treated with GW0742 showed significantly less severe behavioral deficits compared to the control group, accompanied by increased expression of PPAR-beta/delta and Bcl-2, and increased expression of IL-1beta, TNF-alpha, and Bax decreased simultaneously in the GW0742-treated group.	GW0742	18-24	BCL2-associated X protein	Mus musculus	228-231
32049549-8	2020	Mechanistically, pretreatment using nicotinamide (NIC) recovered the AKT activation level and decreased the BAX/BCL-2 ratio.	Niacinamide	36-48	BCL2-associated X protein	Mus musculus	108-111
32049549-8	2020	Mechanistically, pretreatment using nicotinamide (NIC) recovered the AKT activation level and decreased the BAX/BCL-2 ratio.	Niacinamide	50-53	BCL2-associated X protein	Mus musculus	108-111
32061868-7	2020	Moreover, melatonin decreased BAX expression and increased BCL-2 expression (P < 0.05).	Melatonin	10-19	BCL2-associated X protein	Mus musculus	30-33
31933141-11	2020	Intrahippocampally injected antagomir of miR-106a also increased LIMK1 and Bcl-2 levels, decreased the BAX and cleaved caspase3 expression levels in the mice treated with isoflurane.	Isoflurane	171-181	BCL2-associated X protein	Mus musculus	103-106
32256652-13	2020	The antiapoptosis effect of EPS was through reversing apoptotic proteins such as BAX, Caspase-9 and Caspase-3, and Bcl-2.	eps	28-31	BCL2-associated X protein	Mus musculus	81-84
31935479-7	2020	Bax inhibitor peptide V5 rescued 1,2-DCE-induced HCGC apoptosis.	ethylene dichloride	33-40	BCL2-associated X protein	Mus musculus	0-3
32219583-9	2020	KPF attenuated the Cisplatin mediated apoptosis via down-regulating the levels of TP53, Bax/Bcl2 imbalance, activating caspase-3/9 and PARP.	Cisplatin	19-28	BCL2-associated X protein	Mus musculus	88-91
32265701-13	2020	The cellular experiments showed that HD-SB significantly induced cancer cell apoptosis, decreased p-EGFR, HSP90 and bcl-2 expressions, and increased PPARgamma, bax, cleaved caspase 3, cleaved PARP, p-AKT, and p-PI3K expressions compared with HD or SB treatment.	Antimony	40-42	BCL2-associated X protein	Mus musculus	160-163
31808042-4	2020	Linagliptin up-regulated the expression of p-Akt and p-mTOR and regulated the apoptosis factors Bcl-2, Bax, and caspase 9.	linagliptin	0-11	BCL2-associated X protein	Mus musculus	103-106
32218573-7	2020	Probenecid treatment also decreased apoptosis as evidenced by an increase in the level of Bcl-2/Bax.	Probenecid	0-10	BCL2-associated X protein	Mus musculus	96-99
31855734-9	2020	Moreover, in vivo validation studies suggested that the protein expression levels of PTEN, p-AKT, p53, and BAX were indeed regulated in the mouse liver after high-dose FMT administration, indicating hepatocyte apoptosis may be mediated by these three pathways mentioned above.	fmt	168-171	BCL2-associated X protein	Mus musculus	107-110
32210821-7	2020	Administration of recombinant FGF21 to cisplatin-induced AKI mice resulted in significantly decreased blood urea nitrogen (BUN) and serum creatinine levels, as well as significantly reduced protein levels of kidney injury molecule-1 (TIM-1), C-caspase 3, and Bax.	Cisplatin	39-48	BCL2-associated X protein	Mus musculus	259-262
32210821-9	2020	Experiments with an AKI cell model (cisplatin-treated HK-2 cells) yielded similar results as the mouse model; recombinant FGF21 significantly downregulated protein expression levels of TIM-1, C-caspase 3, and Bax.	Cisplatin	36-45	BCL2-associated X protein	Mus musculus	209-212
32143316-6	2020	As an antigen-specific monotherapy, ADi-100 is highly efficacious in reversing elevated hyperglycemia to prevent diabetes, in which increasing apoptosis-inducing BAX content is a promising immune tolerance feature.	adi-100	36-43	BCL2-associated X protein	Mus musculus	162-165
32190177-10	2020	ASX played a protective role by changing the expression of Keap1, Nrf2, HO-1, Bax, Bcl-2, Caspase3, and Caspase9 proteins.	astaxanthine	0-3	BCL2-associated X protein	Mus musculus	78-81
32355829-8	2020	Morphine inhibits the expression of NF-kappaB, Bcl-2, cyclind1, and VEGF while enhancing the expression of Bax in the tumors.	Morphine	0-8	BCL2-associated X protein	Mus musculus	107-110
31774600-6	2020	Also, significant upregulation of Bcl-2 and LC3B expressions, with the downregulation of p62, Bax and caspase-3 expressions were found in TP-treated group.	triptolide	138-140	BCL2-associated X protein	Mus musculus	94-97
32373202-4	2020	Chronic exposure to excess iron induced epithelial-mesenchymal transition (EMT) in normal and cancer cell lines, loss of p53, and suppression of p53 transcriptional activity evidenced from decreased expression of p53 target genes (p21, cyclin D1, Bax, SLC7A11).	Iron	27-31	BCL2-associated X protein	Mus musculus	247-250
32059119-8	2020	Moreover, KMUP-3 attenuated VSMC apoptosis with an increased Bcl-2/Bax ratio and reduced activated caspase-3 expression.	KMUP 1	10-16	BCL2-associated X protein	Mus musculus	67-70
32515175-8	2020	Administration of the antagonist SANT-1 inhibited Shh signaling pathway activity by increasing the expression of Bcl-2 and Bax, and the number of apoptotic cells increased.	SANT-1	33-39	BCL2-associated X protein	Mus musculus	123-126
31978253-12	2020	Strength exercise decreased Bax/Bcl2 ratio in the hippocampus of STZ-injected mice.	Streptozocin	65-68	BCL2-associated X protein	Mus musculus	28-31
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Lead	98-100	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	103-105	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Diethylhexyl Phthalate	107-110	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Lead	114-116	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Diethylhexyl Phthalate	119-122	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	126-128	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Diethylhexyl Phthalate	119-122	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Lead	114-116	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	126-128	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Diethylhexyl Phthalate	119-122	BCL2-associated X protein	Mus musculus	80-83
32016459-12	2020	To explore the molecular basis of this response, the effect of LiCl on the expression of Bax, p53 and Survivin, which are proteins involved in the apoptotic mechanism and in death escape, was analyzed.	Lithium Chloride	63-67	BCL2-associated X protein	Mus musculus	89-92
31767147-9	2020	AM + rutin (100 mg/kg body weight) significantly decreased bax, p53, CCR and increased bcl-2 expression.	Rutin	5-10	BCL2-associated X protein	Mus musculus	59-62
32776015-0	2020	A small-molecule allosteric inhibitor of BAX protects against doxorubicin-induced cardiomyopathy.	Doxorubicin	62-73	BCL2-associated X protein	Mus musculus	41-44
32776015-2	2020	Here we show that BAX is rate-limiting in doxorubicin-induced cardiomyopathy and identify a small-molecule BAX inhibitor that blocks both apoptosis and necrosis to prevent this syndrome.	Doxorubicin	42-53	BCL2-associated X protein	Mus musculus	18-21
32776015-6	2020	This study identifies BAX as an actionable target for doxorubicin-induced cardiomyopathy and provides a prototype small-molecule therapeutic.	Doxorubicin	54-65	BCL2-associated X protein	Mus musculus	22-25
31989218-8	2020	In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio.	celastrol	20-29	BCL2-associated X protein	Mus musculus	173-176
32116763-7	2020	Western blot analysis revealed that levels of Bax and cleaved-caspase 3 proteins were markedly up-regulated in PFOA-treated groups.	perfluorooctanoic acid	111-115	BCL2-associated X protein	Mus musculus	46-49
31989218-8	2020	In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio.	celastrol	34-43	BCL2-associated X protein	Mus musculus	173-176
31989218-8	2020	In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio.	Metformin	46-55	BCL2-associated X protein	Mus musculus	173-176
31957180-4	2020	Moreover, APP-AW, S1, S2 and S3 rescued DEX-induced increase of Bax, cytochrome c and caspase-3 and decrease of Bcl-2, Wnt3, beta-catenin and c-Myc protein expression in MC3T3-E1 cells.	Sulfur	18-20	BCL2-associated X protein	Mus musculus	64-67
32172946-7	2020	Furthermore, DP pretreatment could inhibit the apoptosis of liver cells caused by APAP through up-regulation of Bcl-2 and down-regulation of Bax and caspase-9 protein.	dp	13-15	BCL2-associated X protein	Mus musculus	141-144
31900639-11	2020	Up-regulation of SIRT1 by RSV significantly inhibited RGCs apoptosis, increased p-Akt level, decreased Bax and cleaved caspase-3 expressions, and all these effects were diminished by 100 muM sirtinol.	resveratrol	26-29	BCL2-associated X protein	Mus musculus	103-106
31900639-11	2020	Up-regulation of SIRT1 by RSV significantly inhibited RGCs apoptosis, increased p-Akt level, decreased Bax and cleaved caspase-3 expressions, and all these effects were diminished by 100 muM sirtinol.	sirtinol	191-199	BCL2-associated X protein	Mus musculus	103-106
31809801-5	2020	Moreover, VERU-111 treatment induced apoptosis and modulated the expression of Bid, Bcl-xl, Survivin, Bax, Bcl2 and cleavage in PARP.	R 111	10-18	BCL2-associated X protein	Mus musculus	102-105
32005098-5	2020	Tumors from mice treated with stampidine or stampidine plus paclitaxel displayed unique changes of a signature protein cassette comprised of BRCA1, p21, Bax, and Bcl-2.Conclusion: Stampidine has potent chemopreventive activity and is as effective as the standard chemotherapy drug paclitaxel in the chemical carcinogenesis model of DMBA-induced murine breast cancer.	stampidine	30-40	BCL2-associated X protein	Mus musculus	153-156
32005098-5	2020	Tumors from mice treated with stampidine or stampidine plus paclitaxel displayed unique changes of a signature protein cassette comprised of BRCA1, p21, Bax, and Bcl-2.Conclusion: Stampidine has potent chemopreventive activity and is as effective as the standard chemotherapy drug paclitaxel in the chemical carcinogenesis model of DMBA-induced murine breast cancer.	stampidine	44-54	BCL2-associated X protein	Mus musculus	153-156
32005098-5	2020	Tumors from mice treated with stampidine or stampidine plus paclitaxel displayed unique changes of a signature protein cassette comprised of BRCA1, p21, Bax, and Bcl-2.Conclusion: Stampidine has potent chemopreventive activity and is as effective as the standard chemotherapy drug paclitaxel in the chemical carcinogenesis model of DMBA-induced murine breast cancer.	Paclitaxel	60-70	BCL2-associated X protein	Mus musculus	153-156
31957180-4	2020	Moreover, APP-AW, S1, S2 and S3 rescued DEX-induced increase of Bax, cytochrome c and caspase-3 and decrease of Bcl-2, Wnt3, beta-catenin and c-Myc protein expression in MC3T3-E1 cells.	dextran methacylate phthalate	40-43	BCL2-associated X protein	Mus musculus	64-67
31778727-7	2020	Moreover, tan IIA induced an up-regulation of the Bcl-2/Bax ratio and down-regulation of caspase-3 protein activity.	2-amino-3-(2,5-dihydro-5-oxo-4-isoxazolyl)propanoic acid	10-13	BCL2-associated X protein	Mus musculus	56-59
31820315-12	2020	Moreover, NaAsO2 triggered apoptosis in the liver by upregulating Bax and caspase-3 and downregulating Bcl-2.	Sodium	10-16	BCL2-associated X protein	Mus musculus	66-69
32099340-12	2020	Conclusion: Anwulignan can restore the immune function that is declined in D-gal-induced aging mice partly related to its antioxidant capacity by activating the Nrf2/ARE pathway and downstream enzymes, as well as its anti-apoptotic effect by regulating Caspase-3 and the ratio of Bcl2 to Bax in the spleen.	macelignan	12-22	BCL2-associated X protein	Mus musculus	288-291
31770577-8	2020	Results showed that PA significantly increased ROS generation and the levels of pro-apoptotic protein Bax, and decreased the levels of anti-apoptotic protein Bcl-2 and the mRNA expression and secretion of endothelin-1.	Palmitic Acid	20-22	BCL2-associated X protein	Mus musculus	102-105
31785598-7	2020	Intravenous U46619 significantly decreased renal microcirculation and enhanced gp91 and Bax/Bcl-2 in WT and TXS-/- but not TP-/- in dKO mice.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	12-18	BCL2-associated X protein	Mus musculus	88-91
31673950-0	2020	BAX-Depleted Retinal Ganglion Cells Survive and Become Quiescent Following Optic Nerve Damage.	Retinaldehyde	13-20	BCL2-associated X protein	Mus musculus	0-3
31673950-6	2020	The competency of quiescent RGCs to reactivate their BAX activation mechanism was tested by intravitreal injection of the JNK pathway agonist, anisomycin.	Anisomycin	143-153	BCL2-associated X protein	Mus musculus	53-56
32099340-12	2020	Conclusion: Anwulignan can restore the immune function that is declined in D-gal-induced aging mice partly related to its antioxidant capacity by activating the Nrf2/ARE pathway and downstream enzymes, as well as its anti-apoptotic effect by regulating Caspase-3 and the ratio of Bcl2 to Bax in the spleen.	Galactose	75-80	BCL2-associated X protein	Mus musculus	288-291
32012916-7	2020	Selenium treatment significantly attenuated the CHS- or thapsigargin (Tg, an ER stress activator)-induced apoptosis, potentiation of caspase 3 activity, and the increased protein expression levels of BAX, GRP78, and CHOP.	Selenium	0-8	BCL2-associated X protein	Mus musculus	200-203
32012916-7	2020	Selenium treatment significantly attenuated the CHS- or thapsigargin (Tg, an ER stress activator)-induced apoptosis, potentiation of caspase 3 activity, and the increased protein expression levels of BAX, GRP78, and CHOP.	Thapsigargin	56-68	BCL2-associated X protein	Mus musculus	200-203
31998440-12	2020	Besides, THSG exerted antiapoptosis function by upregulating the level of Bcl-2 and downregulating the levels of BAX and caspase-3 in the hippocampi.	puag-haad	9-13	BCL2-associated X protein	Mus musculus	113-116
32012916-7	2020	Selenium treatment significantly attenuated the CHS- or thapsigargin (Tg, an ER stress activator)-induced apoptosis, potentiation of caspase 3 activity, and the increased protein expression levels of BAX, GRP78, and CHOP.	Thapsigargin	70-72	BCL2-associated X protein	Mus musculus	200-203
31998441-10	2020	Additionally, serotonin promoted hepatocyte apoptosis and autophagy based on B-cell lymphoma-2 (Bcl-2), Bcl-2-asociated X protein (Bax), and Beclin-1 levels and TUNEL staining.	Serotonin	14-23	BCL2-associated X protein	Mus musculus	104-129
31874178-6	2020	Expressions of apoptosis-related proteins including bax, cyt-c, and caspase-9 were significantly up-regulated by exposure to 2.5, 5, 10, or 20 mug MC-LR/mL.	cyanoginosin LR	147-152	BCL2-associated X protein	Mus musculus	52-55
31593881-7	2020	BPA also increased the relative expression of caspase-7, caspase-9, bax, inhibited the relative expression of bcl-2 in F1 females at both PND 21 and 56, and increased the apoptosis rate in the ovaries in F1 mice at PND 56 (P < 0.01).	bisphenol A	0-3	BCL2-associated X protein	Mus musculus	68-71
31998441-10	2020	Additionally, serotonin promoted hepatocyte apoptosis and autophagy based on B-cell lymphoma-2 (Bcl-2), Bcl-2-asociated X protein (Bax), and Beclin-1 levels and TUNEL staining.	Serotonin	14-23	BCL2-associated X protein	Mus musculus	131-134
32990004-6	2020	RESULTS: Memantine altered the Bcl-2, Bax, Casp3, Casp-9 apoptotic protein expression levels.	Memantine	9-18	BCL2-associated X protein	Mus musculus	38-41
33327914-10	2020	Western blot analysis revealed that DHA notably down-regulated the protein expression of full length caspase-3, cleaved caspase-3 and Bax.	Dihydroalprenolol	36-39	BCL2-associated X protein	Mus musculus	134-137
32055597-10	2020	With the administration of EA after ICH, the expression of Bcl-2 was upregulated while the Bax level was downregulated.	echinocystic acid	27-29	BCL2-associated X protein	Mus musculus	91-94
33480238-9	2020	Furthermore, amifostine suppressed neuronal apoptosis, accompanied by the reduction of Bax, cleaved caspase-9, cleaved caspase-3, and Bcl-2 upregulation.	Amifostine	13-23	BCL2-associated X protein	Mus musculus	87-90
31749326-8	2020	In addition, PPAR-gamma was up-regulated by ACART and inhibition of PPAR-gamma abolished the regulatory effects of ACART on cell apoptosis and the expression of Bcl-2, Bax and Cyt-C under H2 O2 treatment.	Water	188-193	BCL2-associated X protein	Mus musculus	168-171
31643023-8	2020	Moreover, the expression of anti-apoptotic protein Bcl-2 was increased, whereas the expression of pro-apoptotic protein Bax was decreased by Dex.	Dexmedetomidine	141-144	BCL2-associated X protein	Mus musculus	120-123
31929757-7	2020	Besides, 25-HC also inhibited the Bax/Bcl-2 ratio and the relative expression of cleaved caspase-3.	25-hydroxycholesterol	9-14	BCL2-associated X protein	Mus musculus	34-37
31566301-6	2020	Moreover, TOCP administration induced placental apoptosis and autophagy by upregulating P53, Bax, Beclin-1, ratio of LC3 II/LC3 I and Atg5 and downregulating Bcl-2 protein.	tri-o-cresyl phosphate	10-14	BCL2-associated X protein	Mus musculus	93-96
32749127-4	2020	We determined experimentally that naringin pretreatment prevents UVB-induced nuclear fragmentation in NIH-3T3 cells, as well as altering UVB-induced apoptotic marker (Bax, BCl-2, Caspase-9, and Caspase-3) expression in them.	naringin	34-42	BCL2-associated X protein	Mus musculus	167-170
31663764-6	2019	We also found that Tf-CT-MEs inhibited tumor cell proliferation, enhanced antiangiogenesis, and induced apoptosis by regulating bax/bcl-2 and the activating caspase-3 pathway.	2-(N-morpholino)ethanesulfonic acid	25-28	BCL2-associated X protein	Mus musculus	128-131
31760035-6	2020	NAS treatment decreased TBI-induced cell death and apoptosis activation (detected by propidium iodide labeling, TUNEL staining, blots for Bcl-2, Bax and caspase-3).	N-acetylserotonin	0-3	BCL2-associated X protein	Mus musculus	145-148
32314723-10	2020	Compared with the CoCl2 group, Res up-regulated the expression of Bcl2 and down-regulated the expression of BAX, cleaved caspase-3 and HIF-1alpha.	cobaltous chloride	18-23	BCL2-associated X protein	Mus musculus	108-111
31445131-7	2019	Besides, the measurement of the effects of TGP treatment on the expressions level of TH, DAT, a-synuclein, p-CREBS133 as well as apoptosis influence was made with the help of western-blot assay with apoptosis-related markers such as Bax and Bcl-2.	tgp	43-46	BCL2-associated X protein	Mus musculus	233-236
31878204-8	2019	These results indicated that hyperoside acted as an anticancer drug through ROS-related apoptosis and its mechanism included activation of the Bax-caspase-3 axis and the inhibition of the NF-kappaB signaling pathway.	hyperoside	29-39	BCL2-associated X protein	Mus musculus	143-146
31445131-11	2019	Besides, TGP treatment helped reversed apoptosis signaling molecules Bcl-2/Bax" reduction; meanwhile improving p-CREBS133 the factor of growth signaling in the substantia nigra" decrease.	tgp	9-12	BCL2-associated X protein	Mus musculus	75-78
31571510-0	2019	Taraxasterol from Taraxacum prevents concanavalin A-induced acute hepatic injury in mice via modulating TLRs/NF-kappaB and Bax/Bc1-2 signalling pathways.	taraxasterol	0-12	BCL2-associated X protein	Mus musculus	123-126
31792327-9	2019	SAL down-regulated the expression levels of TNF-alpha, TGF-beta1, IL-1beta, Bax and up-regulate the expression of Bcl-2, VEGF, Akt and eNOS.	rhodioloside	0-3	BCL2-associated X protein	Mus musculus	76-79
31571510-7	2019	Furthermore, taraxasterol dramatically down-regulated the expressions of T toll-like receptor (TLR2), TLR4 and nuclear factor-kappaappaB (NF-kappaB) p65, and decreased the expression ratio of Bax/Bc1-2 in hepatic tissues.	taraxasterol	13-25	BCL2-associated X protein	Mus musculus	192-195
31571510-8	2019	These findings suggest that taraxasterol prevents Con A-induced acute hepatic injury in mice by inhibiting TLRs/NF-kappaB inflammatory signalling pathway and promoting Bax/Bc1-2 anti-apoptotic signalling pathway.	taraxasterol	28-40	BCL2-associated X protein	Mus musculus	168-171
31159590-9	2019	Importantly, we found that treatment with anagliptin suppressed the mitochondrial-dependent apoptosis pathway by preventing the translocation of cytochrome C, reducing cleavage of caspase-3, and the inhibiting expression of Bax.	anagliptin	42-52	BCL2-associated X protein	Mus musculus	224-227
31563530-7	2019	PCB126 could increase protein expression of Bax, Caspase-3, Caspase-8 and Caspase-9, while the protein expression of Bcl-2 was decreased.	3,4,5,3',4'-pentachlorobiphenyl	0-6	BCL2-associated X protein	Mus musculus	44-47
31639616-7	2019	In addition, MNA treatment suppressed neuronal apoptosis by reducing the number of TUNEL-positive cells, caspase-3 activation and increasing the level of Bcl-2/Bax ratio in the hippocampus and frontal cortex.	N(1)-methylnicotinamide	13-16	BCL2-associated X protein	Mus musculus	160-163
31539617-4	2019	Fisetin inhibited Pb-induced the apoptotic neurodegeneration, as indicated by the decreased levels of Bax and cleaved caspase-3.	fisetin	0-7	BCL2-associated X protein	Mus musculus	102-105
31539617-4	2019	Fisetin inhibited Pb-induced the apoptotic neurodegeneration, as indicated by the decreased levels of Bax and cleaved caspase-3.	Lead	18-20	BCL2-associated X protein	Mus musculus	102-105
31689375-7	2019	Both in diabetic mice and in cultured hippocampal neurons exposed to high glucose, inhibition of Cdk5 activity with roscovitine (Ros) or short hairpin RNA (shRNA) decreased the protein levels of cleaved caspase-3 and the ratio of Bax and Bcl-2.	roscovitine	129-132	BCL2-associated X protein	Mus musculus	230-233
31735662-9	2019	Propofol markedly reduced hepatocyte apoptosis, decreased Bax, Bad, cleaved caspase-3 and increased Bcl-2 expression.	Propofol	0-8	BCL2-associated X protein	Mus musculus	58-61
31839033-0	2019	[BAX Gene Deletion Reduces the Sensitivity of BCR-ABL-Induced B-ALL Cells of Mice to Imatinib].	Imatinib Mesylate	85-93	BCL2-associated X protein	Mus musculus	1-4
32699841-10	2019	Moreover, DOX caused a 49% decline in cardiac BCL2/BAX expression, which was restored with RIPC (p < 0.05 vs. DOX).	Doxorubicin	10-13	BCL2-associated X protein	Mus musculus	51-54
31779213-8	2019	Furthermore, BA relieved testicular injury and reduced the number of apoptotic cells, and it significantly decreased the protein expression of Janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), caspsae-3, and Bcl-2-associated X protein (Bax).	betulinic acid	13-15	BCL2-associated X protein	Mus musculus	243-269
31779213-8	2019	Furthermore, BA relieved testicular injury and reduced the number of apoptotic cells, and it significantly decreased the protein expression of Janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), caspsae-3, and Bcl-2-associated X protein (Bax).	betulinic acid	13-15	BCL2-associated X protein	Mus musculus	271-274
31478183-7	2019	Furthermore, N2L reduced proapoptotic signaling by increasing the expression of anti-apoptotic Bcl-2 and decreasing the protein expression of both pro-apoptotic Bax and cleaved Caspase-3.	n2l	13-16	BCL2-associated X protein	Mus musculus	161-164
31839033-4	2019	RESULTS: In BCR-ABL transfected bone marrow cells treated with imatinib, the numbers of viable cells of BAX deletion group was significantly higher than that of wild type groups with statristcal difference(P<0.05), and effect- and dose-dependency(r=-0.9533 for BAX deletion group, and r=-0.9812 for wild type group).	Imatinib Mesylate	63-71	BCL2-associated X protein	Mus musculus	104-107
31839033-1	2019	OBJECTIVE: To investigate the effect of BAX gene deletion on the sensitivity of BCR-ABL-induced B-ALL cells of mice to imatinib and the related mechanism.	Imatinib Mesylate	119-127	BCL2-associated X protein	Mus musculus	40-43
31839033-4	2019	RESULTS: In BCR-ABL transfected bone marrow cells treated with imatinib, the numbers of viable cells of BAX deletion group was significantly higher than that of wild type groups with statristcal difference(P<0.05), and effect- and dose-dependency(r=-0.9533 for BAX deletion group, and r=-0.9812 for wild type group).	Imatinib Mesylate	63-71	BCL2-associated X protein	Mus musculus	261-264
31839033-7	2019	CONCLUSION: BAX deletion can reduce the sensitivity of BCR-ABL-induced B-ALL cells to imatinib.	lauric acid	59-62	BCL2-associated X protein	Mus musculus	12-15
31853452-11	2019	Expression of Bax and Caspase3 was significantly lower in vitrification group with low-dose selenium, and expression of P53 was significantly upper.	Selenium	92-100	BCL2-associated X protein	Mus musculus	14-17
31839033-7	2019	CONCLUSION: BAX deletion can reduce the sensitivity of BCR-ABL-induced B-ALL cells to imatinib.	Imatinib Mesylate	86-94	BCL2-associated X protein	Mus musculus	12-15
31849693-7	2019	Furthermore, farrerol attenuated the phosphorylation of C-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 mitogen-activated protein kinase (p38); the activation of phosphorylated nuclear factor-kappaB (p-NF-kappaB) and nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3); and the expression of phosphorylated p53 (p-p53), Bax, and cleaved caspase-3.	farrerol	13-21	BCL2-associated X protein	Mus musculus	368-371
31853452-12	2019	Expression of Bax and Fas was significantly lower in vitrification group with high-dose selenium, and expression of P53 was significantly upper (P&lt;0.001).	Selenium	88-96	BCL2-associated X protein	Mus musculus	14-17
31690718-10	2019	Moreover, MPTP led to DNA fragmentation, caspase-3 activation, lipid peroxidation and BAX expression in Wt mice, in the absence of caspase-8 cleavage, suggesting intrinsic apoptosis.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	10-14	BCL2-associated X protein	Mus musculus	86-89
31827674-8	2019	Moreover, aloin inhibited hepatocyte apoptosis and inflammatory response that was caused by the upregulated expression of Bcl-2, the downregulated expression of cleaved caspase3(C-caspase3), Bax, Toll-like receptor 4 (TLR4), FADD, MyD88, TRAF6, phosphorylated IKKalpha/beta (p-IKKalpha/beta), and phosphorylated nuclear factor kappaB p65 (p-NF-kappaB p65).	alloin	10-15	BCL2-associated X protein	Mus musculus	191-194
31673102-8	2019	TG-induced IL-8 expression was reduced in the presence of Api in Bax-dependent manner.	Thapsigargin	0-2	BCL2-associated X protein	Mus musculus	65-68
26142340-8	2019	Berberine treatment dramatically elevated the expression ratio of Bax to Bcl-2.	Berberine	0-9	BCL2-associated X protein	Mus musculus	66-69
31238056-7	2019	Moreover, mitophagy and mitochondrial apoptosis were stimulated in response to the mitochondrial oxidative stress in the hippocampus of tBCCAO-treated mice, and ESC treatment regulated the expression of mitophagy-related factors, including Bnip3, Beclin1, Pink1, and parkin, the LC-3 II/I ratio, and apoptosis-related factors, including p53, Bax, and caspase 3.	tbccao	136-142	BCL2-associated X protein	Mus musculus	342-345
31627170-9	2019	Moreover, IR-induced DNA strand break damage, and the expression of proapoptotic-p53, Bax, Bak protein and antiapoptotic-Bcl-2 protein were reversed in DTT treated mice, and DTT also promoted small intestine repair after radiation exposure via the p53 intrinsic apoptotic pathway.	Dithiothreitol	152-155	BCL2-associated X protein	Mus musculus	86-89
31368586-10	2019	NAC-pretreated cells showed increased anti-apoptotic protein Bcl-2 and decreased pro-apoptotic protein Bax expression.	Acetylcysteine	0-3	BCL2-associated X protein	Mus musculus	103-106
31680772-5	2019	The results showed that RA can effectively inhibit the tumor growth through regulating the ratio of CD4+/CD8+ and the secretion of interleukin (IL)-2 and interferon-gamma, inhibiting the expressions of IL-6, IL-10 and signal transducer and activator of transcription 3, thereby up-regulating Bax and Caspase-3 and down-regulating Bcl-2.	rosmarinic acid	24-26	BCL2-associated X protein	Mus musculus	292-295
31665638-4	2019	Cisplatin induced mtDNA leakage into the cytosol-probably through BCL-2-like protein 4 (BAX) pores in the mitochondrial outer membrane-in tubules, with subsequent activation of the cGAS-STING pathway, thereby triggering inflammation and AKI progression, which is improved in STING-deficient mice.	Cisplatin	0-9	BCL2-associated X protein	Mus musculus	88-91
31494133-5	2019	Besides, EGCG could down-regulate the expression of anti-apoptotic protein Bcl-2, and up-regulate the expression of pro-apoptotic proteins Bax and Caspase-3 in H22 cells.	epigallocatechin gallate	9-13	BCL2-associated X protein	Mus musculus	139-142
31032949-9	2019	High glucose inhibited p-AKT production and B-Cell CLL/Lymphoma 2 expression, and promoted BAX and caspase-3 expression.	Glucose	5-12	BCL2-associated X protein	Mus musculus	91-94
31238056-7	2019	Moreover, mitophagy and mitochondrial apoptosis were stimulated in response to the mitochondrial oxidative stress in the hippocampus of tBCCAO-treated mice, and ESC treatment regulated the expression of mitophagy-related factors, including Bnip3, Beclin1, Pink1, and parkin, the LC-3 II/I ratio, and apoptosis-related factors, including p53, Bax, and caspase 3.	esculetin	161-164	BCL2-associated X protein	Mus musculus	342-345
31660294-11	2019	Moreover, benzo(a)pyrene administration induced the upregulation of PKCalpha, COX-2, and Bcl-2 expression, with the downregulation of BAX and caspase-3 expression.	Benzo(a)pyrene	10-24	BCL2-associated X protein	Mus musculus	134-137
31788433-6	2019	Drug interaction of TAM and SIM was synergistic in T47D by increasing the apoptotic makers Bax/BCL-2 ratio and caspase 3 activity.	Tamoxifen	20-23	BCL2-associated X protein	Mus musculus	91-94
31788433-6	2019	Drug interaction of TAM and SIM was synergistic in T47D by increasing the apoptotic makers Bax/BCL-2 ratio and caspase 3 activity.	Simvastatin	28-31	BCL2-associated X protein	Mus musculus	91-94
31649548-12	2019	We also found that pectolinarigenin inhibited breast cancer cell proliferation and induced apoptosis via mitochondrial-related apoptosis pathway, reduced mitochondrial membrane potential and the expression of Bcl-2, increased expression of Bax, and cleaved caspase-3 as well as disturbed the ROS generation.	pectolinarigenin	19-35	BCL2-associated X protein	Mus musculus	240-243
31401159-8	2019	Sal inhibited oxidative stress by upregulating SOD, GSH-Px and CAT while suppressing colonic apoptosis by downregulating the expression of Bax, caspase-3, and cleaved-caspase-3 and upregulating the expression of Bcl-2.	rhodioloside	0-3	BCL2-associated X protein	Mus musculus	139-142
31243598-4	2019	Overexpression of Bax/Bad significantly promoted aspirin-induced oncosis.	Aspirin	49-56	BCL2-associated X protein	Mus musculus	18-21
31623364-6	2019	The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75NTR receptor signaling pathway was significantly protected in the same group.	Scopolamine	135-137	BCL2-associated X protein	Mus musculus	263-266
31636565-7	2019	In addition, THC exposure increased transcript levels of cannabinoid receptor type 1 (Cb1r) in the parietal cortex and increased the apoptosis regulator BAX in the frontal cortex.	Dronabinol	13-16	BCL2-associated X protein	Mus musculus	133-156
31211943-0	2019	EPO regulates neuroprotective Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) family members GRINA and FAIM2 after cerebral ischemia-reperfusion injury.	tmbim	78-83	BCL2-associated X protein	Mus musculus	44-47
31372877-12	2019	ALA significantly decreased the levels of Bax and cleaved caspase-3, while significantly increasing the level of bcl-2, an anti-apoptotic protein, in the ALA + CIS group than in the CIS group.	alpha-Linolenic Acid	0-3	BCL2-associated X protein	Mus musculus	42-45
31211943-1	2019	BACKGROUND AND PURPOSE: Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) family members exert inhibitory activities in apoptosis and necroptosis.	tmbim	72-77	BCL2-associated X protein	Mus musculus	38-41
31325706-9	2019	Furthermore, QFG inhibited the cellular apoptosis in the jejunum tissue caused by 5-FU via the increasing Bcl-2 expression and decreasing Bax expression.	qfg	13-16	BCL2-associated X protein	Mus musculus	138-141
31325706-9	2019	Furthermore, QFG inhibited the cellular apoptosis in the jejunum tissue caused by 5-FU via the increasing Bcl-2 expression and decreasing Bax expression.	Fluorouracil	82-86	BCL2-associated X protein	Mus musculus	138-141
31366602-2	2019	BAX 826 is a novel polysialylated full-length recombinant factor VIII [polysialyic acid (PSA) rFVIII] with improved pharmacokinetics (PK), prolonged pharmacology, and maintained safety attributes to enable longer-acting rFVIII therapy.	polysialyic acid	71-87	BCL2-associated X protein	Mus musculus	0-3
31695568-12	2019	Finally, Re and Rk3 could upregulate the expression of bcl-2, whereas they could downregulate the expression of bax and caspase-3.	Rhenium	9-11	BCL2-associated X protein	Mus musculus	112-115
31695568-15	2019	Regulating the levels of cytokines, promoting cells enter the normal cell cycle, regulating the balance of bcl-2/bax, and inhibiting the expression of caspase-3 may be the effects of Re and Rk3 on myelosuppression.	Rhenium	0-2	BCL2-associated X protein	Mus musculus	113-116
31485651-0	2019	Sam68 mediates high glucose-induced podocyte apoptosis through modulation of Bax/Bcl-2.	Glucose	20-27	BCL2-associated X protein	Mus musculus	77-80
31432129-7	2019	Furthermore, CAE and nobiletin significantly downregulated the Bax and cleaved caspase-3 protein expression and upregulated the Bcl-2 and Bcl-2/Bax expression in the cortex and hippocampus of Abeta-treated mice.	nobiletin	21-30	BCL2-associated X protein	Mus musculus	63-66
31432129-7	2019	Furthermore, CAE and nobiletin significantly downregulated the Bax and cleaved caspase-3 protein expression and upregulated the Bcl-2 and Bcl-2/Bax expression in the cortex and hippocampus of Abeta-treated mice.	nobiletin	21-30	BCL2-associated X protein	Mus musculus	144-147
31755338-3	2019	Glucose enhances cell apoptosis mediated through PI3K/Akt, ERK1/2, and Bax/Bcl-2 pathways.	Glucose	0-7	BCL2-associated X protein	Mus musculus	71-74
31150651-7	2019	Albiflorin inhibited the mitochondrial pathway of apoptosis by increasing the levels of Bcl-2 and Bcl-xl and decreasing the levels of Bax, caspase-3 and cytochrome c in both the hippocampus and the cortex and by reducing the number of apoptotic cells in the anterior parietal cortex of the APP/PS1 mice.	albiflorin	0-10	BCL2-associated X protein	Mus musculus	134-137
31392591-8	2019	However, the high 15d-PGJ2 concentration treatment induces neuronal apoptosis via increasing the protein levels of Bax, cleaved caspase-3, and DFF45, which further impairs the learning ability of APP/PS1 mice.	15-deoxy-delta(12,14)-prostaglandin J2	18-26	BCL2-associated X protein	Mus musculus	115-118
31082581-7	2019	In addition, in vivo experiments showed that BHPF exposure could induce the expression of oxidative stress genes (Cat, Gpx 3 and Sod 2) and apoptosis genes (Bax, Bcl-2 and Cleaved-caspase 3) and increase the number of atresia follicles in the ovaries.	9,9-Bis(4-hydroxyphenyl)fluorene	45-49	BCL2-associated X protein	Mus musculus	157-160
31362072-7	2019	The decrease in the expression level of apoptotic proteins such as Bax and caspase-3 in ACTPG and alpha-bisabolol treated group indicates that the seaweed and its bioactive compound have anti-apoptotic property.	alpha-Bisabolol	98-113	BCL2-associated X protein	Mus musculus	67-70
31306770-6	2019	Further, propylparaben exposure increased expression of cell cycle regulators (Cdk4, Cdkn1a), an apoptotic factor (Bax), and a key steroidogenic regulator (Star).	propylparaben	9-22	BCL2-associated X protein	Mus musculus	115-118
31572199-10	2019	Meanwhile, dioscin significantly regulated tumor suppressor P53 (P53) expression level and BCL-2-associated X (BAX)/BCL-2 apoptosis regulator (BCL-2) ratio to inhibit cell apoptosis.	dioscin	11-18	BCL2-associated X protein	Mus musculus	91-109
31572199-10	2019	Meanwhile, dioscin significantly regulated tumor suppressor P53 (P53) expression level and BCL-2-associated X (BAX)/BCL-2 apoptosis regulator (BCL-2) ratio to inhibit cell apoptosis.	dioscin	11-18	BCL2-associated X protein	Mus musculus	111-114
31598395-8	2019	Treatment with AZD8055 at 5, 10 and 20 mg/kg/d significantly enhanced NPC cell radiosensitivity in vivo and significantly induced apoptosis and autophagy in tumor tissues, Neither 5 nor 20 mg/kg/d AZD8055 induced significantly pro-apoptosis bax expressions in mouse livers and kidneys.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	15-22	BCL2-associated X protein	Mus musculus	241-244
31431007-5	2019	The inhibition of d-galactose-induced oxidative damage in the liver was correlated with the torularhodin-mediated effects on improving the activity of Nrf2/HO-1, reducing the expression of Bax and NF-kappaB p65 by western blot analysis.	Galactose	18-29	BCL2-associated X protein	Mus musculus	189-192
31431007-5	2019	The inhibition of d-galactose-induced oxidative damage in the liver was correlated with the torularhodin-mediated effects on improving the activity of Nrf2/HO-1, reducing the expression of Bax and NF-kappaB p65 by western blot analysis.	torularhodin	92-104	BCL2-associated X protein	Mus musculus	189-192
31410133-9	2019	Taraxasterol treatment inhibited apoptosis, and reduced the protein levels of p53, Bcl-2 associated X (BAX) and caspase-3.	taraxasterol	0-12	BCL2-associated X protein	Mus musculus	83-101
31349381-6	2019	These effects were associated with enhanced activities of Erk1/2, which in turn promoted Pdx1 expression and increased the ratio of Bcl2/Bax, since inhibition of the Erk1/2 pathway abolished the DP-induced expression of Pdx1 and suppression of apoptosis.	dracorhodin	195-197	BCL2-associated X protein	Mus musculus	137-140
31526502-9	2019	The increased TUNEL-positive cells were detected in kidney tissues of biflavonoids-treated mice, accompanied by elevated expression of proapoptotic protein BAX and unchanged levels of antiapoptotic protein BCL-2, indicating apoptosis was involved in biflavonoids-induced nephrotoxicity.	Biflavonoids	70-82	BCL2-associated X protein	Mus musculus	156-159
31410133-9	2019	Taraxasterol treatment inhibited apoptosis, and reduced the protein levels of p53, Bcl-2 associated X (BAX) and caspase-3.	taraxasterol	0-12	BCL2-associated X protein	Mus musculus	103-106
31286669-6	2019	Mechanistically, cisplatin injection induced the increased apoptosis and regulated the corresponding protein expression of BCL-2, BCL-XL, BAX, cleaved caspase 3 and caspase 12 in the injured kidney tissues.	Cisplatin	17-26	BCL2-associated X protein	Mus musculus	138-141
31326607-3	2019	ROS-mediated apoptosis was accompanied by the induction of the endoplasmic reticulum (ER) stress-mediated apoptotic pathway, involving CHOP/GADD153 upregulation, JNK and p38 MAPK activation, and caspase-12 and caspase-8 activation, and subsequent induction of the mitochondrial apoptotic pathway through BAK and BAX activation, mitochondrial membrane potential (Deltapsim) loss, caspase-9 and caspase-3 activation, PARP cleavage, and nucleosomal DNA fragmentation.	Reactive Oxygen Species	0-3	BCL2-associated X protein	Mus musculus	312-315
31034758-10	2019	The chondrocytes treated with miR-138 mimic and siRNA-NEK2 exhibited reduced expressions of NEK2, beta-catenin, MMP-13, Bax, and p53 and elevated expressions of Col2, Aggrecan, and Bcl-2 as well as phosphorylation levels of beta-catenin along with enhanced chondrocytes" proliferation and suppressed cell apoptosis.	mir-138	30-37	BCL2-associated X protein	Mus musculus	120-123
31144365-8	2019	In addition, the phosphorylation of p53, cathepsin B, and Bax/Bcl-2 protein levels, and the translocation of Bax from the cytosol to mitochondria induced by H2 O2 in C2C12 cells was significantly reduced by PTL.	Hydrogen Peroxide	157-162	BCL2-associated X protein	Mus musculus	58-61
31144365-8	2019	In addition, the phosphorylation of p53, cathepsin B, and Bax/Bcl-2 protein levels, and the translocation of Bax from the cytosol to mitochondria induced by H2 O2 in C2C12 cells was significantly reduced by PTL.	Hydrogen Peroxide	157-162	BCL2-associated X protein	Mus musculus	109-112
31472681-12	2019	Curcumin (20 muM) significantly suppressed PA- or TG-induced decrease in cell viability, caspase 3 activity, and the expression levels of BAX, CHOP, and GRP78.	Curcumin	0-8	BCL2-associated X protein	Mus musculus	138-141
31441515-10	2019	Importantly, GMP-Na2 effectively enhanced the antiapoptosis function by upregulating Bcl-2 expression and downregulating caspase-3 and Bax expressions in vivo and in vitro.	gmp-na2	13-20	BCL2-associated X protein	Mus musculus	135-138
31175966-6	2019	IGF-1 pretreatment also reversed the changes of Bcl-2 and Bax protein expressions in SN in MPTP mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	91-95	BCL2-associated X protein	Mus musculus	58-61
31472681-10	2019	RESULTS: Exposure to 100-400 muM PA reduced cell viability, activated caspase 3, and enhanced the expression levels of the apoptosis-related protein BCL-2-associated X protein (BAX) and ER stress markers glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in MLTC-1 cells.	Palmitic Acid	33-35	BCL2-associated X protein	Mus musculus	149-175
31472681-12	2019	Curcumin (20 muM) significantly suppressed PA- or TG-induced decrease in cell viability, caspase 3 activity, and the expression levels of BAX, CHOP, and GRP78.	Palmitic Acid	43-45	BCL2-associated X protein	Mus musculus	138-141
31472681-10	2019	RESULTS: Exposure to 100-400 muM PA reduced cell viability, activated caspase 3, and enhanced the expression levels of the apoptosis-related protein BCL-2-associated X protein (BAX) and ER stress markers glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in MLTC-1 cells.	Palmitic Acid	33-35	BCL2-associated X protein	Mus musculus	177-180
31472681-12	2019	Curcumin (20 muM) significantly suppressed PA- or TG-induced decrease in cell viability, caspase 3 activity, and the expression levels of BAX, CHOP, and GRP78.	Thapsigargin	50-52	BCL2-associated X protein	Mus musculus	138-141
31450679-3	2019	We also observed that melatonin inhibited apoptosis of mouse Leydig cells, accompanied with increased B-cell lymphoma-2 (BCL-2) and decreased BCL2 associated X (BAX) mRNA and protein expression.	Melatonin	22-31	BCL2-associated X protein	Mus musculus	142-159
31455371-14	2019	C2C12 myotubes exposed to increasing concentrations of pravastatin presented dose-dependent impairment of insulin-induced Akt phosphorylation, increased apoptotic markers (Bax protein and cleaved caspase-3) and augmented superoxide anion production.	Pravastatin	55-66	BCL2-associated X protein	Mus musculus	172-175
31450679-3	2019	We also observed that melatonin inhibited apoptosis of mouse Leydig cells, accompanied with increased B-cell lymphoma-2 (BCL-2) and decreased BCL2 associated X (BAX) mRNA and protein expression.	Melatonin	22-31	BCL2-associated X protein	Mus musculus	161-164
31534532-14	2019	CDDP-induced apoptosis, driven by Bax and caspase-3, was aggravated in Gal-3-/- animals and in WT mice that received Gal-3 inhibitor (CDDP+Davanat-treated mice).	Cisplatin	0-4	BCL2-associated X protein	Mus musculus	34-37
31534548-13	2019	The results suggested that the anticancer molecular mechanism of the combination therapy of glycyrrhizin and doxorubicin in ALG NGPs was performed via regulating apoptosis pathway of Bax/Bcl-2 ratio and caspase-3 activity, which was also verified in H22 tumor-bearing mice.	Glycyrrhizic Acid	92-104	BCL2-associated X protein	Mus musculus	183-186
31534548-13	2019	The results suggested that the anticancer molecular mechanism of the combination therapy of glycyrrhizin and doxorubicin in ALG NGPs was performed via regulating apoptosis pathway of Bax/Bcl-2 ratio and caspase-3 activity, which was also verified in H22 tumor-bearing mice.	Doxorubicin	109-120	BCL2-associated X protein	Mus musculus	183-186
31572580-6	2019	Quantitative analysis showed that the low Met:Cys ratio has obviously decreased the expression of Bax protein and the concentrations of testosterone in male serum, but Prm2, Pgk2, Bcl-2, Bak1, and AR gene were made no difference.	Methionine	42-45	BCL2-associated X protein	Mus musculus	98-101
31572580-6	2019	Quantitative analysis showed that the low Met:Cys ratio has obviously decreased the expression of Bax protein and the concentrations of testosterone in male serum, but Prm2, Pgk2, Bcl-2, Bak1, and AR gene were made no difference.	Cystine	46-49	BCL2-associated X protein	Mus musculus	98-101
31378910-11	2019	AMI mice in the Perindopril group had decreased expression levels of Bax protein and TLR4 and NF-kappaB p50 mRNA and protein, as well as the Bax/Bcl-2 ratio.	Perindopril	16-27	BCL2-associated X protein	Mus musculus	69-72
31201698-7	2019	BPA reduced the transcriptional level of testicular DNA methyltransferase (Dnmt), increased the expression of testicular caspase-7, caspase-9, and bax, and decreased the expression of bcl-2 in F1 mice at PND 56.	bisphenol A	0-3	BCL2-associated X protein	Mus musculus	147-150
31378910-11	2019	AMI mice in the Perindopril group had decreased expression levels of Bax protein and TLR4 and NF-kappaB p50 mRNA and protein, as well as the Bax/Bcl-2 ratio.	Perindopril	16-27	BCL2-associated X protein	Mus musculus	141-144
31108387-7	2019	Furthermore, irisin pretreatment downregulated Bax and cleaved Caspase-3 at the protein level, and increased Bcl-2 protein amounts, significantly reducing apoptosis in the intestine of I/R mice.	irisin	13-19	BCL2-associated X protein	Mus musculus	47-50
30660690-6	2019	The increased ROS production up-regulated the expression of p53 and Bax, and down-regulated Bcl-2 expression, which led to the activation of caspase-3, ultimately initiated cell apoptosis.	Reactive Oxygen Species	14-17	BCL2-associated X protein	Mus musculus	68-71
30793365-6	2019	Finally, this copper complex triggered apoptosis in HepG2 cells via both intrinsic and extrinsic pathway, whereas treatment of normal L929 cells with this complex induce apoptosis only via intrinsic pathway with the upregulation of relative bax/bcl-2 ratio and does not affect the expression level of caspase-8 gene and does not trigger the extrinsic pathway.	Copper	14-20	BCL2-associated X protein	Mus musculus	241-244
30793365-7	2019	Finally, these results obtained from present study confirm the role of a novel Cu complex on the induction of apoptosis process in HepG2 and L929 cells by overexpression of bax, inhibition of bcl-2 and increase of the relative bax/bcl-2 ratio.	Copper	79-81	BCL2-associated X protein	Mus musculus	173-176
30793365-7	2019	Finally, these results obtained from present study confirm the role of a novel Cu complex on the induction of apoptosis process in HepG2 and L929 cells by overexpression of bax, inhibition of bcl-2 and increase of the relative bax/bcl-2 ratio.	Copper	79-81	BCL2-associated X protein	Mus musculus	227-230
31257486-10	2019	The expression levels of Bax, Bcl-2 and survivin were modulated by geniposide.	geniposide	67-77	BCL2-associated X protein	Mus musculus	25-28
31120192-3	2019	We found that SDX decreases cardiac injury during ischaemia reperfusion and decreased myocardial apoptosis and infarct area, which was paralleled by increased superoxide dismutase and reduced malondialdehyde in mice plasm, increased Bcl-2 expression, decreased BAX expression in a mouse model of MI/R.	glucuronyl glucosamine glycan sulfate	14-17	BCL2-associated X protein	Mus musculus	261-264
30854697-10	2019	In histopathological observations, TFPPL-treated mice exhibited reduced hepatocellular Hsp90, TNF-alpha, nuclear factor kappa-light-chain-enhancer of activated B cells-p65 positive cells, and lowered Bax and caspase-3-labeled cells in the livers.	tfppl	35-40	BCL2-associated X protein	Mus musculus	200-203
31602914-9	2019	All Tripterygium Glycosides Tablets increased the MDA and reduced the content of T-SOD,CAT or GSH in liver tissue while inhibited Nrf2,HO-1 and Bcl-2,increased the protein expression level of Bax( except Hunan group).	Glycosides	4-27	BCL2-associated X protein	Mus musculus	192-195
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	97-106	BCL2-associated X protein	Mus musculus	0-3
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	138-147	BCL2-associated X protein	Mus musculus	0-3
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	138-147	BCL2-associated X protein	Mus musculus	0-3
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	138-147	BCL2-associated X protein	Mus musculus	0-3
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	326-335	BCL2-associated X protein	Mus musculus	0-3
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	138-147	BCL2-associated X protein	Mus musculus	0-3
31602914-10	2019	Tripgerygium Glycosides Tablets from 6 manufacturers all resulted in liver function damage and liver histopathological changes,especially in Jiangsu,Hubei and Fujian,and the mechanism may related to inhibit Nrf2/HO-1 oxidative stress pathway and activate Bax/Bcl-2 apoptosis pathway to mediate lipid peroxidation and induce liver cell apoptosis.	Glycosides	0-23	BCL2-associated X protein	Mus musculus	255-258
31059699-5	2019	In an in vitro experiment, T3 inhibited apoptosis in H2O2-treated cardiomyocytes, as evidenced by the decreased expression of Bax, cleaved caspase 3 and 9, and increased expression of Bcl-2.	Hydrogen Peroxide	53-57	BCL2-associated X protein	Mus musculus	126-129
31396089-9	2019	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein homologous protein (CHOP), and p-NF-kB p65 expression and elevation of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha levels in the hippocampus.	Methamphetamine	64-68	BCL2-associated X protein	Mus musculus	107-110
31189740-9	2019	Moreover, overexpressed miR-613, silenced FN1 or LY294002 treatment suppressed proliferation, invasion, migration, and angiogenesis in NPC cells, which was indicated by reduced expression of AKT, mTOR, MMP-2, MMP-9, VEGF, and CD31 as well as decreased ratio of Bcl-2/Bax and increased expression of Cleaved-caspase3.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	49-57	BCL2-associated X protein	Mus musculus	267-270
31138526-5	2019	Spatial activation of p53 target genes in response to bortezomib in the small intestine demonstrated that CDKN1A and BAX were upregulated in the proliferative crypts but not in the differentiated villi of the small intestine; PUMA was specifically activated at the crypt base of p53 wild-type mice.	Bortezomib	54-64	BCL2-associated X protein	Mus musculus	117-120
31295840-7	2019	Anti-apoptotic Bcl-2 protein was significantly downregulated, while apoptotic protein (Bax) was significantly overexpressed in nude mice treated with 100 mg/kg Dis as compared to untreated mice.	diosmetin	160-163	BCL2-associated X protein	Mus musculus	87-90
30943778-9	2019	In addition, the proapoptotic genes Bax and caspase-3 were significantly increased by high dose finasteride, whereas the antiapoptotic gene Bcl-2 was significantly decreased by the low and high doses.	Finasteride	96-107	BCL2-associated X protein	Mus musculus	36-39
31549045-5	2019	Moreover, our results reveal that STN-UDBS or GP-UDBS protects the dopamine (DA) neurons from MPTP neurotoxicity by downregulating Bax (p &lt; 0.001), upregulating Bcl-2 (p &lt; 0.01), blocking cytochrome c (Cyt C) release from mitochondria (p &lt; 0.05), and reducing cleaved-caspase 3 activity (p &lt; 0.01) in the ipsilateral substantia nigra (SN).	Dopamine	67-75	BCL2-associated X protein	Mus musculus	131-134
31549045-5	2019	Moreover, our results reveal that STN-UDBS or GP-UDBS protects the dopamine (DA) neurons from MPTP neurotoxicity by downregulating Bax (p &lt; 0.001), upregulating Bcl-2 (p &lt; 0.01), blocking cytochrome c (Cyt C) release from mitochondria (p &lt; 0.05), and reducing cleaved-caspase 3 activity (p &lt; 0.01) in the ipsilateral substantia nigra (SN).	Dopamine	77-79	BCL2-associated X protein	Mus musculus	131-134
30986644-6	2019	Additionally, TUDCA treatment decreased LPS-induced apoptosis through decreasing TUNEL-positive cells and the overexpression of caspase-3, increasing the ratio of Bcl-2/Bax.	ursodoxicoltaurine	14-19	BCL2-associated X protein	Mus musculus	169-172
32373294-11	2019	Also, treatment with allantoin down-regulated the gene expression of glucose-regulated protein 78 (GRP78), activating transcription factor 6 (AFT6), TNFalpha, sterol regulatory element binding proteins 1c (SREBP1c), fatty acid synthase (FAS), Bax/Bcl2 ratio, caspase3, and P53.	Allantoin	21-30	BCL2-associated X protein	Mus musculus	243-246
31104354-8	2019	Metallothionein transgene reversed L-NAME-induced changes in Bax, Bcl-2, BAD phosphorylation, Caspase 9, Caspase 12 and cleaved Caspase 3.	NG-Nitroarginine Methyl Ester	35-41	BCL2-associated X protein	Mus musculus	61-64
31018046-10	2019	LC3 and Bax signaling pathways were activated in SiO2 -stimulated RAW264.7 cells, showing elevated expression of LC3 and reduced expression of Bax in the melatonin-treated cells.	Silicon Dioxide	49-53	BCL2-associated X protein	Mus musculus	8-11
31018046-10	2019	LC3 and Bax signaling pathways were activated in SiO2 -stimulated RAW264.7 cells, showing elevated expression of LC3 and reduced expression of Bax in the melatonin-treated cells.	Silicon Dioxide	49-53	BCL2-associated X protein	Mus musculus	143-146
31018046-10	2019	LC3 and Bax signaling pathways were activated in SiO2 -stimulated RAW264.7 cells, showing elevated expression of LC3 and reduced expression of Bax in the melatonin-treated cells.	Melatonin	154-163	BCL2-associated X protein	Mus musculus	8-11
31018046-10	2019	LC3 and Bax signaling pathways were activated in SiO2 -stimulated RAW264.7 cells, showing elevated expression of LC3 and reduced expression of Bax in the melatonin-treated cells.	Melatonin	154-163	BCL2-associated X protein	Mus musculus	143-146
30689461-7	2019	The late apoptotic events mediated by H2S and not the TNF-alpha induced early apoptosis correlated significantly with the induction of p53 and Bax expression in LPS-induced macrophages.	Deuterium	38-41	BCL2-associated X protein	Mus musculus	143-146
30942960-10	2019	Also, MOR-treated GMSCs influenced the apoptotic pathway, by reducing Bax, caspase 3, and caspase 9 expressions.	moringin	6-9	BCL2-associated X protein	Mus musculus	70-73
30942960-10	2019	Also, MOR-treated GMSCs influenced the apoptotic pathway, by reducing Bax, caspase 3, and caspase 9 expressions.	gmscs	18-23	BCL2-associated X protein	Mus musculus	70-73
31006097-7	2019	Furthermore, lycopene reduced the ratios of Bax:Bcl-2 and cleaved caspase-3:caspase-3 and the level of cytochrome C, increased the levels of synaptophysin (SYP) and postsynaptic density 95 (PSD95) and activated the PI3K/Akt pathway.	Lycopene	13-21	BCL2-associated X protein	Mus musculus	44-47
31105269-3	2019	Alcohol increased IL-17A production and pro-apoptotic signaling evidenced by Bax, Bim, caspase-3, and caspase-8 increases via endoplasmic reticulum (ER) stress indicated by C/EBP homologous protein (CHOP) upregulation; this was prevented by the ER stress inhibitor, 4-PBA, in isolated crypts in vitro and in vivo.	Alcohols	0-7	BCL2-associated X protein	Mus musculus	77-80
31296984-8	2019	In addition, TP markedly induced apoptosis in MLTC-1 cells via increasing the expressions of Bax, active caspase 3, Cyto c and active caspase 9, and decreasing the level of Bcl-2.	triptolide	13-15	BCL2-associated X protein	Mus musculus	93-96
31217790-5	2019	Moreover, LMP prevented high glucose-induced apoptosis by decreasing the expression of Bax and the activation of caspase-1 and caspase-3.	(2~{s},3~{r},4~{s})-2-[(2~{s},3~{r})-1,3-Bis(Oxidanyl)-1-Oxidanylidene-Butan-2-Yl]-4-[(3~{s},5~{s})-5-(Dimethylcarbamoyl)pyrrolidin-3-Yl]sulfanyl-3-Methyl-3,4-Dihydro-2~{h}-Pyrrole-5-Carboxylic Acid	10-13	BCL2-associated X protein	Mus musculus	87-90
31217790-5	2019	Moreover, LMP prevented high glucose-induced apoptosis by decreasing the expression of Bax and the activation of caspase-1 and caspase-3.	Glucose	29-36	BCL2-associated X protein	Mus musculus	87-90
30515795-8	2019	Inhibition of miR-129-5p is able to increase the antioxidant capacity, EGFR-positive rate and the expressions of EGFR, B-cell lymphoma-2, zonula occluden-1, occludin, and keratinocyte growth factor-2, but decrease the expression of vascular endothelial growth factor, BCL2-associated X protein, interleukin (IL)-1beta, and IL-4.	mir-129-5p	14-24	BCL2-associated X protein	Mus musculus	268-293
31257361-0	2019	Effects of Vitamin A on Expressions of Apoptosis Genes Bax and Bcl-2 in Epithelial Cells of Corneal Tissues Induced by Benzalkonium Chloride in Mice with Dry Eye.	Vitamin A	11-20	BCL2-associated X protein	Mus musculus	55-58
31257361-0	2019	Effects of Vitamin A on Expressions of Apoptosis Genes Bax and Bcl-2 in Epithelial Cells of Corneal Tissues Induced by Benzalkonium Chloride in Mice with Dry Eye.	Benzalkonium Compounds	119-140	BCL2-associated X protein	Mus musculus	55-58
31077207-8	2019	Our results showed that 200-800 muM PA treatment reduces cell viability, induces cell apoptosis, enhances the expression of apoptosis-related genes (Caspase 3 and B-cell lymphoma-2 (BCL-2) associated X protein (BAX)), and activates the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)).	Palmitic Acid	36-38	BCL2-associated X protein	Mus musculus	211-214
31151274-7	2019	In addition, the combined use of JGGC decreased the levels of LRP, P-gp and Bcl-2/Bax when treated with HCPT.	10-hydroxycamptothecin	104-108	BCL2-associated X protein	Mus musculus	82-85
31141948-9	2019	EGFO treatment also attenuated neural apoptosis in scopolamine-treated mice by decreasing the expression of apoptosis-related proteins such as Bax, Bcl2, cleaved caspase-3, and TUNEL staining.	Scopolamine	51-62	BCL2-associated X protein	Mus musculus	143-146
31263496-10	2019	Furthermore, BPA exposure increases the apoptosis of germ cells, which is associated with proapoptotic changes in the levels of Bcl-2 and Bax.	bisphenol A	13-16	BCL2-associated X protein	Mus musculus	138-141
30478761-6	2019	We also found that scopolamine promoted neuronal loss by inducing Bax, Pro-Caspase-3, and Caspase-3 and reducing the levels of the antiapoptotic protein Bcl-2.	Scopolamine	19-30	BCL2-associated X protein	Mus musculus	66-69
30959158-9	2019	Moreover, H2S reduced caspase-3/9 activity, Bax/Bcl-2 ratio, and LOX-1 mRNA expression in VSMCs stimulated with oxidized low-density lipoprotein.	Hydrogen Sulfide	10-13	BCL2-associated X protein	Mus musculus	44-47
31214044-8	2019	Moreover, tempol treatment decreased pro-apoptotic protein expressions (cleaved caspase-3 and Bax) and increased anti-apoptotic Bcl-2 in liver, as well as reducing apoptotic cells of TUNEL staining, which suggested apoptotic effects of tempol treatment.	tempol	10-16	BCL2-associated X protein	Mus musculus	94-97
31077207-9	2019	Melatonin treatment (1-10 muM) suppresses 400 muM PA-induced cell viability decrease, cell apoptosis, Caspase 3 activation, and BAX, CHOP, and GRP78 expression.	Palmitic Acid	50-52	BCL2-associated X protein	Mus musculus	128-131
31077207-9	2019	Melatonin treatment (1-10 muM) suppresses 400 muM PA-induced cell viability decrease, cell apoptosis, Caspase 3 activation, and BAX, CHOP, and GRP78 expression.	Melatonin	0-9	BCL2-associated X protein	Mus musculus	128-131
31210848-11	2019	AEEF inhibited apoptotic signals by regulating phosphorylated c-Jun N-terminal kinases (p-JNK), phosphorylated protein kinase B (p-Akt), Bcl-2-associated X protein (BAX), and phosphorylated Tau (p-Tau).	aeef	0-4	BCL2-associated X protein	Mus musculus	137-163
31068571-10	2019	Furthermore, Ami decreased the expression of ROCK2, NHE1, calpain1, and caspase-3 and increased the Bcl-1/Bax ratio in the hippocampus of LPS-challenged mice.	Amiloride	13-16	BCL2-associated X protein	Mus musculus	106-109
30802836-6	2019	The apoptosis of oocyte regulated by the expression of Bax and Bcl-2 protein was obviously affected by deltamethrin.	decamethrin	103-115	BCL2-associated X protein	Mus musculus	55-58
30734460-7	2019	In addition, DOX downregulated survival proteins (p-Akt, Bcl-2) with concomitant upregulation in Erk (1/2), Bax and cleaved caspase-3 expressions.	Doxorubicin	13-16	BCL2-associated X protein	Mus musculus	108-111
30844437-7	2019	Furthermore, 150 kGy gamma-irradiated hesperidin decreased the expression of Bcl-2 and pro-caspases-3 and -9, increased the expression of Bax and cytosolic cytochrome c, and increased the cleavage of poly ADP ribose polymerase.	Hesperidin	38-48	BCL2-associated X protein	Mus musculus	138-141
30097849-3	2019	This study demonstrated that triclocarban that was used at environmentally relevant concentrations induced apoptosis in mouse embryonic neurons, inhibited sumoylation, and changed the epigenetic status, as evidenced by impaired activities of HDAC, sirtuins, and DNMT, global DNA hypomethylation, and alterations of methylation levels of bax, bcl2, Ahr, and Car genes.	triclocarban	29-41	BCL2-associated X protein	Mus musculus	337-340
31631597-13	2019	In vitro and in vivo, HCQ+DOC upregulated the mRNA and protein expressions of Beclin-1, P62 and Bax ( P<0.05).	Hydroxychloroquine	22-26	BCL2-associated X protein	Mus musculus	96-99
30995739-9	2019	Moreover, proline dehydrogenase (PRODH) was verified to regulate the levels of l-proline and downstream apoptotic factors (Bax, Bcl-2, and cleaved Caspase-3) compared with the control (p &lt; 0.05).	Proline	79-88	BCL2-associated X protein	Mus musculus	123-126
31013842-13	2019	In addition, RSV decreased the protein expression of PCNA, fibronectin, and upregulated the ratio of Bax (Bcl-2-associated X) and Bcl-2 (B-cell lymphoma/leukemia 2) in vivo.	Resveratrol	13-16	BCL2-associated X protein	Mus musculus	101-104
31013842-13	2019	In addition, RSV decreased the protein expression of PCNA, fibronectin, and upregulated the ratio of Bax (Bcl-2-associated X) and Bcl-2 (B-cell lymphoma/leukemia 2) in vivo.	Resveratrol	13-16	BCL2-associated X protein	Mus musculus	106-124
30594716-8	2019	Furthermore, acrylamide treatment inhibited proliferation and induced apoptosis of placentas, as shown by decreased Ki67-positive cells and Bcl-2 protein, and increased the expression of Bax, cleaved-caspase-3, and cleaved-caspase-8 proteins.	Acrylamide	13-23	BCL2-associated X protein	Mus musculus	187-190
30797149-7	2019	Similarly, scutellarin administration inhibited apoptosis triggered by cisplatin through reducing the expressions of Cleaved caspase-3, Cleaved PARP, p53, and the ratio of Bax/Bcl-2.	scutellarin	11-22	BCL2-associated X protein	Mus musculus	172-175
30797149-7	2019	Similarly, scutellarin administration inhibited apoptosis triggered by cisplatin through reducing the expressions of Cleaved caspase-3, Cleaved PARP, p53, and the ratio of Bax/Bcl-2.	Cisplatin	71-80	BCL2-associated X protein	Mus musculus	172-175
30213181-8	2019	5-Fluorouracil treatment also accelerated the expression of the pro-apoptotic protein BAX and decelerated the expression of the anti-apoptotic protein Bcl-xL on melanoma cell line.	Fluorouracil	0-14	BCL2-associated X protein	Mus musculus	86-89
30601695-5	2019	Our data indicated that lunasin attenuated H2O2-induced, mitochondria-dependent endothelial apoptosis via down-regulating Bax and up-regulating Bcl-2, inhibiting the mitochondrial depolarization, and reducing the release of cytochrome c, as well as decreasing the activation of caspase-9 and caspase-3 in vitro and in vivo.	Hydrogen Peroxide	43-47	BCL2-associated X protein	Mus musculus	122-125
30976171-8	2019	Phosphorylation of MAPKs, Bax, and nuclear AIF was gradually increased by treatment with 5 mM of glutamate and decreased by co-treatment with Rb2.	Glutamic Acid	97-106	BCL2-associated X protein	Mus musculus	26-29
30720072-8	2019	Furthermore, restoration of Bax by pc-DNA-Bax inhibits the protective effect of miR-124 in H2O2-treated BV-2 cells.	Hydrogen Peroxide	91-95	BCL2-associated X protein	Mus musculus	28-31
30720072-8	2019	Furthermore, restoration of Bax by pc-DNA-Bax inhibits the protective effect of miR-124 in H2O2-treated BV-2 cells.	Hydrogen Peroxide	91-95	BCL2-associated X protein	Mus musculus	42-45
30884890-9	2019	Moreover, hesperetin rescued LPS-induced neuronal apoptosis by reducing the expression of phosphorylated-c-Jun N-terminal kinases (p-JNK), B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), and Caspase-3 protein and promoting the Bcl-2 protein level.	hesperetin	10-20	BCL2-associated X protein	Mus musculus	187-190
30583225-9	2019	Our results also showed decreased levels of phase I enzymes (Cyt P450 and-Cyt b5) with increased levels of phase II enzymes (GR, GST and GSH) and increased expression of Bax, caspase-3 and caspase-9 with decreased expression of mutated p53 and Bcl-2 in animals treated with DMBA and D-carvone at 20 mg dose.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	274-278	BCL2-associated X protein	Mus musculus	170-173
30583225-9	2019	Our results also showed decreased levels of phase I enzymes (Cyt P450 and-Cyt b5) with increased levels of phase II enzymes (GR, GST and GSH) and increased expression of Bax, caspase-3 and caspase-9 with decreased expression of mutated p53 and Bcl-2 in animals treated with DMBA and D-carvone at 20 mg dose.	carvone	283-292	BCL2-associated X protein	Mus musculus	170-173
30599373-13	2019	CONCLUSIONS: Our findings have demonstrated that protein levels of pERK and BAX may be relevant to the role of GLP-1 in antidepressant effects of metformin and exercise, which may provide a novel topic for future clinical research.	Metformin	146-155	BCL2-associated X protein	Mus musculus	76-79
30218457-0	2019	Sodium selenite induces apoptosis via ROS-mediated NF-kappaB signaling and activation of the Bax-caspase-9-caspase-3 axis in 4T1 cells.	Sodium Selenite	0-15	BCL2-associated X protein	Mus musculus	93-96
30711419-7	2019	In addition, the colon of DNBS-injected Fpr1 KO mice displayed a lower degree of expression of Bax and higher expression of Bcl-2 compared correspondent WT mice.	2,4-dinitrofluorobenzene sulfonic acid	26-30	BCL2-associated X protein	Mus musculus	95-98
30219962-9	2019	RESULTS: The percentage of apoptotic cell in the CIH group was significantly higher than that of normoxia group; meanwhile, Bax and cleaved caspase-3 protein levels were increased in the CIH group than those of normoxia group (all p &lt; 0.05).	cih	187-190	BCL2-associated X protein	Mus musculus	124-127
30819186-14	2019	Testosterone also increased Bax expression, decreased Bcl-2 expression and induced a loss of DeltaPsim.	Testosterone	0-12	BCL2-associated X protein	Mus musculus	28-31
30657151-6	2019	CGA significantly inhibited Pb-induced increase of cytoplasmic NF-kappaB, Bax, cytochrome C, and caspase-9 protein expressions.	Chlorogenic Acid	0-3	BCL2-associated X protein	Mus musculus	74-77
30657151-6	2019	CGA significantly inhibited Pb-induced increase of cytoplasmic NF-kappaB, Bax, cytochrome C, and caspase-9 protein expressions.	Lead	28-30	BCL2-associated X protein	Mus musculus	74-77
30769948-5	2019	Treatment with R-PHQ and S-PHQ clearly induced the apoptosis of tumor cells, significantly increased the expression of Bax, and remarkably inhibited the expression of Bcl-2 and vascular endothelial growth factor (VEGF) in H22 tumor tissues.	r-phq	15-20	BCL2-associated X protein	Mus musculus	119-122
30391286-9	2019	Acetate treatment of tumor cells inhibited tumor cell survival accompanied by induction of apoptotic cell death, associated with modulated expression of cell survival regulatory HIF1alpha, ROS, p53, Caspase 3, Bax and HSP70 along with the elevated level of cytosolic cytochrome c. Acetate treatment also modulated the expression of pH regulators MCT-1 and V-ATPase accompanied by altered pH homeostasis.	Acetates	0-7	BCL2-associated X protein	Mus musculus	210-213
30537677-15	2019	Knockdown of GSK3beta alleviated Dex-induced osteoblast and MC3T3-E1 cell apoptosis by decreasing the expressions of Bax, cleaved-caspase 3, cleaved-caspase 9 and increasing the expression of Bcl-2.	Dexamethasone	33-36	BCL2-associated X protein	Mus musculus	117-120
30407505-11	2019	Elevated expression of apoptosis-associated protein Bax and cleaved-caspase 3 was also reversed by rhodomyrtone treatment.	rhodomyrtone	99-111	BCL2-associated X protein	Mus musculus	52-55
30414103-5	2019	Cd accumulation was recorded in the cortical homogenates, accompanied by elevated levels of lipid peroxidation, nitric oxide, tumor necrosis factor-alpha, interleukin-1beta, and the pro-apoptotic mRNA Bax and caspase-3.	Cadmium	0-2	BCL2-associated X protein	Mus musculus	201-204
30668397-11	2019	Combination treatment of dendrobine with cisplatin showed enhanced cytotoxicity through stimulation of JNK/p38 stress signaling pathways and, consequently, the induction of apoptosis involving pro-apoptotic proteins Bax and Bim.	dendrobine	25-35	BCL2-associated X protein	Mus musculus	216-219
30668397-11	2019	Combination treatment of dendrobine with cisplatin showed enhanced cytotoxicity through stimulation of JNK/p38 stress signaling pathways and, consequently, the induction of apoptosis involving pro-apoptotic proteins Bax and Bim.	Cisplatin	41-50	BCL2-associated X protein	Mus musculus	216-219
30906210-6	2019	Furthermore, farrerol effectively suppressed mitochondrial dysfunction by reducing JNK phosphorylation, Bax mitochondrial translocation, AIF and cytochrome c release.	farrerol	13-21	BCL2-associated X protein	Mus musculus	104-107
30700973-0	2018	The Effect of Fucoidan on Cellular Oxidative Stress and the CatD-Bax Signaling Axis in MN9D Cells Damaged by 1-Methyl-4-Phenypyridinium.	1-methyl-4-phenypyridinium	109-135	BCL2-associated X protein	Mus musculus	65-68
30700973-8	2018	After pepstatin A treatment, Bax expression was significantly downregulated.FUC reversed the reduction of superoxide dismutase (SOD) L-Glutathione(GSH), decreased cell viability, and apoptosis induced by MPP+ in 6 h, suggesting that Fucoidan can attenuate damage to MN9D cells induced by MPP+.	pepstatin	6-17	BCL2-associated X protein	Mus musculus	29-32
30700973-8	2018	After pepstatin A treatment, Bax expression was significantly downregulated.FUC reversed the reduction of superoxide dismutase (SOD) L-Glutathione(GSH), decreased cell viability, and apoptosis induced by MPP+ in 6 h, suggesting that Fucoidan can attenuate damage to MN9D cells induced by MPP+.	fucoidan	76-79	BCL2-associated X protein	Mus musculus	29-32
30393195-12	2019	At that time, cocaine treatment decreased Bcl-2 and Bcl-xL levels, and increased Bax, cytosolic cytochrome c, and cleaved caspase-3 levels.	Cocaine	14-21	BCL2-associated X protein	Mus musculus	81-84
31468453-7	2019	The expression of Bax and Bcl-2 were disturbed by As exposure, which were reversed by taurine.	Taurine	86-93	BCL2-associated X protein	Mus musculus	18-21
31468453-8	2019	These results indicated that taurine expose protective effect on As-exposed primary cortical neurons and its mechanism maybe involved the regulation of Bax/Bcl-2.	Taurine	29-36	BCL2-associated X protein	Mus musculus	152-155
31468453-8	2019	These results indicated that taurine expose protective effect on As-exposed primary cortical neurons and its mechanism maybe involved the regulation of Bax/Bcl-2.	Arsenic	65-67	BCL2-associated X protein	Mus musculus	152-155
31468455-10	2019	This indicated that taurine may reduce apoptosis by controlling balance of Bcl-2 and Bax.	Taurine	20-27	BCL2-associated X protein	Mus musculus	85-88
31468455-12	2019	Thus, it was clear that taurine reduces apoptosis via Akt/Bad pathway in HT-22 cells exposed to HG which further improves downstream balance of Bcl-2 and Bax.	Taurine	24-31	BCL2-associated X protein	Mus musculus	154-157
31179723-8	2019	Multiple apoptosis related genes including p53, Bax and Fas were upregulated by quercetin in tumor tissue and the ratio of Bax/Bcl-2 was increased accordingly.	Quercetin	80-89	BCL2-associated X protein	Mus musculus	48-51
31179723-9	2019	Our results demonstrated that quercetin, as the main effective component of the YYQFT, has potent inhibitory activity on non-small cell lung cancer by regulating the ratio of Bax/Bcl-2.	Quercetin	30-39	BCL2-associated X protein	Mus musculus	175-178
30697271-9	2019	Moreover, THSG was identified to reverse the elevation of caspase-3, caspase-9 and Bax and the reduction of Bcl-2 induced by H2O2.	thsg	10-14	BCL2-associated X protein	Mus musculus	83-86
30551525-0	2019	Puerarin attenuates neurological deficits via Bcl-2/Bax/cleaved caspase-3 and Sirt3/SOD2 apoptotic pathways in subarachnoid hemorrhage mice.	puerarin	0-8	BCL2-associated X protein	Mus musculus	52-55
30551525-2	2019	But whether puerarin can reduce brain nerve damage after SAH is not clear.In this study, we hypothesized that puerarin had the neuroprotective effect after SAH, and this protection could be mediated by bothBcl-2/Bax/Cleaved caspase-3 and SIRT3/SOD2 apoptotic signaling pathways.	puerarin	110-118	BCL2-associated X protein	Mus musculus	212-215
30551525-7	2019	In addition, obviously higher ratio of Blc-2/Bax and decreased expression of cleaved caspase-3 in puerarin-treated SAH micecomparing with vehicle-treated SAH animals had been found.	puerarin	98-106	BCL2-associated X protein	Mus musculus	45-48
31663350-8	2019	RESULTS: Co-treatment of atorvastatin + tamoxifen could strongly enhance the expression of pro/apoptotic factors of Bax and cytochrome c in melanoma cells compared to the tamoxifen and atorvastatin groups.	12-(4'-azido-2'-nitrophenoxy)dodecanoyl-coenzyme A	9-11	BCL2-associated X protein	Mus musculus	116-119
31663350-8	2019	RESULTS: Co-treatment of atorvastatin + tamoxifen could strongly enhance the expression of pro/apoptotic factors of Bax and cytochrome c in melanoma cells compared to the tamoxifen and atorvastatin groups.	atorvastatin	25-37	BCL2-associated X protein	Mus musculus	116-119
31530262-7	2019	In addition, in GA muscle of the mice fed with DDC-supplemented diet-induced CLD showed increased myonuclear apoptosis compared with the GA muscle of the control diet-fed mice, as evidenced by increased apoptotic nuclei number, caspase-8 and caspase-9 expression, enzymatic activity of caspase-3 and BAX/BCL-2 ratio.	Zalcitabine	47-50	BCL2-associated X protein	Mus musculus	300-303
30408539-0	2019	The functional role of Bax/Bak in palmitate-induced lipoapoptosis.	Palmitates	34-43	BCL2-associated X protein	Mus musculus	23-26
30408539-5	2019	Results showed that palmitate induced caspase-dependent apoptosis in wild-type Bax/Bak MEF cells, whereas a caspase-independent cell death was induced by palmitate in Bax/Bak knockout MEF cells, suggesting requirement of Bax/Bak in palmitate-induced caspase activation.	Palmitates	20-29	BCL2-associated X protein	Mus musculus	79-82
32450040-7	2019	Furthermore, the expression profiles of beta-catenin, Bcl-2, and Bax reversed with the administration of laminarin (P < 0.05).	laminaran	105-114	BCL2-associated X protein	Mus musculus	65-68
29424794-8	2019	Sirt1 blocker nicotinamide and Nrf2 siRNA restrained the levels of GRP78, CHOP, Bax, and active caspase 3.	Niacinamide	14-26	BCL2-associated X protein	Mus musculus	80-83
30278210-8	2019	Arsenite induced testicular apoptosis with a significant increase in Bax mRNA and protein levels, especially the caspase-3 activation.	arsenite	0-8	BCL2-associated X protein	Mus musculus	69-72
30587838-6	2018	High glucose triggered cell apoptosis via the the loss of mitochondrial membrane potential, depletion of adenosine triphosphate, upregulation of caspases 9 and 3, enhancement of cytochrome c release, and subsequent interruption of the Bax/Bcl-2 balance.	Glucose	5-12	BCL2-associated X protein	Mus musculus	235-238
30361442-7	2018	We also found that DOX-induced CDK2 activation in the mouse heart is associated with up-regulation of the pro-apoptotic BCL2 family member BCL2-like 11 (Bim), a BH3-only protein essential for triggering Bax/Bak-dependent mitochondrial outer membrane permeabilization.	Doxorubicin	19-22	BCL2-associated X protein	Mus musculus	203-206
30232032-10	2018	Furthermore, BA treatment increased the expression levels of B-cell lymphoma 2 (Bcl-2), decreased Bcl-2-associated X (Bax), and inhibited the levels of active caspase-3.	betulinic acid	13-15	BCL2-associated X protein	Mus musculus	98-116
30232032-10	2018	Furthermore, BA treatment increased the expression levels of B-cell lymphoma 2 (Bcl-2), decreased Bcl-2-associated X (Bax), and inhibited the levels of active caspase-3.	betulinic acid	13-15	BCL2-associated X protein	Mus musculus	118-121
30618732-9	2018	Furthermore, quercetin rescued the mitochondrial apoptotic pathway and neuronal degeneration by regulating Bax/Bcl2, and decreasing activated cytochrome c, caspase-3 activity and cleaving PARP-1 in the cortical and hippocampal regions of the mouse brain.	Quercetin	13-22	BCL2-associated X protein	Mus musculus	107-110
29990555-5	2018	Meanwhile, western blotting analysis showed that the FA-AAP-CDDP complex induced apoptosis by activating Bax, Cytochrome-c, and Caspase-3, and downregulating Bcl-2, which suggested that the FA-AAP-CDDP complex may induce apoptosis through the endogenetic-mitochondrion signaling apoptosis pathways and intrinsic apoptotic pathways.	fa-aap-cddp	53-64	BCL2-associated X protein	Mus musculus	105-108
31949647-12	2018	The results indicated that PFOA could accelerate the apoptosis of uterine cells, and lead to slow embryo development or abortion by regulating the expression of Fas, FasL, Bax, Bcl-2 and Caspase-3 in uterine cells.	perfluorooctanoic acid	27-31	BCL2-associated X protein	Mus musculus	172-175
30323140-8	2018	RA (20 and 40 mg/kg) greatly improved neurological function, reduced infarct volume, decreased cell apoptosis, upregulated Bcl-2 protein and mRNA expression, downregulated Bax protein and mRNA expression, increased HO-1 and Nrf2 protein and mRNA expression, increased superoxide dismutase activity, and decreased malondialdehyde levels in ischemic brain tissue of model mice.	rosmarinic acid	0-2	BCL2-associated X protein	Mus musculus	172-175
30323140-9	2018	However, intraperitoneal injection of a HO-1 inhibitor (10 mg/kg zinc protoporphyrin IX) reversed the neuroprotective effects of RA on HO-1 enzyme activity and Bcl-2 and Bax protein expression.	protoporphyrin IX	70-87	BCL2-associated X protein	Mus musculus	170-173
30533172-10	2018	Coherently, apoptotic gene expressions (Casp3, Casp9, Bax, and Parp8) were significantly increased in the retina with increasing dosages of H2O2, while Bcl2 expression was mildly decreased.	Hydrogen Peroxide	140-144	BCL2-associated X protein	Mus musculus	54-57
30585262-9	2018	DHT treatment promoted bone marrow cell homing to ischemic tissue shown by significantly higher SRY expression compared to placebo-treated females as well as reduced apoptotic features in DHT-treated females, including increased Bcl-2 expression, reduced Bax levels and decreased TUNEL staining.	Dihydrotestosterone	0-3	BCL2-associated X protein	Mus musculus	255-258
30165128-6	2018	Induction of apoptosis and oxidative stress was attenuated in a dose-dependent manner by suppressing Bax, caspase-8, caspase-9 and heme oxygenase-1 (HO-1) protein expression in mice administrated with ChA.	Chlorogenic Acid	201-204	BCL2-associated X protein	Mus musculus	101-104
30171970-8	2018	In addition, PQ reduced cellular beta-catenin, p-GSK-3beta, and cyclin-D1 and increased the radio of Bax/Bcl2.	Paraquat	13-15	BCL2-associated X protein	Mus musculus	101-104
30218952-10	2018	Polydatin also inhibited apoptosis in mice with colitis by downregulating the expression of the pro-apoptotic proteins Bax, caspase 3 and cleaved caspase 3 and increasing the expression of the anti-apoptotic protein Bcl-2.	polydatin	0-9	BCL2-associated X protein	Mus musculus	119-122
30402026-11	2018	Fimasartan caused a significant decrease in caspase-3 activity and the level of Bax, and increased the Bcl-2 level.	fimasartan	0-10	BCL2-associated X protein	Mus musculus	80-83
30416757-8	2018	Baf-A1 co-treatment with TMZ significantly decrease Mcl-1 expression compared to TMZ while increase Bax expression in C2C12 cells (Bcl2 and Bcl-XL do not significantly change in Baf-A1/TMZ co-treatment).	Temozolomide	25-28	BCL2-associated X protein	Mus musculus	100-103
29594946-5	2018	Simultaneously, compared with the control group, the expression levels of Bax, Bcl-2, Cyt c, caspase-3, and caspase-9 were up-regulated after fluoride treatment.	Fluorides	142-150	BCL2-associated X protein	Mus musculus	74-77
30114659-6	2018	Apoptosis-related protein cleaved caspase-3 and pro-apoptotic protein Bax expression levels were up-regulated, and the anti-apoptotic protein Bcl-2 expression level was down-regulated in TiO2-NPs-treated cells.	titanium dioxide	187-191	BCL2-associated X protein	Mus musculus	70-73
30041155-3	2018	The results indicated that appropriate ZnCl2 levels can enhance the cell proliferation, whereas high levels of ZnCl2 could apparently inhibit cell growth, exaggerate the generation of both hydrogen peroxide and hydroxyl radicals, collapse the mitochondrial membrane potential, and accelerate cytochrome c release into cytosol, decrease the ATP production, elevate the Bax production, and reduce the Bcl-2 expression, thereby disrupting the mitochondrial homeostasis.	zinc chloride	111-116	BCL2-associated X protein	Mus musculus	368-371
30100034-10	2018	Capsaicin also decreased cleaved caspase-3, caspase-3/9, and Bax protein expression, effects abolished by TRPV1 blockade.	Capsaicin	0-9	BCL2-associated X protein	Mus musculus	61-64
32185983-10	2018	The mechanisms of apoptosis induced by EFA may be associated with decreasing Bcl-2 protein expression and increasing p53, Bax, Caspase-3, and Caspase-8 proteins expression.	efa	39-42	BCL2-associated X protein	Mus musculus	122-125
30066882-10	2018	Erastin exposure upregulated and activated p53 and thus, transcriptionally activated its downstream target genes, including p21 and Bax, in lung cancer A549 cells dependent on erastin-induced ROS.	erastin	0-7	BCL2-associated X protein	Mus musculus	132-135
30066882-10	2018	Erastin exposure upregulated and activated p53 and thus, transcriptionally activated its downstream target genes, including p21 and Bax, in lung cancer A549 cells dependent on erastin-induced ROS.	erastin	176-183	BCL2-associated X protein	Mus musculus	132-135
30066882-10	2018	Erastin exposure upregulated and activated p53 and thus, transcriptionally activated its downstream target genes, including p21 and Bax, in lung cancer A549 cells dependent on erastin-induced ROS.	Reactive Oxygen Species	192-195	BCL2-associated X protein	Mus musculus	132-135
29557179-7	2018	SKEO pre-treatment potentially increased Bcl-2 expression and decreased BAX expression in sperm of G4 compared with G2 and G3.	skeo	0-4	BCL2-associated X protein	Mus musculus	72-75
29982767-6	2018	We found: (1) structural and functional maturation was similar in WT and MT-TG ECTs; (2) Cd exposure negatively impacted ECT cell survival, maturation, and function; and (3) MT-ECTs showed reduced Cd toxicity as defined by reduced cleaved caspase 3, reduced Bax/Bcl2 ratio, reduced TdT-mediated dUTP nick-end labeling positive cells, reduced CM loss after Cd treatment, and delayed onset of cardiac dysfunction after Cd treatment.	Cadmium	89-91	BCL2-associated X protein	Mus musculus	258-261
30261648-6	2018	Bax protein expression was high in FSS-plus melatonin with chloral hydrate treatment.	Melatonin	44-53	BCL2-associated X protein	Mus musculus	0-3
30261648-6	2018	Bax protein expression was high in FSS-plus melatonin with chloral hydrate treatment.	Chloral Hydrate	59-74	BCL2-associated X protein	Mus musculus	0-3
30107910-5	2018	While the ubiquinol treatment significantly decreased active Bax protein expression in the ischemic retina, phosphorylation of Bad at serine 112 and Bcl-xL protein expression were preserved in the ubiquinol-treated ischemic retina at 12 h. Consistently, the ubiquinol treatment prevented apoptotic cell death by blocking caspase-3 cleavage.	ubiquinol	10-19	BCL2-associated X protein	Mus musculus	61-64
30107910-5	2018	While the ubiquinol treatment significantly decreased active Bax protein expression in the ischemic retina, phosphorylation of Bad at serine 112 and Bcl-xL protein expression were preserved in the ubiquinol-treated ischemic retina at 12 h. Consistently, the ubiquinol treatment prevented apoptotic cell death by blocking caspase-3 cleavage.	ubiquinol	197-206	BCL2-associated X protein	Mus musculus	61-64
30107910-5	2018	While the ubiquinol treatment significantly decreased active Bax protein expression in the ischemic retina, phosphorylation of Bad at serine 112 and Bcl-xL protein expression were preserved in the ubiquinol-treated ischemic retina at 12 h. Consistently, the ubiquinol treatment prevented apoptotic cell death by blocking caspase-3 cleavage.	ubiquinol	197-206	BCL2-associated X protein	Mus musculus	61-64
30107910-6	2018	These results suggest that the ubiquinol enhances RGC survival by modulating the Bax/Bad/Bcl-xL-mediated apoptotic pathway in the ischemic retina.	ubiquinol	31-40	BCL2-associated X protein	Mus musculus	81-84
29790427-9	2018	Moreover, the protein expression levels of tumor necrosis factor alpha (TNF-alpha) and the Bcl-2-associated X protein (Bax)/b cell leukemia/lymphoma 2 protein (Bcl-2) ratio were significantly lower at brain injury sites in mice of group MG than those of group PBS.	Lead	260-263	BCL2-associated X protein	Mus musculus	91-117
29790427-9	2018	Moreover, the protein expression levels of tumor necrosis factor alpha (TNF-alpha) and the Bcl-2-associated X protein (Bax)/b cell leukemia/lymphoma 2 protein (Bcl-2) ratio were significantly lower at brain injury sites in mice of group MG than those of group PBS.	Lead	260-263	BCL2-associated X protein	Mus musculus	119-122
30073232-7	2018	Gene expression analysis of TNF-alpha, IL-6, COX-2, NF-kappaB, Bax and Caspase 3 suggested that pre-treatment with DHICA downregulates the above-mentioned genes and simultaneously upregulates Bcl2 expression.	5,6-dihydroxy-2-indolylcarboxylic acid	115-120	BCL2-associated X protein	Mus musculus	63-66
30096284-3	2018	We found that ERalpha and/or ERbeta activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze (MWM) and Y-maze tests and suppress apoptosis as evidenced by decreased caspase-3 activity and increased ratio of Bcl-2/Bax.	NAD	90-93	BCL2-associated X protein	Mus musculus	269-272
30241783-8	2018	The protective effects of PPX patch was also associated with downregulation of the Bax/Bcl-2 ratio and Apaf-1, inhibition of cytochrome c release and inactivation of caspase-9 and caspase-3.	paclitaxel poliglumex	26-29	BCL2-associated X protein	Mus musculus	83-86
28448247-5	2018	The exposure of the glutamate treatment caused neuronal cell death through an alteration of Bax/Bcl-2 expression and translocation of mitochondrial apoptosis-inducing factor (AIF) to the cytoplasm of HT-22 cells.	Glutamic Acid	20-29	BCL2-associated X protein	Mus musculus	92-95
30127597-7	2018	Results: Baicalin administration significantly improved neurobehavioral function, alleviated brain edema, and reduced apoptosis-positive cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay accompanied with the upregulation of B-cell lymphoma 2 (Bcl-2) and downregulation of Bcl-2-associated X protein (Bax) and cleaved-caspase 3 by Western blot.	baicalin	9-17	BCL2-associated X protein	Mus musculus	306-332
30127597-7	2018	Results: Baicalin administration significantly improved neurobehavioral function, alleviated brain edema, and reduced apoptosis-positive cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay accompanied with the upregulation of B-cell lymphoma 2 (Bcl-2) and downregulation of Bcl-2-associated X protein (Bax) and cleaved-caspase 3 by Western blot.	baicalin	9-17	BCL2-associated X protein	Mus musculus	334-337
30074018-16	2018	However, combined SC79 and LY294002 treatment abolished SC79-induced p-Akt activity, inhibited anti-apoptotic bcl-2 and promoted anti-apoptotic Bax expression in MCAO mice.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	27-35	BCL2-associated X protein	Mus musculus	144-147
30061214-6	2018	Dietary quercetin also caused a significant increase in Bax/Bcl2 ratio protein expression.	Quercetin	8-17	BCL2-associated X protein	Mus musculus	56-59
29365285-5	2018	The intrinsic apoptotic pathway was activated in the hippocampal neurons following pilocarpine-induced SE, as evidenced by increased levels of cleaved caspase-3 and Bax, downregulation of Bcl-2, and the release of cytochrome c from mitochondria to cytoplasm.	Pilocarpine	83-94	BCL2-associated X protein	Mus musculus	165-168
29948678-8	2018	Maternal exposure to BPA increased Bax and decreased Bcl-2 in testicular and ovary tissues in the offspring mice.	bisphenol A	21-24	BCL2-associated X protein	Mus musculus	35-38
29948678-9	2018	Lycopene decreased Bax in testis and ovary and increased Bcl-2 in ovary tissues in the offspring mice.	Lycopene	0-8	BCL2-associated X protein	Mus musculus	19-22
30112029-7	2018	ECH or PFT-alpha treatment also alleviated dexamethasone"s action of inhibiting Bcl-2 expression as well as dexamethasone"s action of stimulating on the expression of p53 and Bax.	Dexamethasone	108-121	BCL2-associated X protein	Mus musculus	175-178
29975840-5	2018	DHM suppressed Pb-induced apoptosis, as indicated by the decreased levels of Bax and cleaved caspase-3.	dihydromyricetin	0-3	BCL2-associated X protein	Mus musculus	77-80
29975840-5	2018	DHM suppressed Pb-induced apoptosis, as indicated by the decreased levels of Bax and cleaved caspase-3.	Lead	15-17	BCL2-associated X protein	Mus musculus	77-80
30044372-11	2018	After IVF, the hatched blastocyst formation rate in the 30 mug/mL melatonin-treated group (85.70%) was significantly higher than that of the control (72.10%), and it was the same for the BCL2/BAX expression ratio.	Melatonin	66-75	BCL2-associated X protein	Mus musculus	192-195
30041644-8	2018	RESULTS: RIN5F cells treated with STZ showed increase in the expression of NF-kB and Bax and decrease in IkB, Bcl-2 and PDX1.	Streptozocin	34-37	BCL2-associated X protein	Mus musculus	85-88
30036972-6	2018	Furthermore, catechin and procyanidin A2 could inhibit Abeta-induced apoptosis in BV-2 cells by upregulating Bcl-2 and downregulating Bax protein expression.	Catechin	13-21	BCL2-associated X protein	Mus musculus	134-137
30116260-5	2018	Fucosterol also inhibited apoptosis and autophagy by upregulating Bcl-2, which decreased levels of functional Bax and Beclin-1.	fucosterol	0-10	BCL2-associated X protein	Mus musculus	110-113
30093935-8	2018	We also provide evidence that RSV administration reduced LPS-induced apoptosis of MH-S cells by altering the unbalance of Bax/Bcl-2 and inhibiting LPS-induced autophagy.	Resveratrol	30-33	BCL2-associated X protein	Mus musculus	122-125
29996549-7	2018	Furthermore, we report that Na2S (a stable precursor of H2S) toxicity is, at least in part, reverted by the Bax inhibitor V5 and by necrostatin, a potent necroptosis inhibitor.	sodium sulfide	28-32	BCL2-associated X protein	Mus musculus	108-111
29996549-7	2018	Furthermore, we report that Na2S (a stable precursor of H2S) toxicity is, at least in part, reverted by the Bax inhibitor V5 and by necrostatin, a potent necroptosis inhibitor.	Hydrogen Sulfide	56-59	BCL2-associated X protein	Mus musculus	108-111
29575236-12	2018	Western blot analysis also indicated that TMZ but not DMC more significantly decreased p-Akt and increased cleaved-caspase-3 and Bax expression.These findings suggested a fact that TMZ appear to be more effective in controlling the growth of glioblastoma than DMC in an orthotopic glioblastoma xenograft model.	Temozolomide	42-45	BCL2-associated X protein	Mus musculus	129-132
29575236-12	2018	Western blot analysis also indicated that TMZ but not DMC more significantly decreased p-Akt and increased cleaved-caspase-3 and Bax expression.These findings suggested a fact that TMZ appear to be more effective in controlling the growth of glioblastoma than DMC in an orthotopic glioblastoma xenograft model.	Temozolomide	181-184	BCL2-associated X protein	Mus musculus	129-132
29786737-6	2018	Finally, EFAA prevented mitochondrial dysfunction via regulating apoptotic signaling molecules including phosphorylated Akt (p-Akt), phosphorylated tau (p-tau), Bax, and cytochrome c in the brain tissues.	efaa	9-13	BCL2-associated X protein	Mus musculus	161-164
29680708-5	2018	We also showed that resveratrol treatment decreased IL-1beta, IL-6, TNF-alpha, PCNA, Bcl-2, and acetyl-p65 levels, but increased Bax and caspase 3 levels in hippocampus, suggesting a suppressive effect of resveratrol on cellular neuroinflammation and proliferation while a promotive effect on apoptosis of microglia in hippocampus.	Resveratrol	20-31	BCL2-associated X protein	Mus musculus	129-132
29704481-7	2018	GT/vitexin also inhibited glutamate induced Bax expression.	Glutamic Acid	26-35	BCL2-associated X protein	Mus musculus	44-47
29574133-7	2018	Furthermore, kaempferol markedly attenuated APAP-induced serum TNF-alpha and IL-6 productions, downregulated APAP-induced phosphorylations of JNK and ERK, and decreased early hepatic apoptosis via decreasing Bax/Bcl-2 ratio and caspase 3 activation.	kaempferol	13-23	BCL2-associated X protein	Mus musculus	208-211
29574133-7	2018	Furthermore, kaempferol markedly attenuated APAP-induced serum TNF-alpha and IL-6 productions, downregulated APAP-induced phosphorylations of JNK and ERK, and decreased early hepatic apoptosis via decreasing Bax/Bcl-2 ratio and caspase 3 activation.	Acetaminophen	44-48	BCL2-associated X protein	Mus musculus	208-211
29574133-7	2018	Furthermore, kaempferol markedly attenuated APAP-induced serum TNF-alpha and IL-6 productions, downregulated APAP-induced phosphorylations of JNK and ERK, and decreased early hepatic apoptosis via decreasing Bax/Bcl-2 ratio and caspase 3 activation.	Acetaminophen	109-113	BCL2-associated X protein	Mus musculus	208-211
29872034-8	2018	Increased levels of SOD2, Bax, and cleaved caspase-3 following SAH were reduced in the SAH + melatonin-treated group; reduced levels of Sirt3 and Bcl-2 following SAH were increased in the SAH + melatonin-treated group.	Melatonin	93-102	BCL2-associated X protein	Mus musculus	26-29
29579708-7	2018	Compared with methionine-treated animals, mice that treated with methionine and punicalagin remarkably displayed less apoptosis, indicated by the lower level of proapoptotic protein (Bax, caspases- 3, 9 and p53) and higher levels of antiapoptotic Bcl-2 protein than those in hyperhomocysteinemic mice.	Methionine	65-75	BCL2-associated X protein	Mus musculus	183-186
29949176-13	2018	LSESr treatment significantly enhanced Bcl-2 expression and reduced Bax expression compared to that of DHT treated mice (p<0.05).	lsesr	0-5	BCL2-associated X protein	Mus musculus	68-71
29568865-0	2018	Trifluoperazine induces apoptosis through the upregulation of Bax/Bcl-2 and downregulated phosphorylation of AKT in mesangial cells and improves renal function in lupus nephritis mice.	Trifluoperazine	0-15	BCL2-associated X protein	Mus musculus	62-65
29442721-8	2018	Additionally, real-time PCR data analysis shown an increased in the expression of p53, Bax, caspase-9, caspase-3 and decreased the level of Bcl-2, by this means specifying that apoptosis induced by TiO2 NPs occurs via the caspase-dependent pathway.	titanium dioxide	198-202	BCL2-associated X protein	Mus musculus	87-90
29926836-8	2018	Western blot assay showed that astragaloside IV reduced cytochrome c release induced by H2O2, inhibited Bax and caspase-3 expression, and increased Bcl-2 expression.	astragaloside	31-44	BCL2-associated X protein	Mus musculus	104-107
29756138-8	2018	Our results showed that CMP in combination with 5-FU reversed intestinal shortening (p &lt; 0.01) and alleviated 5-FU-induced colon injury (p &lt; 0.001) via suppression of ROS production; increasing the levels of CAT, GSH-Px and GSH; decreasing expression of NF-kappaB, p-p38 and Bax; and elevating the levels of Nrf2 and Bcl-2.	Fluorouracil	48-52	BCL2-associated X protein	Mus musculus	281-284
29883380-3	2018	Evo significantly enhanced cell viability, inhibited the accumulation of reactive oxygen species, ameliorated mitochondrial function, increased the B-cell lymphoma-2 protein content, and inhibited the high expression levels of Bax, Bad, and cleaved-caspase-3 and -8 in l-Glu-induced HT22 cells.	evodiamine	0-3	BCL2-associated X protein	Mus musculus	227-230
28874056-9	2018	INNOVATION: CP alterations in iron contents were mediated through DMT1(-IRE) and changes in ROS levels, which in turn attenuated the progression of AD through the Erk/p38 and Bcl-2/Bax signaling pathways.	Iron	30-34	BCL2-associated X protein	Mus musculus	181-184
28874056-9	2018	INNOVATION: CP alterations in iron contents were mediated through DMT1(-IRE) and changes in ROS levels, which in turn attenuated the progression of AD through the Erk/p38 and Bcl-2/Bax signaling pathways.	Reactive Oxygen Species	92-95	BCL2-associated X protein	Mus musculus	181-184
29372592-0	2018	Rasagiline delays retinal degeneration in a mouse model of retinitis pigmentosa via modulation of Bax/Bcl-2 expression.	rasagiline	0-10	BCL2-associated X protein	Mus musculus	98-101
29372592-4	2018	Rasagiline is an antiparkinsonian drug that has shown neuroprotective effects in part attributed to a modulation of Bax/Bcl-2 expression.	rasagiline	0-10	BCL2-associated X protein	Mus musculus	116-119
29723988-7	2018	Western blotting analysis of liver tissues also proved evidence that &amp;alpha;-MG partially inhibited the activation of apoptotic signaling pathways via increasing the expression of Bcl-2 and decreasing Bax and cleaved caspase 3 proteins.	Adenosine Monophosphate	70-73	BCL2-associated X protein	Mus musculus	205-208
29589006-7	2018	In addition, DHQ reduced phosphorylation of NF-kB/p65, and inhibited the expressions of pro-apoptotic factors (p53 and Bax), while it up-regulated the expression of the anti-apoptotic factor Bcl-2.	taxifolin	13-16	BCL2-associated X protein	Mus musculus	119-122
29720871-13	2018	We also observed that quercetin could inhibit palmitic acid-induced cell apoptosis via suppressing the activation of caspase-3, -9, -12; increasing the ratio of Bcl-2/BAX and reversing the impaired mitochondrial membrane potential.	Quercetin	22-31	BCL2-associated X protein	Mus musculus	167-170
29720871-13	2018	We also observed that quercetin could inhibit palmitic acid-induced cell apoptosis via suppressing the activation of caspase-3, -9, -12; increasing the ratio of Bcl-2/BAX and reversing the impaired mitochondrial membrane potential.	Palmitic Acid	46-59	BCL2-associated X protein	Mus musculus	167-170
29686615-6	2018	Furthermore, LC53 decreased the phosphorylation of p65, expression of HSP90, Bax, and cleaved-caspase-3 in EIU.	lc53	13-17	BCL2-associated X protein	Mus musculus	77-80
30966454-5	2018	Meanwhile, the transplanted S180 tumor cells exhibited obvious apoptotic phenotype after PPs treatment by arresting the cell cycle in S phase, down-regulating the Bcl-2 expressions and up-regulating the Bax levels.	Pentosan Sulfuric Polyester	89-92	BCL2-associated X protein	Mus musculus	203-206
29360439-5	2018	Our data indicated that DHA synergized with ABT-263 to trigger Bax-dependent apoptosis in NSCLC cells in culture.	artenimol	24-27	BCL2-associated X protein	Mus musculus	63-66
29360439-5	2018	Our data indicated that DHA synergized with ABT-263 to trigger Bax-dependent apoptosis in NSCLC cells in culture.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	44-47	BCL2-associated X protein	Mus musculus	63-66
29481770-11	2018	Moreover, hesperidin induced apoptosis of tumor cells which appeared as DNA fragmentation by down-regulation of Bcl2 as anti-apoptotic gene and stimulation of Caspase3 and Bax genes expression as apoptotic genes.	Hesperidin	10-20	BCL2-associated X protein	Mus musculus	172-175
29353886-5	2018	In this study, we demonstrate that single-agent ABT-199 efficiently displaces BAX from BCL-2 complexes but fails to maintain a significant antitumor activity over time in most MYC+/BCL2+DHL cell lines and primary cultures, as well as in a xenograft mouse model of the disease.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	48-51	BCL2-associated X protein	Mus musculus	78-81
29628888-6	2018	Furthermore, Lico A not only significantly modulated apoptosis-related protein by increasing Bcl-2 expression, and decreasing Bax and caspase-3 cleavage expression, but also efficiently alleviated mitochondrial dysfunction by reducing c-jun N-terminal kinase phosphorylation and translocation, inhibiting Bax mitochondrial translocation, apoptosis-inducing factor and cytochrome c release.	licochalcone A	13-19	BCL2-associated X protein	Mus musculus	126-129
29628888-6	2018	Furthermore, Lico A not only significantly modulated apoptosis-related protein by increasing Bcl-2 expression, and decreasing Bax and caspase-3 cleavage expression, but also efficiently alleviated mitochondrial dysfunction by reducing c-jun N-terminal kinase phosphorylation and translocation, inhibiting Bax mitochondrial translocation, apoptosis-inducing factor and cytochrome c release.	licochalcone A	13-19	BCL2-associated X protein	Mus musculus	305-308
29588573-7	2018	Vit also enhanced the activation of PI3K and Akt and suppressed the ratio of Bax/Bcl-2 and caspase-3 activity in MPTP-treated mice.	vitexin	0-3	BCL2-associated X protein	Mus musculus	77-80
29588573-7	2018	Vit also enhanced the activation of PI3K and Akt and suppressed the ratio of Bax/Bcl-2 and caspase-3 activity in MPTP-treated mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	113-117	BCL2-associated X protein	Mus musculus	77-80
29538417-7	2018	Furthermore, BB treatment substantially upregulated the expression of tight junction (TJ) proteins (zonula occludens-1, zonula occludens-2, claudin-1, occludin) and mRNA expression of mucins (mucin-1 and mucin-2), and decreased the Bax/Bcl-2 ratio.	berberrubine	13-15	BCL2-associated X protein	Mus musculus	232-235
29129596-6	2018	Abeta25-35 induced learning impairment, oxidative stress, Bax induction and BDNF alteration at lower dose in NE-100-treated mice or S1RKO mice as compared to WT animals.	Amyloid beta-peptide(25-35)	0-10	BCL2-associated X protein	Mus musculus	58-61
29440900-16	2018	Furthermore, TiO2 NPs treatment impaired the formation of intricate networks of fetal vessels and reduced the number of uNK cells, and inhibited proliferation and induced apoptosis of placenta by nuclear pyknosis, the activation of caspase-3 and upregulation of Bax protein and downregulation of Bcl-2 protein on GD 13.	titanium dioxide	13-17	BCL2-associated X protein	Mus musculus	262-265
29317168-6	2018	We further demonstrated that chebulinic acid significantly decreased the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK1/2, JNK, and p38, as well as inhibiting pro-apoptotic Bax and increasing anti-apoptotic Bcl-2 protein expression.	chebulinic acid	29-44	BCL2-associated X protein	Mus musculus	203-206
29317168-8	2018	In conclusion, our results in this study suggest that chebulinic acid is a potent protectant against glutamate-induced neuronal cell death via inhibiting ROS production, Ca2+ influx, and phosphorylation of MAPKs, as well as reducing the ratio of Bax to Bcl-2, which contribute to oxidative stress-mediated neuronal cell death.	chebulinic acid	54-69	BCL2-associated X protein	Mus musculus	246-249
29129496-4	2018	In this study, Runx2 protein levels were decreased in the intestinal epithelial cells (IECs) of CD patients and in a mouse 2, 4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis model; in contrast, the expression levels of p53 and Bax, a p53-target gene, were increased.	Trinitrobenzenesulfonic Acid	160-164	BCL2-associated X protein	Mus musculus	235-238
29441017-14	2018	DHTS increased the expression of several apoptosis-related proteins, including caspase9, caspase3, PARP, AIF, BAX, cytochrome c, caspase8 and FADD and significantly inhibited angiogenesis, as indicated by reduced tube formation and diminished expression of vascular endothelial cell growth factor receptor 2 and matrix metalloproteinase 9.	dhts	0-4	BCL2-associated X protein	Mus musculus	110-113
29191769-6	2018	Moreover, western blotting demonstrated that BBR effectively inhibited apoptosis via reducing cytochrome c release, Bax/Bcl-2 ratio and caspase-3/-9 cleavage in vitro and in vivo.	bbr	45-48	BCL2-associated X protein	Mus musculus	116-119
29329317-9	2018	Silencing of Nox4 rescued the production of ROS, downregulated pro-inflammatory markers (particularly phospho-p38) implicated in CIAKI, and reduced Bax and caspase 3/7 activity, which resulted in increased cellular survival in iohexol-treated HK-2 cells.	nox4	13-17	BCL2-associated X protein	Mus musculus	148-151
29080788-6	2018	In addition, l-theanine significantly increased the mRNA and protein expression of Bcl-2 and decreased the expression of Bax, anti- and pro-apoptotic molecules, respectively, compared with levels in the ETEC control group.	theanine	13-23	BCL2-associated X protein	Mus musculus	121-124
29488395-5	2018	Our results show that ZnO nanoparticles induce the release of cytochorme c, decrease the intracellular ATP level, collapse the mitochondrial membrane potential, elevate the ROS level, inhibit total antioxidant enzyme activities and increase the Bax and Caspase 3 levels whereas it decrease the Bcl-2 expression, leading to cell death.	Zinc Oxide	22-25	BCL2-associated X protein	Mus musculus	245-248
30110677-12	2018	Furthermore, CDDP increased the expression of Bax and decreased Bcl-2 expression in renal tissue.	cddp	13-17	BCL2-associated X protein	Mus musculus	46-49
29518773-9	2018	Treatment of mouse liver FL83B cells with t-BHP activated caspase 3, increased the expression of apoptotic molecules, caused cytochrome c release, and induced Bcl-2, Bax and IRE1alpha/TRAF2 complex formation.	bicyclo(2.2.1)hept-5-en-2-yl phenyl sulfoxide	44-47	BCL2-associated X protein	Mus musculus	166-169
29794468-10	2018	RESULTS: Allicin significantly suppressed CCA cell proliferation by activating the caspase cascade, inducing apoptosis, and reducing the expression of proteins downstream of STAT3, such as B-cell lymphoma 2 (Bcl-2), while upregulating Bcl-2-associated X (Bax) protein.	allicin	9-16	BCL2-associated X protein	Mus musculus	235-253
29794468-10	2018	RESULTS: Allicin significantly suppressed CCA cell proliferation by activating the caspase cascade, inducing apoptosis, and reducing the expression of proteins downstream of STAT3, such as B-cell lymphoma 2 (Bcl-2), while upregulating Bcl-2-associated X (Bax) protein.	allicin	9-16	BCL2-associated X protein	Mus musculus	255-258
29250157-6	2018	The activity of tumor necrosis factor alpha, interleukin-6, TGF-beta1, malondialdehyde, superoxide dismutase and ROS were effectively inhibited, and the protein expression of caspase-3 and Bax were clearly suppressed by treatment with myrtol in a mouse model of PTKO.	myrtol	235-241	BCL2-associated X protein	Mus musculus	189-192
29250157-7	2018	In conclusion, the results demonstrated that myrtol treatment improved PTKO through the suppression of inflammation, oxidative stress, ROS, TGF-beta1 and Bax/caspase-3 in mice, and myrtol may be a potential agent for clinical therapy.	myrtol	45-51	BCL2-associated X protein	Mus musculus	154-157
29115406-8	2018	The NF-kappaB inhibitor, caffeic acid phenethyl ester (CAPE), mimicked the protective effects of BBR, as evidenced by the increased expression of nephrin and podocin, and the decreased the expression of caspase-3 and the ratio of Bax/Bcl-2.	caffeic acid phenethyl ester	55-59	BCL2-associated X protein	Mus musculus	230-233
29115406-8	2018	The NF-kappaB inhibitor, caffeic acid phenethyl ester (CAPE), mimicked the protective effects of BBR, as evidenced by the increased expression of nephrin and podocin, and the decreased the expression of caspase-3 and the ratio of Bax/Bcl-2.	Berberine	97-100	BCL2-associated X protein	Mus musculus	230-233
30045633-5	2018	QFG increased the expression of Fas, FasL, and Bax ( P &lt; .05).	qfg	0-3	BCL2-associated X protein	Mus musculus	47-50
29490300-11	2018	Meanwhile, PA treatment induced an increase in Bax protein expression and a decrease in Bcl-2 protein expression, with Bax translocation to the mitochondria.	Palmitic Acid	11-13	BCL2-associated X protein	Mus musculus	47-50
29490300-11	2018	Meanwhile, PA treatment induced an increase in Bax protein expression and a decrease in Bcl-2 protein expression, with Bax translocation to the mitochondria.	Palmitic Acid	11-13	BCL2-associated X protein	Mus musculus	119-122
28795366-0	2018	Ru(II)/diphenylphosphine/pyridine-6-thiolate complexes induce S-180 cell apoptosis through intrinsic mitochondrial pathway involving inhibition of Bcl-2 and p53/Bax activation.	pyridine-6-thiolate	25-44	BCL2-associated X protein	Mus musculus	161-164
27957682-2	2018	Activation of c-Jun NH2-terminal kinase (JNK) may contribute to this death by the induction and phosphorylation of pro-apoptotic Bcl-2 proteins, such as Bax, that are involved in cytochrome c release from mitochondria and reactive oxygen species (ROS) production.	Reactive Oxygen Species	222-245	BCL2-associated X protein	Mus musculus	153-156
27957682-2	2018	Activation of c-Jun NH2-terminal kinase (JNK) may contribute to this death by the induction and phosphorylation of pro-apoptotic Bcl-2 proteins, such as Bax, that are involved in cytochrome c release from mitochondria and reactive oxygen species (ROS) production.	Reactive Oxygen Species	247-250	BCL2-associated X protein	Mus musculus	153-156
29115645-7	2018	In addition, apoptosis induced by 3-BrPA and SCT was initiated by the upregulation of Bax and downregulation of Bcl-2, which promote cytochrome c release and subsequently activate caspase-9 and -3, and ultimately execute mitochondria-mediated apoptosis.	bromopyruvate	34-40	BCL2-associated X protein	Mus musculus	86-89
28591009-9	2018	SB203580 attenuates the LPS-induced increase in apoptosis, caspase-3, and BAX/Bcl-2 in WT IECs.	SB 203580	0-8	BCL2-associated X protein	Mus musculus	74-77
29138212-0	2017	Bax-inhibiting peptide attenuates bleomycin-induced lung injury in mice.	Bleomycin	34-43	BCL2-associated X protein	Mus musculus	0-3
29138212-3	2017	Bax-inhibiting peptide V5 (BIP-V5) exhibits membrane permeability and inhibits the activation of Bax.The purpose of this study was to investigate whether the control of Bax activity by BIP-V5 reduces the degree of bleomycin-induced lung injury.	Bleomycin	214-223	BCL2-associated X protein	Mus musculus	0-3
29207476-10	2017	Hesperidin inhibited high glucose-induced cell apoptosis by attenuating the downregulation of caspase-9, caspase-3, and Bax/Bcl-2.	Hesperidin	0-10	BCL2-associated X protein	Mus musculus	120-123
29207476-10	2017	Hesperidin inhibited high glucose-induced cell apoptosis by attenuating the downregulation of caspase-9, caspase-3, and Bax/Bcl-2.	Glucose	26-33	BCL2-associated X protein	Mus musculus	120-123
29312803-4	2017	Co-treatment of sorafenib and VPA synergistically inhibited HCC cell viability, induced cell apoptosis, along with the up-regulation of p21, Bax, cleaved caspase9, cleaved caspase3, cleaved PARP and down-regulation of Bcl-xL, suggesting this combination activated intrinsic apoptotic pathway.	Valproic Acid	30-33	BCL2-associated X protein	Mus musculus	141-144
29174851-7	2017	The expression of Bax, Bcl-2, Beclin-1, LC3, P62 and caspase 9 were markedly affected by quercetin pretreatment.	Quercetin	89-98	BCL2-associated X protein	Mus musculus	18-21
29024717-7	2017	Supplementation of cisplatin-intoxicated mice with AGBE also significantly reduced apoptotic protein levels of Bax, cleaved caspase-3, cytochrome c and increased anti-apoptotic protein Bcl-2.	Cisplatin	19-28	BCL2-associated X protein	Mus musculus	111-114
29024717-7	2017	Supplementation of cisplatin-intoxicated mice with AGBE also significantly reduced apoptotic protein levels of Bax, cleaved caspase-3, cytochrome c and increased anti-apoptotic protein Bcl-2.	agbe	51-55	BCL2-associated X protein	Mus musculus	111-114
29039475-6	2017	t-Butylhydroquinone, an Nrf2 activator, significantly attenuated IIR-induced intestinal injury and apoptosis, with inhibition of the overexpression of the inflammatory cytokines, Bax and caspase-3 protein and partial restoration of Bcl-2 protein expression.	2-tert-butylhydroquinone	0-19	BCL2-associated X protein	Mus musculus	179-182
29383091-4	2017	Moreover, splenocytes from sodium fluoride-treated mice showed high expression of pro-apoptotic proteins, including Bim, Bax, Bak, caspase-3 and poly ADP-ribose polymerase, and low expression of the anti-apoptotic proteins BcL-2 and BcL-xL.	Sodium Fluoride	27-42	BCL2-associated X protein	Mus musculus	121-124
29171326-10	2017	By treating with EDN (10, 20 and 40 muM), expression of caspase-3, caspase-9, Bax, P53 and phosphorylated JNK in A549 cells were significantly upregulated, whereas expression of Bcl-2 and Akt phosphorylation were significantly down-regulated.	eudesmin	17-20	BCL2-associated X protein	Mus musculus	78-81
29179722-10	2017	The caspase-9 and caspase-3 cascade was activated by the AG-PEG-SS-PLA/PTX nanomicelles through upregulation of the pro-apoptotic proteins Bax and Bid and suppression of the anti-apoptotic protein Bcl-2, thereby increasing apoptosis.	Paclitaxel	71-74	BCL2-associated X protein	Mus musculus	139-142
29166724-8	2017	Masson staining results showed that the degree of myocardial fibrosis in MI+ Sch B group was significantly less than that of MI+ vehicle group.Moreover, Sch B could down-regulate some inflammatory cytokines, like NF-kappaB TGF-beta TNF-alpha and IL-1beta, activate Akt-eNOS pathway, upgrade Bcl-2 and downgrade Bax and reduce cell apoptosis as compared with MI+ vehicle group (all P&lt;0.05).	schizandrin B	77-82	BCL2-associated X protein	Mus musculus	311-314
29145236-7	2017	Western blot analyses showed that nitrite pretreatment resulted in up-regulation of antiapoptotic factors Bcl-2 and p21waf1/cip1 signal proteins, but down-regulation of the proapoptotic factor Bax signal protein.	Nitrites	34-41	BCL2-associated X protein	Mus musculus	193-196
28900799-6	2017	The mRNA expressions of Caspase-8, Caspase-9, Apaf1, and Bax were increased and, meanwhile, the mRNA expression of Bcl-2 was decreased in response to ONOO- treatment.	onoo	150-154	BCL2-associated X protein	Mus musculus	57-60
28892788-8	2017	Moreover, dose-dependent activation of caspase-3 and decreased Bcl2/Bax proportion were observed after triptolide treatment.	triptolide	103-113	BCL2-associated X protein	Mus musculus	68-71
29262627-8	2017	Interestingly, we found a cell survival response, induced by cholesterol, judged by a decrement in Bax to Bcl2 ratio.	Cholesterol	61-72	BCL2-associated X protein	Mus musculus	99-102
28158949-9	2017	MsrA deletion exacerbated cisplatin-induced increases in Bax to Bcl-2 ratio, cleaved caspase-3 level, and apoptosis, whereas MsrA overexpression attenuated cisplatin-induced oxidative stress and apoptosis.	Cisplatin	26-35	BCL2-associated X protein	Mus musculus	57-60
29212221-7	2017	More importantly, CAPE-pNO2 dramatically induced cell apoptosis via significant down-regulation of pro-caspase-3, pro-caspase-9, Bcl-2, Cyclin B1 and Cdc2 and up-regulation of cleaved-caspase-3, Bax, CytoC and P21Cip1.	cape-pno2	18-27	BCL2-associated X protein	Mus musculus	195-198
28922986-12	2017	In connection with that, DIM significantly attenuated DOX-induced apoptosis by upregulation of Bcl-2 expression and downregulation of Bax and caspase-3 expression.	Doxorubicin	54-57	BCL2-associated X protein	Mus musculus	134-137
28544535-7	2017	beta-Cryptoxanthin was more effective than astaxanthin and vitamin E because it reduced cardiac mitochondrial swelling, mitochondrial depolarization, the Bax/Bcl-2 ratio, and plasma and cardiac thiobarbituric acid reactive substances levels more significantly than its counterparts.	Beta-Cryptoxanthin	0-18	BCL2-associated X protein	Mus musculus	154-157
28544535-7	2017	beta-Cryptoxanthin was more effective than astaxanthin and vitamin E because it reduced cardiac mitochondrial swelling, mitochondrial depolarization, the Bax/Bcl-2 ratio, and plasma and cardiac thiobarbituric acid reactive substances levels more significantly than its counterparts.	Vitamin E	59-68	BCL2-associated X protein	Mus musculus	154-157
28508993-8	2017	14,15-EET could reduce neuronal apoptosis through upregulation of the ratio of Bcl-2 (anti-apoptotic protein) to Bax (apoptosis protein) and inhibition of Bax aggregation onto mitochondria.	14,15-epoxy-5,8,11-eicosatrienoic acid	0-9	BCL2-associated X protein	Mus musculus	113-116
28508993-8	2017	14,15-EET could reduce neuronal apoptosis through upregulation of the ratio of Bcl-2 (anti-apoptotic protein) to Bax (apoptosis protein) and inhibition of Bax aggregation onto mitochondria.	14,15-epoxy-5,8,11-eicosatrienoic acid	0-9	BCL2-associated X protein	Mus musculus	155-158
28735240-5	2017	L-Cysteine treatment significantly attenuated brain edema and decreased infarct volume and neuronal cell death, as shown by a decrease in the Bax/Bcl-2 ratio, suppression of caspase-3 activation, and reduced phosphorylation of Akt and ERK at 72h after HI.	Cysteine	0-10	BCL2-associated X protein	Mus musculus	142-145
28957350-12	2017	CyA pretreatment and/or RIP3(-/-) mice decreased Bax/Bcl2 expression; however, it did lead to an overall change in the levels of AST, ALT and LDH or necrotic injury.	Cyclosporine	0-3	BCL2-associated X protein	Mus musculus	49-52
28959203-7	2017	Furthermore, METH elevated the production of reactive oxygen species (ROS) and induced the dysfunction of mitochondrial characterized by a Bcl2/Bax ratio decrease, mitochondrial membrane potential collapse, and cytochrome c. ER stress release was partially reversed by ROS inhibition, and cytochrome c release was partially blocked by knockdown of CHOP.	Methamphetamine	13-17	BCL2-associated X protein	Mus musculus	144-147
28869535-7	2017	For POD 2, MitoTEMPO treatment suppressed the expression of p53 and the ratio of Bax/Bcl2 and upregulated the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) in ischemic aged skeletal muscles.	MitoTEMPO	11-20	BCL2-associated X protein	Mus musculus	81-84
28623147-8	2017	Western blot analysis and immunofluorescence revealed that H2O2 and LPS-induced neuronal toxicity down-regulated the activation of ErbB receptors and Akt1, and the ratio of Bcl2/Bax, which was reversed by rNrg1beta.	Hydrogen Peroxide	59-63	BCL2-associated X protein	Mus musculus	178-181
28734031-9	2017	In SY-SY5Y cells, MPP+ significantly suppressed DEC1 expression and increased the cleaved caspase 3/caspase 3 and Bax/Bcl-2.	mangion-purified polysaccharide (Candida albicans)	18-21	BCL2-associated X protein	Mus musculus	114-117
27987330-6	2017	As to the mechanisms, exposure of neuro-2a cells to dexmedetomidine substantially attenuated I/R-induced translocation of Bax protein from the cytosol to mitochondria and reduction in the mitochondrial membrane potential (MMP).	Dexmedetomidine	52-67	BCL2-associated X protein	Mus musculus	122-125
27987330-10	2017	Taken together, this study has shown the neuroprotective effects of dexmedetomidine against I/R-induced apoptotic insults via an intrinsic Bax-mitochondria-cytochrome c-caspase protease pathway.	Dexmedetomidine	68-83	BCL2-associated X protein	Mus musculus	139-142
28911736-6	2017	Moreover, 2,4-D exposure up-regulated the expression of p53 and Bax protein and down-regulated the expression of Bcl-2 protein in the testis.	2,4-Dichlorophenoxyacetic Acid	10-15	BCL2-associated X protein	Mus musculus	64-67
28841638-0	2017	Cerebrovascular Protective Effect of Boldine Against Neural Apoptosis via Inhibition of Mitochondrial Bax Translocation and Cytochrome C Release.	boldine	37-44	BCL2-associated X protein	Mus musculus	102-105
28841638-8	2017	Additionally, the level of the Bax in mitochondria (mit) and cytosol was elevated in the TBI-treated group as compared to the sham group.	Thioacetazone	89-92	BCL2-associated X protein	Mus musculus	31-34
28526415-8	2017	Consistently, LNK specific siRNA further decreased the Akt Ser-473 phosphorylation reduced by palmitate and located on upstream of Bax and cytochrome C. The siRNA-mediated LNK knockdown exacerbated mitochondrial membrane depolarization and mitochondrial-derived reactive oxygen species production induced by palmitate, whereas overexpression of LNK attenuated that.	Serine	59-62	BCL2-associated X protein	Mus musculus	131-134
28526415-8	2017	Consistently, LNK specific siRNA further decreased the Akt Ser-473 phosphorylation reduced by palmitate and located on upstream of Bax and cytochrome C. The siRNA-mediated LNK knockdown exacerbated mitochondrial membrane depolarization and mitochondrial-derived reactive oxygen species production induced by palmitate, whereas overexpression of LNK attenuated that.	Reactive Oxygen Species	262-285	BCL2-associated X protein	Mus musculus	131-134
29050341-9	2017	Taken together, these results suggest that GOH treatment alleviates LPS-induced ALI via inhibiting pulmonary inflammation and apoptosis, a finding that might be associated with the inhibition of TLR4-mediated NF-kappaB and Bcl-2/Bax signalling pathways.	5-[2-Cyclopropyl-5-(1h-Pyrrol-1-Yl)-1,3-Oxazol-4-Yl]-1h-1,2,3,4-Tetrazole	43-46	BCL2-associated X protein	Mus musculus	229-232
28798484-5	2017	In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2.	epigallocatechin gallate	15-19	BCL2-associated X protein	Mus musculus	144-147
28798484-5	2017	In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2.	Hydrogen Peroxide	61-65	BCL2-associated X protein	Mus musculus	144-147
28549670-13	2017	Bax/Bcl-2 ratio were significantly increased in the vancomycin-treated kidney.	Vancomycin	52-62	BCL2-associated X protein	Mus musculus	0-3
28582759-10	2017	Moreover, alpha-mangostin promoted the apoptosis of skin tumor dose-dependently by up-regulating of Bax, cleaved caspase-3, cleaved PARP and Bad, and down-regulating of Bcl-2 and Bcl-xl.	mangostin	10-25	BCL2-associated X protein	Mus musculus	100-103
28494419-7	2017	In addition, MPP+-induced changes of Bcl-2 and Bax mRNA and protein expressions were also reversed by TF pretreatment.	mangion-purified polysaccharide (Candida albicans)	13-17	BCL2-associated X protein	Mus musculus	47-50
27678165-8	2017	In addition, the protein expression levels of cleaved Caspase-3 and Bax increased and the protein expression level of Bcl-2 decreased in MC3T3-E1 cells exposed to Dex.	Dexamethasone	163-166	BCL2-associated X protein	Mus musculus	68-71
28954469-2	2017	Our current study was aimed to explore the effect of L-arginine on skin fibroblast (L929) signaling pathways involved in cell proliferation (Akt-pAkt kinase, Erk/pErk1/2 kinase, JNK/pJNK kinase and pStat-1), apoptosis (Bcl2 and Bax) and immune defense (NF-kappaB and CD26).	Arginine	53-63	BCL2-associated X protein	Mus musculus	228-231
28954469-5	2017	The exposure of skin fibroblasts to L-arginine increased anti-apoptotic Bcl2/Bax stoichiometry ratio (p&lt;0.05), obtained by calculation of their individual quantities.	Arginine	36-46	BCL2-associated X protein	Mus musculus	77-80
28689387-5	2017	GB also significantly increased Bcl-2/Bax ratio, reduced the expression of caspase-3, and protected against OGD/R-induced neuronal apoptosis.	ginkgolide B	0-2	BCL2-associated X protein	Mus musculus	38-41
31086091-10	2019	Astragaloside IV promoted cell viability and balanced Bcl-2 and Bax expression in vitro, reduced the rate of apoptosis, decreased the expression of P62, and increased the expression of LC3II/LC3I in HT22 cells after OGD/R.	astragaloside A	0-16	BCL2-associated X protein	Mus musculus	64-67
31191799-9	2019	Moreover, AMO-155 reversed the H2O2-induced downregulation of Bcl-2 and XIAP and upregulation of Bax and cleaved-caspase-3.	amo-155	10-17	BCL2-associated X protein	Mus musculus	97-100
31191799-9	2019	Moreover, AMO-155 reversed the H2O2-induced downregulation of Bcl-2 and XIAP and upregulation of Bax and cleaved-caspase-3.	Hydrogen Peroxide	31-35	BCL2-associated X protein	Mus musculus	97-100
30381745-5	2019	Treatment with 400 muM GA significantly inhibited PCNA and Cyclin B1 expression, however up-regulated BAX and Caspase-3 expression, caused mitochondrial membrane depolarization, activated Caspase-3, and induced DNA damage, thus, markedly increased the numbers of dead cells.	Gallic Acid	23-25	BCL2-associated X protein	Mus musculus	102-105
30885636-9	2019	Western blot and RT-PCR were performed to detect the effect of exenatide on apoptosis-related genes (Bcl-2 and Bax) and inflammation-related genes and/or proteins (tumour necrosis factor-alpha, interleukin-6, nuclear factor-kappaB, and p53).	Exenatide	63-72	BCL2-associated X protein	Mus musculus	111-114
30710579-13	2019	Activation of primary macrophage cultures with Poly (I:C) induced translocation of IRF3 to the mitochondria, where it associated with Bax and activated caspases 3 and 9, processes indicative of activation of the RIPA pathway.	Poly I-C	47-56	BCL2-associated X protein	Mus musculus	134-137
30785197-12	2019	Moreover, the undifferentiated spermatogonia numbers were decreased by 60% in 5 mg/kg/day glyphosate group, which could be due to the alterations in the expression of genes involved in germ cell differentiation such as Sall4 and Nano3 and apoptosis as Bax and Bcl2.	glyphosate	90-100	BCL2-associated X protein	Mus musculus	252-255
31844611-13	2019	In addition, Dex significantly increased Bax expression and reduced Bcl-2 expression.	Dexamethasone	13-16	BCL2-associated X protein	Mus musculus	41-44
30520250-7	2019	However, phytol treatment reduced the expression of Bax, caspase-3, and caspase-9 protein and maintained the constant expression of anti-apoptotic protein Bcl-2.	Phytol	9-15	BCL2-associated X protein	Mus musculus	52-55
30802477-2	2019	In HUVE cells, high glucose decreased cell viability, reduced Bcl-2 mRNA expression and increased Bax mRNA expression.	Glucose	20-27	BCL2-associated X protein	Mus musculus	98-101
31001113-5	2019	Moreover, co-treatment of alteronol and ADM (i) remarkably activated p38 and JNK kinases, (ii) elevated ROS levels, (iii) triggered mitochondrial dysfunction, (iv) released cytochrome c into the cytoplasm, (v) upregulated apoptosis-related proteins, e.g., cleaved PARP, Bax, and cleaved caspase-3/9, and (vi) downregulated the expression of Bcl-2, followed by apoptosis.	alteronol	26-35	BCL2-associated X protein	Mus musculus	270-273
30914735-3	2019	ACEE treatment increased expression of p53 and Bax, as well as cleavage of caspase-3 and PARP, while reducing expression of survivin and Bcl-2.	acee	0-4	BCL2-associated X protein	Mus musculus	47-50
30458235-11	2019	Gene expression of Bax and caspase 3 was decreased in both the lung and submandibular gland with nitrate treatment, indicating attenuation of apoptosis.	Nitrates	97-104	BCL2-associated X protein	Mus musculus	19-22
30992737-8	2019	Results: VSMC apoptosis, caspase-3 activity, and Bax were increased by corticosterone, and cell death was paralleled by marked loss of miR-25.	Corticosterone	71-85	BCL2-associated X protein	Mus musculus	49-52
30641432-5	2019	Additionally five flavonoids inhibited hepatocyte apoptosis through increasing Bcl-2/Bax ratio and suppressing the Caspase family proteins.	Flavonoids	18-28	BCL2-associated X protein	Mus musculus	85-88
31128015-10	2019	Investigation of the underlying mechanism revealed that TC triggered apoptotic death of the SNU-4235 cells which was also associated with enhancement of the expression of Bax and decrease in the expression of Bcl-2.	Technetium	56-58	BCL2-associated X protein	Mus musculus	171-174
30799248-10	2019	Treatment of 4T1 cells with the CEAA increased Bax protein levels accompanied by decreased Bcl-2 expression, in the presence of cleaved caspase-3 and cytosolic calcium mobilization, suggesting mitochondrial involvement in breast cancer cell death induced by the CEAA in this cell line.	ceaa	32-36	BCL2-associated X protein	Mus musculus	47-50
30791594-8	2019	After treatment with COS, significantly elevated concentrations of Bax and reduced expression of Bcl-2 in tumor tissues, as well as elevated levels of TNF- alpha , IL-2, Fas and Fas-L in mice serum were observed (p &lt; 0.05).	carbonyl sulfide	21-24	BCL2-associated X protein	Mus musculus	67-70
30597130-8	2019	Silibinin activated AKT signaling pathway and decreased the levels of p-GSK-3beta, Bax and cleaved caspase-3.	Silybin	0-9	BCL2-associated X protein	Mus musculus	83-86
30833897-5	2019	GLA downregulated pro-apoptotic proteins (Bax, cleaved-caspase 9 and cleaved-caspase 3) and upregulated anti-apoptotic proteins (HAX-1 and Bcl-2) in the cardiac tissues.	glabridin	0-3	BCL2-associated X protein	Mus musculus	42-45
30521994-7	2019	The anti-apoptotic property of ebselen was demonstrated by its effectiveness against the increase in the ratios of Bax/Bcl-2, cleaved PARP/PARP and the cleaved caspase-3 levels in the hippocampus of icv STZ mice.	ebselen	31-38	BCL2-associated X protein	Mus musculus	115-118
30447495-15	2019	In contrast, Bax expression was significantly higher in the aging group compared with all other groups (P &lt; 0.01), and the Bcl-2/Bax ratio was markedly reduced in aging group compared with control, Ica 100 and 200 groups (P &lt; 0.01), and Ica 50 group (P &lt; 0.05).	icariin	201-204	BCL2-associated X protein	Mus musculus	13-16
30447495-15	2019	In contrast, Bax expression was significantly higher in the aging group compared with all other groups (P &lt; 0.01), and the Bcl-2/Bax ratio was markedly reduced in aging group compared with control, Ica 100 and 200 groups (P &lt; 0.01), and Ica 50 group (P &lt; 0.05).	icariin	201-204	BCL2-associated X protein	Mus musculus	132-135
30447495-17	2019	Ovarian Bcl-2 protein levels and the Bcl-2/Bax ratio were significantly higher in the Ica 100 group than those in the Ica 50, 200 and aging groups (P &lt; 0.05), and were similar or reduced (P &lt; 0.05), respectively, compared to those in control group.	icariin	86-89	BCL2-associated X protein	Mus musculus	43-46
30447495-19	2019	These findings suggest that Ica can improve ovarian follicular development, inhibit follicular atresia, decrease FSH and LH levels and increase E2, upregulate ovarian AMH expression and increase the Bcl-2/Bax ratio in aging mice.	icariin	28-31	BCL2-associated X protein	Mus musculus	205-208
30686973-7	2018	More importantly, Baicalin enhanced autophagy by detecting the autophagy markers (LC3, Beclin 1, and p62) using western blot and LC3 immunofluorescence staining, ameliorating mitochondrial apoptotic pathway evidenced by restoration of the TBI-induced translocation of Bax and cytochrome C. However, simultaneous treatment with 3-MA inhibited Baicalin-induced autophagy and abolished its protective effects on mitochondrial apoptotic pathway.	baicalin	18-26	BCL2-associated X protein	Mus musculus	268-271
31468417-8	2019	Then the heat stress group cells were cultivated in a 43  C thermostatic water bath for 6 h under heat stress, and then re-incubated under 37  C for 1 h. The results showed that compared with the control group, expression levels of Bax, Caspase-9, Caspase-3, Cyt-c, P53 and other pro-apoptosis factors in HS groups were significantly increased (P &lt; 0.05), while expression levels of anti-apoptosis factor Bcl-2 showed a significant decrease (P &lt; 0.05).	Water	73-78	BCL2-associated X protein	Mus musculus	232-235
31096772-9	2019	Fisetin inhibited anti-apoptotic protein Bcl-2 and Bcl-xL and increased pro-apoptotic protein Bax and Bak.	fisetin	0-7	BCL2-associated X protein	Mus musculus	94-97
30451117-7	2019	Our results also showed that both berberine and cinnamic acid-induced apoptosis by increasing the Bax/Bcl-2 ratio (74.1 and 45.1, respectively) and caspase-3 expression (14.3- and 11.6-fold increase, respectively).	Berberine	34-43	BCL2-associated X protein	Mus musculus	98-101
30451117-7	2019	Our results also showed that both berberine and cinnamic acid-induced apoptosis by increasing the Bax/Bcl-2 ratio (74.1 and 45.1, respectively) and caspase-3 expression (14.3- and 11.6-fold increase, respectively).	cinnamic acid	48-61	BCL2-associated X protein	Mus musculus	98-101
31663350-8	2019	RESULTS: Co-treatment of atorvastatin + tamoxifen could strongly enhance the expression of pro/apoptotic factors of Bax and cytochrome c in melanoma cells compared to the tamoxifen and atorvastatin groups.	Tamoxifen	40-49	BCL2-associated X protein	Mus musculus	116-119
31663350-9	2019	CONCLUSION: In general, we conclude that the atorvastatin-induced increase in Bax and cytochrome c gene expression might be a permissive response to tamoxifen-induced cell death (Fig.	atorvastatin	45-57	BCL2-associated X protein	Mus musculus	78-81
31663350-9	2019	CONCLUSION: In general, we conclude that the atorvastatin-induced increase in Bax and cytochrome c gene expression might be a permissive response to tamoxifen-induced cell death (Fig.	Tamoxifen	149-158	BCL2-associated X protein	Mus musculus	78-81
29804319-9	2019	Furthermore, upregulation of miR-219 inhibits positive expression of Bax, caspase-9, and caspase-3 proteins, leading to the suppression of hippocampal neuronal cell apoptosis.	mir-219	29-36	BCL2-associated X protein	Mus musculus	69-72
31830892-5	2019	Furthermore, anthocyanins reduced tumor weight and volume in a colon tumor mouse model and downregulated the expression of PI3K protein, inhibited AKT expression and phosphorylation, decreased the Bcl-2 and Bax ratio and reduced survivin protein expression in the tumor tissue.	Anthocyanins	13-25	BCL2-associated X protein	Mus musculus	207-210
31830892-7	2019	Mechanistically, anthocyanins enhanced the Bcl-2/Bax and caspase-dependent apoptotic pathways through targeting the PI3K/AKT/survivin pathway, resulting in impairment of growth of CRC.	Anthocyanins	17-29	BCL2-associated X protein	Mus musculus	49-52
30539784-8	2019	In line with this, rifampicin decreased the number of apoptotic cells in the corpus callosum thereby diminishing the expression of cleaved caspase-3 and Bax, as well as increasing Bcl-2.	Rifampin	19-29	BCL2-associated X protein	Mus musculus	153-156
30408539-5	2019	Results showed that palmitate induced caspase-dependent apoptosis in wild-type Bax/Bak MEF cells, whereas a caspase-independent cell death was induced by palmitate in Bax/Bak knockout MEF cells, suggesting requirement of Bax/Bak in palmitate-induced caspase activation.	Palmitates	154-163	BCL2-associated X protein	Mus musculus	167-170
30408539-5	2019	Results showed that palmitate induced caspase-dependent apoptosis in wild-type Bax/Bak MEF cells, whereas a caspase-independent cell death was induced by palmitate in Bax/Bak knockout MEF cells, suggesting requirement of Bax/Bak in palmitate-induced caspase activation.	Palmitates	154-163	BCL2-associated X protein	Mus musculus	167-170
30408539-5	2019	Results showed that palmitate induced caspase-dependent apoptosis in wild-type Bax/Bak MEF cells, whereas a caspase-independent cell death was induced by palmitate in Bax/Bak knockout MEF cells, suggesting requirement of Bax/Bak in palmitate-induced caspase activation.	Palmitates	154-163	BCL2-associated X protein	Mus musculus	167-170
30408539-5	2019	Results showed that palmitate induced caspase-dependent apoptosis in wild-type Bax/Bak MEF cells, whereas a caspase-independent cell death was induced by palmitate in Bax/Bak knockout MEF cells, suggesting requirement of Bax/Bak in palmitate-induced caspase activation.	Palmitates	154-163	BCL2-associated X protein	Mus musculus	167-170
30408539-6	2019	More importantly, we found that the status of Bax/Bak is a determinant that governs the decision between the pro-survival or pro-death function of autophagy in response to palmitate exposure, and Bax/Bak is required for palmitate-induced activation of endoplasmic reticulum (ER) stress and subsequently ER stress-mediated apoptosis.	Palmitates	172-181	BCL2-associated X protein	Mus musculus	46-49
30408539-6	2019	More importantly, we found that the status of Bax/Bak is a determinant that governs the decision between the pro-survival or pro-death function of autophagy in response to palmitate exposure, and Bax/Bak is required for palmitate-induced activation of endoplasmic reticulum (ER) stress and subsequently ER stress-mediated apoptosis.	Palmitates	172-181	BCL2-associated X protein	Mus musculus	196-199
30745820-11	2019	Furthermore, ICA significantly inhibited the expression of ER stress apoptotic proteins caspase-12, CHOP, Bax/Bcl-2, caspase-9 and caspase-3.	icariin	13-16	BCL2-associated X protein	Mus musculus	106-109
30662289-8	2019	Moreover, ginsenoside Rk1 supplementation suppressed activation of apoptotic pathways by increasing Bcl-2 and decreasing Bax protein expression levels, which was shown using western blotting analysis.	Ginsenosides	10-21	BCL2-associated X protein	Mus musculus	121-124
30227242-9	2019	In vitro study showed endogenous visfatin inhibition by FK866 increased expression of PCNA and BCL2 increased catalase activity while FK866 treatment decreased expression of active caspase3 and BAX with decreased SOD and GPx activity.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	134-139	BCL2-associated X protein	Mus musculus	194-197
30315841-6	2019	TCE-induced DNA damage was associated with significant activation of PARP-1 and increases in caspase-3, cleaved caspase-8 and -9, and alterations in Bcl-2 and Bax in the livers.	Trichloroethylene	0-3	BCL2-associated X protein	Mus musculus	159-162
30315841-8	2019	Interestingly, NAC supplementation not only attenuated elevated 8-OHdG, PARP-1, caspase-3, cleaved caspase-9, and Bax, but also the TCE-mediated autoimmune response supported by significantly reduced serum anti-ssDNA antibodies.	Acetylcysteine	15-18	BCL2-associated X protein	Mus musculus	114-117
30643390-8	2019	Lower LC3II/LC3I and BAX/BCL-2 ratios in denervated muscles were also detected after catalpol treatment.	catalpol	85-93	BCL2-associated X protein	Mus musculus	21-24
30594149-9	2018	Pro-apoptotic protein, Bcl-2 associated x (Bax), exhibited a slight, but significant decrease with rapamycin treatment, while its anti-apoptotic counterpart, B cell lymphoma-2 (Bcl-2), was to a similar degree upregulated.	Sirolimus	99-108	BCL2-associated X protein	Mus musculus	23-41
30594149-9	2018	Pro-apoptotic protein, Bcl-2 associated x (Bax), exhibited a slight, but significant decrease with rapamycin treatment, while its anti-apoptotic counterpart, B cell lymphoma-2 (Bcl-2), was to a similar degree upregulated.	Sirolimus	99-108	BCL2-associated X protein	Mus musculus	43-46
30594149-13	2018	Additionally, inhibition of caspase-9 and -3 activation and stimulation of protective autophagy reduces cell death, while a decrease in the Bax/Bcl-2 ratio and an increase in pMAPK promotes cell survival during CoCl2 exposure.	cobaltous chloride	211-216	BCL2-associated X protein	Mus musculus	140-143
30622447-7	2018	Pretreatment with LDR significantly prevented DOX-induced cardiotoxicity likely through preventing DOX-induced mitochondrial Bcl2/Bax dyshomeostasis-induced caspase-3 cleavage-dependent apoptosis.	Doxorubicin	46-49	BCL2-associated X protein	Mus musculus	130-133
30622447-7	2018	Pretreatment with LDR significantly prevented DOX-induced cardiotoxicity likely through preventing DOX-induced mitochondrial Bcl2/Bax dyshomeostasis-induced caspase-3 cleavage-dependent apoptosis.	Doxorubicin	99-102	BCL2-associated X protein	Mus musculus	130-133
30195209-6	2018	Moreover, SO2 and arsenic co-exposure changed the mRNA levels of Bax and Bcl-2, decreased serum testosterone levels, and downregulated the expression of steroidogenic-related genes (LHR, StAR, and ABP) in mice.	Arsenic	18-25	BCL2-associated X protein	Mus musculus	65-68
30025915-13	2018	Meanwhile, metformin down-regulated the anti-apoptotic protein B cell lymphoma 2 (Bcl-2) but up-regulated the pro-apoptotic protein Bcl2-associated X (BAX), which suggests the involvement of the mitochondrial-mediated apoptosis pathway.	Metformin	11-20	BCL2-associated X protein	Mus musculus	132-149
30025915-13	2018	Meanwhile, metformin down-regulated the anti-apoptotic protein B cell lymphoma 2 (Bcl-2) but up-regulated the pro-apoptotic protein Bcl2-associated X (BAX), which suggests the involvement of the mitochondrial-mediated apoptosis pathway.	Metformin	11-20	BCL2-associated X protein	Mus musculus	151-154
30581978-5	2018	However, GAPT and donepezil showed improved memory performance, less Abeta accumulation, increased neuron and synapse number, as well as restored balance of Bcl-2/Bax.	Donepezil	18-27	BCL2-associated X protein	Mus musculus	163-166
30531685-9	2018	In addition, it was revealed that resveratrol elevated ROS concentration and expression of biomarker of cell death Bax, while inhibiting Bcl2, an anti-apoptotic protein, and reinforcing expression of p53.	Resveratrol	34-45	BCL2-associated X protein	Mus musculus	115-118
30544760-7	2018	Furthermore, Cd triggered an apoptotic cascade via upregulation of caspase-3 and Bax and downregulation of Bcl-2.	Cadmium	13-15	BCL2-associated X protein	Mus musculus	81-84
30564112-11	2018	In addition, NaIO3-induced retinal damage was related to apoptosis via caspase 8 and caspase 9, but not the caspase 3 pathways, which led to upregulation of Bax and p53, downregulation of Bcl-2, and increase in Jc-1-positive cells in mice.	sodium iodate	13-18	BCL2-associated X protein	Mus musculus	157-160
30316072-7	2018	In addition, Nar enhanced anti-apoptotic Bcl-2 expression, decreased pro-apoptotic Bax expression and inhibited caspase-3 activation in liver tissue in mice exposed to PFOS.	naringin	13-16	BCL2-associated X protein	Mus musculus	83-86
29990555-5	2018	Meanwhile, western blotting analysis showed that the FA-AAP-CDDP complex induced apoptosis by activating Bax, Cytochrome-c, and Caspase-3, and downregulating Bcl-2, which suggested that the FA-AAP-CDDP complex may induce apoptosis through the endogenetic-mitochondrion signaling apoptosis pathways and intrinsic apoptotic pathways.	fa-aap-cddp	190-201	BCL2-associated X protein	Mus musculus	105-108
30272354-5	2018	In LM3 cells, capsaicin and sorafenib combination treatment achieved a markedly stronger induction of apoptosis by increasing caspase-3, Bax and poly(ADP-ribose) polymerase activity and inhibiting Bcl-2, and induction of autophagy by upregulating the levels of beclin-1 and LC3A/B II, enhancing P62 degradation.	Capsaicin	14-23	BCL2-associated X protein	Mus musculus	137-140
30272354-5	2018	In LM3 cells, capsaicin and sorafenib combination treatment achieved a markedly stronger induction of apoptosis by increasing caspase-3, Bax and poly(ADP-ribose) polymerase activity and inhibiting Bcl-2, and induction of autophagy by upregulating the levels of beclin-1 and LC3A/B II, enhancing P62 degradation.	Sorafenib	28-37	BCL2-associated X protein	Mus musculus	137-140
30218672-9	2018	Moreover, donepezil can also improve PCP-induced schizophrenia-like cognitive deficits by inhibiting neuronal apoptosis and regulating synaptic plasticity, which was possible through the up-regulation of p-Akt, p-GSK-3beta, Bcl-2 and the down-regulation of Bax, Caspase-3.	Donepezil	10-19	BCL2-associated X protein	Mus musculus	257-260
30218672-9	2018	Moreover, donepezil can also improve PCP-induced schizophrenia-like cognitive deficits by inhibiting neuronal apoptosis and regulating synaptic plasticity, which was possible through the up-regulation of p-Akt, p-GSK-3beta, Bcl-2 and the down-regulation of Bax, Caspase-3.	Phencyclidine	37-40	BCL2-associated X protein	Mus musculus	257-260
30469321-5	2018	Western blotting showed that PDQ reversed the CDDP-induced (1) downregulation of Sirtuin-1 (Sirt-1), nuclear-related factor 2 (Nrf2), and Bcl-2, and (2) upregulation of NF-kappaB, Nox-4, Bax, caspase-9, and caspase-3.	Cisplatin	46-50	BCL2-associated X protein	Mus musculus	187-190
30074260-6	2018	Quantitative polymerase chain reaction revealed that melatonin significantly upregulated the transcription of catalase, superoxide dismutase 2, glutathione peroxidase, and the antiapoptotic factors Bcl-2 and Bcl-x while downregulated the transcription of pro-apoptotic genes p53 and Bax.	Melatonin	53-62	BCL2-associated X protein	Mus musculus	283-286
30713662-7	2019	Moreover, DAS pretreatment regulated the expression of cleaved caspase 3, Bax and Bcl-2 in the liver and suppressed APAP-/CCl4-induced hepatocyte apoptosis.	allyl sulfide	10-13	BCL2-associated X protein	Mus musculus	74-77
30314494-9	2018	CTPG treatment significantly increased Bax/Bcl-2 ratio, reduced Deltapsim and enhanced the release of cytochrome c. The levels of cleaved caspase-8 and caspase-9 in both extrinsic and intrinsic signaling pathways were significantly increased that sequentially activated caspase-7 and -3 to cleave PARP.	ctpg	0-4	BCL2-associated X protein	Mus musculus	39-42
29520724-3	2018	We found AlCl3 inhibited MC3T3-E1 cell survival rate and caused apoptosis, as evidenced by CCK-8 assay, Annexin V/PI double staining, and increased expressions of Bcl-2, Bax, and Caspase-3 genes.	Aluminum Chloride	9-14	BCL2-associated X protein	Mus musculus	170-173
30075314-7	2018	Furthermore, DAS pretreatment attenuated LPS/D-GalN-induced hepatocyte apoptosis, as evidenced by TUNEL staining and protein expression of cleaved caspase3, Bax and Bcl-2 in liver.	allyl sulfide	13-16	BCL2-associated X protein	Mus musculus	157-160
30568691-9	2018	Bax, caspase-9 genes" expression and caspase-9 enzymatic activity were significantly increased, while Bcl-2 gene expression was significantly decreased in PEITC treated mice.	phenethyl isothiocyanate	155-160	BCL2-associated X protein	Mus musculus	0-3
30056207-4	2018	We found that exposure to genistein had no effect on follicle number, but it did affect the expression of apoptotic regulatory genes (Bax, Bcl-2, Bid, and Dffa) in the ovary.	Genistein	26-35	BCL2-associated X protein	Mus musculus	134-137
30377135-10	2018	Exposure to high glucose obviously increased [Ca2 +]I in the podocytes to cause activation of calcineurin and the subsequent increment of nuclear accumulation of NFAT2 and Bax expression.	Glucose	17-24	BCL2-associated X protein	Mus musculus	172-175
30377135-11	2018	CONCLUSIONS: High glucose-induced apoptosis in podocytes is mediated by calcineurin/NFAT2/Bax signaling pathway, which may serve as a potential target for therapeutic intervention.	Glucose	18-25	BCL2-associated X protein	Mus musculus	90-93
30232347-9	2018	Moreover, the expression of Bcl-2, HO-1, and Sirt1 in liver, KCs, and hepatocytes by hydrogen gas were increased, whereas caspase activation, Bax, and acetylation of p53 were suppressed by hydrogen gas.	Hydrogen	189-197	BCL2-associated X protein	Mus musculus	142-145
30275707-8	2018	Additionally, oldhamianoside treatment inhibited the expression of VEGF and VEGFR2 and decreased the expression of caspase-3 and Bax/Bcl-2 ratio.	oldhamianoside	14-28	BCL2-associated X protein	Mus musculus	129-132
29792955-6	2018	Furthermore, administration of fisetin suppressed neuron cell death and apoptosis, increased the expression of B-cell lymphoma 2 (Bcl-2), while decreased the expression of Bcl-2-associated X protein (Bax) and caspase-3 after TBI.	fisetin	31-38	BCL2-associated X protein	Mus musculus	172-198
29792955-6	2018	Furthermore, administration of fisetin suppressed neuron cell death and apoptosis, increased the expression of B-cell lymphoma 2 (Bcl-2), while decreased the expression of Bcl-2-associated X protein (Bax) and caspase-3 after TBI.	fisetin	31-38	BCL2-associated X protein	Mus musculus	200-203
30224925-14	2018	DOX significantly decreased Bax and increased cytochrome c expressions in the cytoplasm, whereas Bax was upregulated and cytochrome c was downregulated in the mitochondria, which were reversed by SYKT treatment.	Doxorubicin	0-3	BCL2-associated X protein	Mus musculus	28-31
29886239-11	2018	In the western blot analysis, PDSN exerted its neuroprotective effect via the upregulation of Bcl-2 and downregulation of Bax and caspase-3.	protodioscin	30-34	BCL2-associated X protein	Mus musculus	122-125
30159329-5	2018	Moreover, with the treatment of aflatoxins, proline dehydrogenase (PRODH) and proapoptotic factors (Bax, Caspase-3) were upregulated, while the inhibitor of apoptosis Bcl-2 was downregulated, at both the mRNA and the protein levels, comparing with the control (P &lt; 0.05).	Aflatoxins	32-42	BCL2-associated X protein	Mus musculus	100-103
30122899-11	2018	In addition, SIN treatment promoted the apoptosis of B16-F10 cells in a dose-dependent manner, as demonstrated by the increase in apoptotic cells, Bax/Bcl-2 ratio, and caspase-3 activity.	sinomenine	13-16	BCL2-associated X protein	Mus musculus	147-150
29951932-4	2018	We found that 50 microM minocycline protected against neuronal apoptosis induced by OGD/R injury, with increased expression ratio of Bcl-2/Bax and reduced expression of caspase-3.	Minocycline	24-35	BCL2-associated X protein	Mus musculus	139-142
30070339-9	2018	RTG treatment also decreased the Bax/Bcl-2 ratio and cleaved caspase 3 expression in the ischemic tissues.	ezogabine	0-3	BCL2-associated X protein	Mus musculus	33-36
29717768-10	2018	In addition, co-administration of breviscapine with CCl4 decreased the apoptotic response by enhancing B-cell lymphoma-2 (Bcl-2) levels, while reducing Bcl-2-associated X protein, apoptotic protease activating factor 1, caspase-3 and PARP activity.	breviscapine	34-46	BCL2-associated X protein	Mus musculus	152-218
30048421-5	2018	In addition, APS also decreased the bax/bcl2 ratio, and cytochrome-c and caspase-3 protein content (P<0.01) in substantia nigra in our mouse PD model.	aps	13-16	BCL2-associated X protein	Mus musculus	36-39
29986533-6	2018	Indeed, CBG pre-treatment inhibited apoptosis, as shown by the reduction of caspase 3 activation and Bax expression, while Bcl-2 levels increased.	cannabigerol	8-11	BCL2-associated X protein	Mus musculus	101-104
29781855-10	2018	In addition, systemic AMD3100 increased local provasculogenic factors (hypoxia-inducible factor 1 alpha, stromal cell-derived factor 1 alpha, and vascular endothelial growth factor; P <= 0.05) and decreased local proapoptotic factors (p53, PUMA, and Bax; P <= 0.05).	plerixafor	22-29	BCL2-associated X protein	Mus musculus	250-253
29806073-8	2018	Collectively, we demonstrate that Taraxasterol inhibits the growth of liver cancer at least partially by enhancing Hint1 expression to regulate Bax, Bcl2, and cyclin D1 expression.	taraxasterol	34-46	BCL2-associated X protein	Mus musculus	144-147
30030951-5	2018	Hence we used real-time PCR to identify alterations in mRNA expression of genes involved in apoptotic pathway, including p53, Bax and Bcl-2 between the morphine-treated and TQ plus morphine-treated mice.	Morphine	152-160	BCL2-associated X protein	Mus musculus	126-129
30030951-5	2018	Hence we used real-time PCR to identify alterations in mRNA expression of genes involved in apoptotic pathway, including p53, Bax and Bcl-2 between the morphine-treated and TQ plus morphine-treated mice.	Morphine	181-189	BCL2-associated X protein	Mus musculus	126-129
30030951-7	2018	In the morphine group, compared to control group, a significant increase in P53 and Bax mRNA expression and a significant decrease in Bcl-2 mRNA expression were observed (p &amp;lt; 0.01).	Morphine	7-15	BCL2-associated X protein	Mus musculus	84-87
30030951-9	2018	Interestingly, TQ (9 and 18 mg/kg) plus morphine caused a significant decrease in p53 and Bax and a significant increase in Bcl2 mRNA expression, compared to morphine-treated group (p &amp;lt; 0.01).	thymoquinone	15-17	BCL2-associated X protein	Mus musculus	90-93
30030951-9	2018	Interestingly, TQ (9 and 18 mg/kg) plus morphine caused a significant decrease in p53 and Bax and a significant increase in Bcl2 mRNA expression, compared to morphine-treated group (p &amp;lt; 0.01).	Morphine	40-48	BCL2-associated X protein	Mus musculus	90-93
30018728-9	2018	In addition, MitoQ treatment reduced Bax protein translocation to mitochondria and cytochrome c release into the cytosol.	mitoquinone	13-18	BCL2-associated X protein	Mus musculus	37-40
29549731-10	2018	In addition, treatment with LCE in BPA-treated TM4 sertoli cells recovered cell viability by attenuating Bax expression and activating caspase 3 and PARP.	LCE	28-31	BCL2-associated X protein	Mus musculus	105-108
29549731-10	2018	In addition, treatment with LCE in BPA-treated TM4 sertoli cells recovered cell viability by attenuating Bax expression and activating caspase 3 and PARP.	bisphenol A	35-38	BCL2-associated X protein	Mus musculus	105-108
29264673-5	2018	Moreover, ODN blocked the inhibition of the anti-apoptotic gene Bcl-2, and the stimulation of the pro-apoptotic genes Bax and caspase-3, induced by MPTP in the substantia nigra pars compacta.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	148-152	BCL2-associated X protein	Mus musculus	118-121
29795372-6	2018	Interestingly, siFAM188B treatment induced the upregulation and activation of p53, and consequently increased p53-regulated pro-apoptotic proteins, PUMA and BAX.	sifam188b	15-24	BCL2-associated X protein	Mus musculus	157-160
29789603-6	2018	Compared to the single treatment, QC plus vorinostat significantly induced apoptosis, disrupted the mitochondrial transmembrane potential, and decreased Mcl-1 and Bcl-2/Bax ratio.	Vorinostat	42-52	BCL2-associated X protein	Mus musculus	169-172
29867489-10	2018	Mechanistically, EAEO significantly decreased the ratio of Bcl-2/Bax and resulted in the activation of caspase-9 and -3.	eaeo	17-21	BCL2-associated X protein	Mus musculus	65-68
29448197-7	2018	Furthermore, the expression of mRNA in PI3K, BAD, Bcl-2, Bax and caspase-9 were significantly increased in the fluoride group (P &lt; 0.01), while the expression of PDK1 was markedly decreased (P &lt; 0.01).	Fluorides	111-119	BCL2-associated X protein	Mus musculus	57-60
29448197-8	2018	The expression of protein in BAD, Bcl-2 and Bax were significantly increased in the fluoride group (P &lt; 0.01), while the expression of PDK1 and P-AKT1 was markedly decreased (P &lt; 0.01).	Fluorides	84-92	BCL2-associated X protein	Mus musculus	44-47
29534229-17	2018	Cy increased the expression of BAX (P &lt; 0.01) and decreased the expression of BCLX-L compared to control ovaries (P &lt; 0.01).	Cyclophosphamide	0-2	BCL2-associated X protein	Mus musculus	31-34
29534229-18	2018	The ovarian BCLX-L:BAX ratio was also lower in Cy-treated mice (P &lt; 0.05).	Cyclophosphamide	47-49	BCL2-associated X protein	Mus musculus	19-22
29484386-7	2018	In addition, pretreatment with mangiferin markedly reduced Dex-induced BMP2 and p-Smad-1 downregulation, and corrected the expression of differentiation- and apoptosis-associated markers, including alkaline phosphatase, OSX, OCN, OPG, RANK, RANKL, Bcl-2 and Bax, which were altered by Dex treatment.	mangiferin	31-41	BCL2-associated X protein	Mus musculus	258-261
29484386-7	2018	In addition, pretreatment with mangiferin markedly reduced Dex-induced BMP2 and p-Smad-1 downregulation, and corrected the expression of differentiation- and apoptosis-associated markers, including alkaline phosphatase, OSX, OCN, OPG, RANK, RANKL, Bcl-2 and Bax, which were altered by Dex treatment.	Dexamethasone	59-62	BCL2-associated X protein	Mus musculus	258-261
29555474-6	2018	RESULTS: DMOG caused hepatocytes damage evidenced by increase in HIF-1alpha, cell death and apoptosis genes p27 and Bax, with concurrent decrease of cell proliferation genes PCNA and CyclinD1.	oxalylglycine	9-13	BCL2-associated X protein	Mus musculus	116-119
29760794-8	2018	Combined treatment of Yangyin Fuzheng Decoction and cisplatin further increased p53 and Bax levels and suppressed Bcl-2 level.	Cisplatin	52-61	BCL2-associated X protein	Mus musculus	88-91
29431616-8	2018	Also, PXR-dependent was the binge EtOH-induced inhibition of hepatic Akr1b8 mRNA, and protein levels of aldehyde dehydrogenase (ALDH) 1A1 and anti-apoptotic Bcl-2, but increased pro-apoptotic Bax protein expression, leading to increases in residual EtOH concentration and the cellular oxidative stress marker, malondialdehyde.	Ethanol	34-38	BCL2-associated X protein	Mus musculus	192-195
29566706-20	2018	Dexmedetomidine increased p-Akt in a time- and dose-dependent manner, and down-regulated the expression of caspase 3 and Bax and up-regulated the Bcl-2 expression in PMVECs.	Dexmedetomidine	0-15	BCL2-associated X protein	Mus musculus	121-124
29556195-7	2018	The expression levels of Bax and Caspase-3 in the untreated CVMC group were significantly higher than those of the normal group and were apparently reduced in the ivabradine-treated group versus the untreated CVMC group.	cvmc	60-64	BCL2-associated X protein	Mus musculus	25-28
29556195-7	2018	The expression levels of Bax and Caspase-3 in the untreated CVMC group were significantly higher than those of the normal group and were apparently reduced in the ivabradine-treated group versus the untreated CVMC group.	Ivabradine	163-173	BCL2-associated X protein	Mus musculus	25-28
29556195-7	2018	The expression levels of Bax and Caspase-3 in the untreated CVMC group were significantly higher than those of the normal group and were apparently reduced in the ivabradine-treated group versus the untreated CVMC group.	cvmc	209-213	BCL2-associated X protein	Mus musculus	25-28
29556195-9	2018	These results indicate that ivabradine could attenuate the expression of Caspase-3 by downregulation of Bax and upregulation of Bcl-2 to prevent the deterioration of cardiac function resulting from ventricular myocyte loss by cardiomyocyte apoptosis.	Ivabradine	28-38	BCL2-associated X protein	Mus musculus	104-107
29480020-7	2018	Treatment with quercetin in the pristane-induced LN mice model was nephroprotective, decreasing proteinuria levels and significantly lowering tissue expression of IL-6, TNF-alpha, TGF-beta1, Bax and TBARS.	Quercetin	15-24	BCL2-associated X protein	Mus musculus	191-194
29480020-7	2018	Treatment with quercetin in the pristane-induced LN mice model was nephroprotective, decreasing proteinuria levels and significantly lowering tissue expression of IL-6, TNF-alpha, TGF-beta1, Bax and TBARS.	pristane	32-40	BCL2-associated X protein	Mus musculus	191-194
29128415-11	2018	In addition, by using the alpha7nAChR agonist PNU282987, the p38 phosphorylation level decreases, rescues the biochemical changes which are tightly associated with Abeta-induced apoptosis, such as Bcl2/Bax level, cytochrome c (Cyt c) release.	PNU-282987	46-55	BCL2-associated X protein	Mus musculus	202-205
29415054-10	2018	COS significantly inhibited reactive oxygen species, MDA5 and IREalpha mRNA and protein expressions, cell apoptosis and Bax and Caspase-3 mRNA and protein expressions, and significantly increased superoxide dismutase-1 mRNA expression, and Bcl-2 and Caspase-8 mRNA and protein expression (all P&lt;0.05).	carbonyl sulfide	0-3	BCL2-associated X protein	Mus musculus	120-123
29289836-6	2018	Cleaved-caspase-8, cleaved-caspase-9 and cleaved-caspase-3 were up-regulated after Brevilin A treatment, together with an increase of Bax protein expression, while Bcl-2 was reduced.	brevilin A	83-93	BCL2-associated X protein	Mus musculus	134-137
29151191-6	2018	The protein expressions of ATM, CHK-2, P53, E2F1, P73, BAX, Caspase-9, and Caspase-3 were significantly increased, while expressions of RAD51 were down-regulated after SiNP exposure by days 15.	sinp	168-172	BCL2-associated X protein	Mus musculus	55-58
29132812-5	2018	In addition, the FA-AAP-CDDP complex significantly promoted the expression of Bax and caspase-3 protein, but inhibited the expression of Bcl-2 protein, which activated the mitochondrial apoptotic pathway of tumor cells in nude mice.	fa-aap-cddp	17-28	BCL2-associated X protein	Mus musculus	78-81
29174113-10	2018	Rotenone decreased the protein levels of Bcl-2 and increased the protein levels of Bax, cleaved caspase-3 and cleaved caspase-9, and this effect was reversed by ghrelin treatment.	Rotenone	0-8	BCL2-associated X protein	Mus musculus	83-86
29174113-10	2018	Rotenone decreased the protein levels of Bcl-2 and increased the protein levels of Bax, cleaved caspase-3 and cleaved caspase-9, and this effect was reversed by ghrelin treatment.	Ghrelin	161-168	BCL2-associated X protein	Mus musculus	83-86
29657400-0	2018	The effect of moderate exercise on the elevation of Bax/Bcl-2 ratio in oral squamous epithelial cells induced by benzopyrene.	Benzopyrenes	113-124	BCL2-associated X protein	Mus musculus	52-55
29657400-8	2018	Conclusion: Moderate exercise could increase the Bax/Bcl-2 ratio in oral squamous epithelial cells induced by benzopyrene.	Benzopyrenes	110-121	BCL2-associated X protein	Mus musculus	49-52
29374767-9	2018	In vivo, compared to mice treated with 5-FU alone, UA treatment was significantly more effective in suppressing the tumor growth without affecting body weight, and in regulating the amount of Bax and Bcl2 in tumor tissues.	usnic acid	51-53	BCL2-associated X protein	Mus musculus	192-195
29364179-5	2018	Upon histopathological and immunohistochemical examination, the mean pathology scores and the percentages of caspase-3-, Bax-, and CK-positive regions were significantly higher in the tulathromycin- and/or DFS-treated groups than in control mice.	tulathromycin	184-197	BCL2-associated X protein	Mus musculus	121-124
29364179-5	2018	Upon histopathological and immunohistochemical examination, the mean pathology scores and the percentages of caspase-3-, Bax-, and CK-positive regions were significantly higher in the tulathromycin- and/or DFS-treated groups than in control mice.	Diclofenac	206-209	BCL2-associated X protein	Mus musculus	121-124
29484272-14	2018	Moreover, curcumin treatment improved cell viability, reduced cell apoptosis, increased Bcl-2 protein levels while decreased Bax and caspase-3 expressions in mouse N2a cells after OGD/R injury.	Curcumin	10-18	BCL2-associated X protein	Mus musculus	125-128
29484272-15	2018	Besides, curcumin treatment inhibited Bax activation and maintained mitochondrial membrane integrity.	Curcumin	9-17	BCL2-associated X protein	Mus musculus	38-41
29484272-17	2018	Moreover, our results for the first time demonstrated curcumin inhibited ischemia-induced mitochondrial apoptosis via restricting Bax activation, which may be one of the possible mechanisms underlying the neuroprotective effects of curcumin.	Curcumin	54-62	BCL2-associated X protein	Mus musculus	130-133
29484272-17	2018	Moreover, our results for the first time demonstrated curcumin inhibited ischemia-induced mitochondrial apoptosis via restricting Bax activation, which may be one of the possible mechanisms underlying the neuroprotective effects of curcumin.	Curcumin	232-240	BCL2-associated X protein	Mus musculus	130-133
29138110-2	2018	The present study tested the hypothesis that ethanol exposure during the period of naturally occurring neuronal death causes a time- and Bax-dependent neuronal loss.	Ethanol	45-52	BCL2-associated X protein	Mus musculus	137-140
29138110-3	2018	Wild-type and Bax knockout mice were given a pair of injections (two hours apart) of ethanol (2.5 g/kg) or saline on postnatal day (P) 4, P7, P10, or P13.	Ethanol	85-92	BCL2-associated X protein	Mus musculus	14-17
29138110-11	2018	Thus, ethanol-induced death of cortical neurons is Bax-dependent, occurs concurrently in all layers, but does not correspond to lamina- and age-dependent expression of DNA fragmentation.	Ethanol	6-13	BCL2-associated X protein	Mus musculus	51-54
29737213-0	2018	Pachymic Acid Sensitizes Gastric Cancer Cells to Radiation Therapy by Upregulating Bax through Hypoxia.	pachymic acid	0-13	BCL2-associated X protein	Mus musculus	83-86
29737213-4	2018	Changes in Bax and HIF1[Formula: see text] expressions were assessed in GC cells following PA treatment.	pachymic acid	91-93	BCL2-associated X protein	Mus musculus	11-14
29737213-7	2018	PA greatly enhanced the sensitivity of GC cells to radiation in vitro and in vivo, upregulated Bax expression and inhibited hypoxia.	pachymic acid	0-2	BCL2-associated X protein	Mus musculus	95-98
29737213-11	2018	PA treatment induces the expression of pro-apoptotic factor Bax by inhibiting hypoxia/HIF1[Formula: see text], supporting the therapeutic potential of PA in radiation therapy against GC.	pachymic acid	0-2	BCL2-associated X protein	Mus musculus	60-63
29737213-11	2018	PA treatment induces the expression of pro-apoptotic factor Bax by inhibiting hypoxia/HIF1[Formula: see text], supporting the therapeutic potential of PA in radiation therapy against GC.	pachymic acid	151-153	BCL2-associated X protein	Mus musculus	60-63
30439699-10	2018	AMO-124 decreased the expression of Bax and cleaved-caspase-3 and upregulated the expression of Bcl-2 in H2O2-treated NRVMs.	amo-124	0-7	BCL2-associated X protein	Mus musculus	36-39
29115406-8	2018	The NF-kappaB inhibitor, caffeic acid phenethyl ester (CAPE), mimicked the protective effects of BBR, as evidenced by the increased expression of nephrin and podocin, and the decreased the expression of caspase-3 and the ratio of Bax/Bcl-2.	caffeic acid phenethyl ester	25-53	BCL2-associated X protein	Mus musculus	230-233
28592707-10	2018	In Study 2, pitavastatin prolonged hind-limb survival after the surgery with increased BCL2-to-BAX protein ratio and inactivated JNK.	pitavastatin	12-24	BCL2-associated X protein	Mus musculus	95-98
30144066-9	2018	Downregulation of miR-340-5p and upregulation of FMOD decreased the expressions of Runx2, Bax, and ERK1/2, and cell apoptosis of chondrocytes, and increased the expressions of FMOD, Col II, Bcl-2, Sox9, and PCNA, and cell proliferation.	mir-340-5p	18-28	BCL2-associated X protein	Mus musculus	90-93
28795366-0	2018	Ru(II)/diphenylphosphine/pyridine-6-thiolate complexes induce S-180 cell apoptosis through intrinsic mitochondrial pathway involving inhibition of Bcl-2 and p53/Bax activation.	ru(ii)	0-6	BCL2-associated X protein	Mus musculus	161-164
28795366-0	2018	Ru(II)/diphenylphosphine/pyridine-6-thiolate complexes induce S-180 cell apoptosis through intrinsic mitochondrial pathway involving inhibition of Bcl-2 and p53/Bax activation.	benzyl diphenylphosphine	7-24	BCL2-associated X protein	Mus musculus	161-164
29115547-8	2018	Hesperidin also significantly suppressed the protein expression levels of p53 and Bax/Bcl-2, and induced the expression of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) in mice with AMI.	Hesperidin	0-10	BCL2-associated X protein	Mus musculus	82-85
30380983-7	2018	In addition, THSG increased Bcl-2 and decreased Bax and Caspase-3 expression by protecting neuronal survival.	thsg	13-17	BCL2-associated X protein	Mus musculus	48-51
29425659-14	2018	SP suppressed APAP-induced JNK phosphorylation and increased the ratio of Bcl-2/Bax.	sp	0-2	BCL2-associated X protein	Mus musculus	80-83
29416617-6	2018	Pretreatment of DOX-treated mice with LDR also decreased DOX-induced cardiac cell apoptosis (TUNEL staining and cleaved caspase-3) and mitochondrial apoptotic pathway (increased p53, Bax, and caspase-9 expression and decreased Bcl2 expression and DeltaPsim dissipation).	Doxorubicin	16-19	BCL2-associated X protein	Mus musculus	183-186
29312803-4	2017	Co-treatment of sorafenib and VPA synergistically inhibited HCC cell viability, induced cell apoptosis, along with the up-regulation of p21, Bax, cleaved caspase9, cleaved caspase3, cleaved PARP and down-regulation of Bcl-xL, suggesting this combination activated intrinsic apoptotic pathway.	Sorafenib	16-25	BCL2-associated X protein	Mus musculus	141-144
29285094-8	2017	Meanwhile, AS-IV remarkably rescued MPP+-induced cell viability reduction, increase in cell apoptosis rate, and upregulation of p-JNK, Bax/Bcl-2 ratio and caspase-3 activity in vitro.	mangion-purified polysaccharide (Candida albicans)	36-40	BCL2-associated X protein	Mus musculus	135-138
31966560-5	2017	Moreover, after inhibitor PD98059 treated mouse peritoneal macrophages infected with XJ-MTB, Bcl-2, Bax and Mcl-1 were reduced, while Cytochrome-c and Caspase-8 protein levels were significantly increased, and Cytochrome-c protein levels was significant higher than Caspase-8 (P&lt;0.05).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	26-33	BCL2-associated X protein	Mus musculus	100-103
28641471-11	2017	ZEA treatment also led to increased apoptosis in the spleen and Peyer"s patches; these changes were associated with changes in the ratios of Bax:Bcl-2.	Zearalenone	0-3	BCL2-associated X protein	Mus musculus	141-144
29053994-10	2017	Furthermore, Bcl-2 and the Bax/Bcl-2 ratio were partially rescued in myoblasts by resveratrol treatment.	Resveratrol	82-93	BCL2-associated X protein	Mus musculus	27-30
28852940-7	2017	Silibinin suppressed the activation of caspase-3 by inhibiting Jun N-terminal kinase phosphorylation and the downstream hippocampal Bax/Bcl-2 ratio.	Silybin	0-9	BCL2-associated X protein	Mus musculus	132-135
28228044-10	2017	Furthermore, the apoptotic cell death was attenuated in mice treated with WFA (31.48 +- 2.50% vs. 50.08 +- 2.08%) accompanied by decreased bax and increased bcl-2.	withaferin A	74-77	BCL2-associated X protein	Mus musculus	139-142
28973639-6	2017	Moreover, the activation of p53 and Bax with the inhibition of Bcl-2 might be the reason for the upregulation of caspase-3 in the apoptosis, as detected by TdT-mediated dUTP nick-end labeling assay in the testes induced by 1,2-DCE.	deoxyuridine triphosphate	169-173	BCL2-associated X protein	Mus musculus	36-39
28973639-6	2017	Moreover, the activation of p53 and Bax with the inhibition of Bcl-2 might be the reason for the upregulation of caspase-3 in the apoptosis, as detected by TdT-mediated dUTP nick-end labeling assay in the testes induced by 1,2-DCE.	ethylene dichloride	223-230	BCL2-associated X protein	Mus musculus	36-39
28856937-6	2017	In vivo, AP/PTX-SLNs were revealed to be much more effective in suppressing tumor growth in B16F10-bearing mice and in eliminating cancer cells in the lungs than single drug (AP or PTX)-loaded SLNs via a synergistic effect through reducing the Bcl-2/Bax ratio.	Paclitaxel	12-15	BCL2-associated X protein	Mus musculus	250-253
28991675-11	2017	In addition, NaB resulted in increased level of Bcl-2 and decreased level of Bax.	nab	13-16	BCL2-associated X protein	Mus musculus	77-80
29160373-5	2017	RESULTS: TSA significantly increased the expression of p-Akt, p-GSK-3beta proteins and the levels of SOD, Bcl-2, reduced the infarct volume and the levels of MDA, ROS, TNF-alpha, IL-1beta, Bax, Caspase-3, TUNEL and attenuated neurological deficit in mice with transient MCAO, LY294002 weakened such effect of TSA dramatically.	trichostatin A	9-12	BCL2-associated X protein	Mus musculus	189-192
28810537-8	2017	Cilostazol also significantly inhibited Bax and cleaved caspase-3 levels and restored the Bcl-2 levels.	Cilostazol	0-10	BCL2-associated X protein	Mus musculus	40-43
28669743-7	2017	These results indicated that inhibition of P2X7R with BBG promoted neuronal survival, not through the activation of survival kinase pathways, but possibly by improved intracellular Ca2+ overload and decreased the levels of Caspase 1, IL-1beta and Bax proteins.	coomassie Brilliant Blue	54-57	BCL2-associated X protein	Mus musculus	247-250
32188225-6	2017	Compared with the BMF group, the CSA and flavone groups had significantly higher and expressions of caspase family proteins (all P<0.05) whereas the levels of Cyt C, PS, Ca2+, and expressions of Bak and Bax were reduced (all P<0.05).	Cyclosporine	33-36	BCL2-associated X protein	Mus musculus	203-206
32188225-6	2017	Compared with the BMF group, the CSA and flavone groups had significantly higher and expressions of caspase family proteins (all P<0.05) whereas the levels of Cyt C, PS, Ca2+, and expressions of Bak and Bax were reduced (all P<0.05).	flavone	41-48	BCL2-associated X protein	Mus musculus	203-206
32188225-7	2017	More importantly, the flavone group had higher levels of Cyt C, Ca2+ and expressions of Bak and Bax compared with the CSA group (all P<0.05), while the levels of PS and caspase family proteins were reduced (all P<0.05).	flavone	22-29	BCL2-associated X protein	Mus musculus	96-99
28849116-10	2017	Caspase-3/-9, Bax/Bcl-2, TLR4 and NF-kappaB protein expression were reduced in CIA mice following scutellarin treatment.	scutellarin	98-109	BCL2-associated X protein	Mus musculus	14-17
29065794-8	2017	Resveratrol also reduced cell viability, altered the expression of apoptotic markers (Bax and Bcl2), and increased expression of gamma-H2A.x (indicative marker of DNA fragmentation) and p53 (a critical DNA damage response protein).	Resveratrol	0-11	BCL2-associated X protein	Mus musculus	86-89
28959203-7	2017	Furthermore, METH elevated the production of reactive oxygen species (ROS) and induced the dysfunction of mitochondrial characterized by a Bcl2/Bax ratio decrease, mitochondrial membrane potential collapse, and cytochrome c. ER stress release was partially reversed by ROS inhibition, and cytochrome c release was partially blocked by knockdown of CHOP.	Reactive Oxygen Species	269-272	BCL2-associated X protein	Mus musculus	144-147
28962142-9	2017	In the low selenium-treated group, the expression of Bax protein increased, whereas the expression of Bcl-2 protein decreased.	Selenium	11-19	BCL2-associated X protein	Mus musculus	53-56
28713987-12	2017	In addition, the cleaved caspase-3 levels, and the ratio of Bax to Bcl-2 in the CAE + A779 group presented a significant rise compared with the CAE group.	Ceruletide	80-83	BCL2-associated X protein	Mus musculus	60-63
28560697-10	2017	Western blot analysis indicated that the expression level of cardiac caspase-3, caspase-8, Bax and BNIP3 were up-regulated due to DOX injection (9 mg/kg).	Doxorubicin	130-133	BCL2-associated X protein	Mus musculus	91-94
28820432-7	2017	Finally, the expression of Jag1 and apoptosis markers such as Bax and cyclin-dependent kinase inhibitor 1A (CDKN1A) was decreased in podocytes derived from db/db mice treated with fasudil.	fasudil	180-187	BCL2-associated X protein	Mus musculus	62-65
28668383-10	2017	Furthermore, it"s found that expression of cytochrome C, as well as the restoration of Bcl-2/Bax and Bcl-xl/Bax ratio in the presence of Berberine, led to a decline in the apoptotic rate.	Berberine	137-146	BCL2-associated X protein	Mus musculus	93-96
28668383-10	2017	Furthermore, it"s found that expression of cytochrome C, as well as the restoration of Bcl-2/Bax and Bcl-xl/Bax ratio in the presence of Berberine, led to a decline in the apoptotic rate.	Berberine	137-146	BCL2-associated X protein	Mus musculus	108-111
29113340-6	2017	Analgecine treatments also activated apoptotic signaling with increased levels of pro-apoptotic proteins, including cytochrome c, caspase-3, cleaved caspase-3, caspase-9, p53 and Bax, and decreased Bcl2.	analgecine	0-10	BCL2-associated X protein	Mus musculus	179-182
28784995-6	2017	Meanwhile, overexpression of miR-98 reversed H2O2-induced Bcl-2 downregulation and Bax elevation and significantly reduced JC-1 monomeric cells.	Hydrogen Peroxide	45-49	BCL2-associated X protein	Mus musculus	83-86
28529240-4	2017	Mn-induced mitochondria-related apoptotic characteristics, such as caspase-3 and -9 activation, cytochrome c release, Bax increase, and Bcl-2 decrease, were significantly suppressed by curcumin.	Curcumin	185-193	BCL2-associated X protein	Mus musculus	118-121
28726929-8	2017	Sesamin decreased the levels of p-JNK protein, which in turn inactivated pro-apoptotic signaling events by restoring the balance between mitochondrial pro-apoptotic Bcl-2 and Bax proteins.	sesamin	0-7	BCL2-associated X protein	Mus musculus	175-178
29082365-13	2017	CONCLUSION: Continuous exposure of 2 MAC sevoflurane in 2 lit/min O2 simultaneous during prepubertal may create more testicular tissue damage in terms of cellular and molecular function compared to continuous exposure to lower level of sevoflurane by increase in ratio of Bax/Bcl2 and apoptosis in germ cells after puberty.	Sevoflurane	41-52	BCL2-associated X protein	Mus musculus	272-275
29082365-13	2017	CONCLUSION: Continuous exposure of 2 MAC sevoflurane in 2 lit/min O2 simultaneous during prepubertal may create more testicular tissue damage in terms of cellular and molecular function compared to continuous exposure to lower level of sevoflurane by increase in ratio of Bax/Bcl2 and apoptosis in germ cells after puberty.	Oxygen	66-68	BCL2-associated X protein	Mus musculus	272-275
29082365-13	2017	CONCLUSION: Continuous exposure of 2 MAC sevoflurane in 2 lit/min O2 simultaneous during prepubertal may create more testicular tissue damage in terms of cellular and molecular function compared to continuous exposure to lower level of sevoflurane by increase in ratio of Bax/Bcl2 and apoptosis in germ cells after puberty.	Sevoflurane	236-247	BCL2-associated X protein	Mus musculus	272-275
28709158-10	2017	The results showed that DEX decreased TUNEL-positive cells induced by heatstroke in a Bax/Bcl-2-related manner.	Dexmedetomidine	24-27	BCL2-associated X protein	Mus musculus	86-89
28749416-3	2017	In 25 mM of l-Glu-damaged HT22 cells, a 3-h pretreatment with AC strongly improved cell viability, reduced the proportion of apoptotic cells, restored mitochondrial function, inhibited the over-production of intracellular reactive oxygen species (ROS) and Ca2+, and suppressed the high expression levels of cleaved-caspase-3, calpain 1, apoptosis-inducing factor (AIF) and Bax.	Glutamic Acid	12-17	BCL2-associated X protein	Mus musculus	373-376
28749416-3	2017	In 25 mM of l-Glu-damaged HT22 cells, a 3-h pretreatment with AC strongly improved cell viability, reduced the proportion of apoptotic cells, restored mitochondrial function, inhibited the over-production of intracellular reactive oxygen species (ROS) and Ca2+, and suppressed the high expression levels of cleaved-caspase-3, calpain 1, apoptosis-inducing factor (AIF) and Bax.	Actinium	62-64	BCL2-associated X protein	Mus musculus	373-376
28732510-7	2017	RESULTS: We demonstrated that 2ccPA suppressed the CoCl2-induced increase in the Bax/Bcl-2 protein expression ratio and phosphorylation levels of p38MAPK and JNK protein.	2-carba-cyclic phosphatidic acid	30-35	BCL2-associated X protein	Mus musculus	81-84
28732510-7	2017	RESULTS: We demonstrated that 2ccPA suppressed the CoCl2-induced increase in the Bax/Bcl-2 protein expression ratio and phosphorylation levels of p38MAPK and JNK protein.	cobaltous chloride	51-56	BCL2-associated X protein	Mus musculus	81-84
28371286-11	2017	Our in vitro results indicate that ginsenoside Rg1 treatment increases intracellular oxidative stress, decreases mitochondrial membrane potential, increases the Bax/Bcl-2 ratio, and activates caspase-9 and caspase-3, but not caspase-8.	Ginsenosides	35-46	BCL2-associated X protein	Mus musculus	161-164
28560451-6	2017	The results also showed that PPE treatment inhibited mitogen-activated protein kinase phosphorylation, prevented the activation of pro-apoptotic protein caspase-3, decreased the levels of apoptosis-inducing Bax protein, and increased the levels of the anti-apoptotic mediator, Bcl-2, induced by AMK in the mouse cochlea.	ppe	29-32	BCL2-associated X protein	Mus musculus	207-210
28751809-5	2017	mRNA for anti-apoptotic Bcl-2 was decreased and that for pro-apoptotic Bax was increased in the carcinoma tissue of CR, l-1-deoxynojirimycin and H-1-deoxynojirimycin groups.	Chromium	116-118	BCL2-associated X protein	Mus musculus	71-74
28751809-5	2017	mRNA for anti-apoptotic Bcl-2 was decreased and that for pro-apoptotic Bax was increased in the carcinoma tissue of CR, l-1-deoxynojirimycin and H-1-deoxynojirimycin groups.	CHEMBL369297	120-140	BCL2-associated X protein	Mus musculus	71-74
28751809-5	2017	mRNA for anti-apoptotic Bcl-2 was decreased and that for pro-apoptotic Bax was increased in the carcinoma tissue of CR, l-1-deoxynojirimycin and H-1-deoxynojirimycin groups.	h-1-deoxynojirimycin	145-165	BCL2-associated X protein	Mus musculus	71-74
31210848-11	2019	AEEF inhibited apoptotic signals by regulating phosphorylated c-Jun N-terminal kinases (p-JNK), phosphorylated protein kinase B (p-Akt), Bcl-2-associated X protein (BAX), and phosphorylated Tau (p-Tau).	aeef	0-4	BCL2-associated X protein	Mus musculus	165-168