Ignet

Gene Information

Gene symbol: BAX

Gene name: BCL2-associated X protein

HGNC ID: 959

Synonyms: BCL2L4

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	AKT1	1 hits
3	BCL2	1 hits
4	BCL2L1	1 hits
5	CASP3	1 hits
6	CASP9	1 hits
7	CAT	1 hits
8	CYCS	1 hits
9	FOXM1	1 hits
10	GPT	1 hits
11	INS	1 hits
12	LEP	1 hits
13	MAPK1	1 hits
14	NGF	1 hits
15	NOS2A	1 hits
16	PARP1	1 hits
17	PDCD4	1 hits
18	PIK3CA	1 hits
19	SOD1	1 hits
20	SPHK1	1 hits
21	TNF	1 hits
22	TP53	1 hits
23	TXNIP	1 hits
24	XIAP	1 hits

Related Sentences

#	PMID	Sentence
1	21269661	The aim of the study was to determine in a rat model of streptozotocin-induced diabetic nephropathy the expression of: WT-1 (for podocyte loss in the glomerulus), TGF-beta 1 (for tissue damage), caspase-3 and bax (for glomerular apoptosis) and the possible protective effects of an angiotensin II type 1 receptor blocker.
2	21269661	We conclude that the decrease in the number of podocytes is an early marker of diabetic nephropathy, AT1 receptor blocker has renoprotective effects on the regulation of renal hemodynamics and on the control of tissue damage by preventing podocyte loss, which leads to decrease of bax and caspase-3 expressions of apoptosis related proteins, and may prevent glomerular cell apoptosis via angiotensin II.
3	9398849	However, IR-induced apoptosis and Bax induction were completely normal; both of which are mediated by p53.
4	11813268	This effect was correlated with a marked decrease of Bcl-2 mRNA expression (without any major change of Bax mRNA) and a marked increase of inducible nitric oxide synthase mRNA.
5	15153564	Caspase-3 activity was also increased, and the authors linked it to a low PI3K-induced activation of the apoptotic system that includes a conformational change in Bax and release of cytochrome C.
6	15705778	We therefore generated a stable transfected beta-cell line (INS-1) overexpressing human TXNIP and found that TXNIP overexpression induced apoptosis as assessed by Bax, Bcl2, caspase-3, and cleaved caspase-9 as well as Hoechst staining.
7	16114068	The subcellular localizations of Bcl-2, an antiapoptotic protein, and Bax, a proapoptotic protein, within RIN cells were altered with TNF-alpha treatment such that the two were colocalized with mitochondria in the perinuclear region.
8	16282055	LWDHP can up-regulate the expression of bcl-2 and down-regulate the expression of Bax at transcription level, which maybe contribute to the anti-apoptosis effects of LWDHP.
9	16243419	Compared with untreated control group, polyphenols (100 microg/ml) reduced the expression of Bcl-2 whereas those of Bax and Caspase-3 were increased.
10	17053028	In this study, we demonstrate that diazoxide prevents the onset and development of diabetes in OLETF rats by inhibiting beta-cell apoptosis via increasing p38beta MAPK, elevating Bcl-2/Bax ratio, and ameliorating insulin secretory capacity and action.
11	17287463	V5 treatment upregulated expression of anti-apoptotic proteins Bcl-2 and XIAP (X-linked inhibitor of apoptosis protein) by more than 3- and 11-fold and downregulated expression of apoptosis-inducing proteins Bax, Bad, and nuclear factor-kappaB-p65 by 10, 30, and nearly 50%, respectively.
12	17456851	FFA-induced inhibition of insulin secretion was not associated with increased transcript levels of the apoptosis markers Bax (BclII-associated X protein) and caspase-3.
13	17473225	Phosphorylation of Akt was analyzed by Western blot and apoptosis by Blc-2 and Bax measurements.
14	17318810	At the protein level, leptin increased BCL-2 and decreased Bax, altering the BCL-2 : Bax ratio.
15	17318810	We conclude that leptin reduces apoptosis in beta-cells at physiological concentrations, possibly via its ability to up-regulate BCL-2 and Bax expression.
16	19455054	BHE elevated antiapoptotic proteins Bcl-2 and heme oxygenase-1 and stimulated the phosphorylation of survival protein Akt simultaneously decreasing the apoptotic proteins Bax and Src.
17	20395372	In addition, Bcl-2 transfection inhibited apoptosis and attenuated albumin-induced Bax translocation to mitochondria and cytochrome c release from the organelles, further confirming a role for the intrinsic pathway of apoptosis in albuminuria-associated tubular apoptosis.
18	20406798	The following measures were assessed in the left ventricle: size of MI, systolic and diastolic function by echocardiography, cytokines by ELISA (TNF-alpha, IL-1beta, IL-6, and IL-10), gene expression by real-time PCR (Bax, Fas, p53, Bcl-2, HIF1-alpha, VEGF, and IL8r), caspase-3 activity by spectrofluorometric assay, glucose transporter type 1 and 4 (GLUT-1 and GLUT-4) protein expression by western blotting, and capillary density and fibrosis by histological analysis.
19	20660595	This was followed by Bax translocation to the mitochondria with subsequent cytochrome c release, opening of the permeability transition pore, and apoptosis.
20	19848202	They were sacrificed at 28 weeks old for observing serum fasting blood glucose (FBG), triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST) by automatic biochemistry; liver cell apoptosis by flow cytometry; pathomorphology by electron microscope; and mRNA expressions of bcl-2 and bax genes by RT-PCR; as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), Na(+)-K(+)-ATPase; and content of malondialdehyde (MDA) in liver tissue by spectrophotometer.
21	19848202	In KKAy mice, blood levels of FBG, TG, TC, ALT, AST and liver cell apoptosis rate were higher; the bax mRNA expression was higher and bcl-2 mRNA was lower markedly; the activities of SOD, GSH-Px, Na(+)-K(+)-ATPase in liver tissue were lower, and MDA content was higher than those in the normal control significantly (all P <0.01).
22	20650802	Compared with the NC group, the rats in the DM group showed significantly decreased body weight (P<0.05), increased blood glucose at o and 120 min after oral glucose administration, decreased expressions of Bcl-2 (P<0.01), increased expression of Bax (P<0.01), and increased islet cell apoptosis (P<0.05).
23	20650802	Diazoxide treatment significantly decreased the body weight (P<0.05), decreased the blood glucose, increased Bcl-2 expression (P<0.01), decreased Bax expression (P<0.05), and reduced the islet cell apoptosis (P>0.05) of the diabetic rats.
24	20541824	The expression of iNOS and the promoting apoptosis gene Bax and Fas were significantly up-regulated by the induction of IL-1beta and TNF-alpha.
25	20541824	Silencing iNOS by RNAi prevented the up-regulation of Bax and Fas induced by cytokine, thus reduced apoptosis of islets and recovered the insulin secretion index (3.43+/-0.24 vs 1.87+/-0.31, P<0.01).
26	20803707	The results showed that treatment with GlcN induced HIT-T15 cell death via apoptotic pathway, inhibited the expression of Bcl-2 and Bcl-xL, enhanced the expression of Bax, Bid and caspase-3, reduced the production of ATP and decreased in insulin secretion.
27	20960169	Bax expression was elevated in diabetic 2-cell embryos, but caspase-3 expression did not significantly differ between diabetic and nondiabetic 2-cell embryos.
28	20889222	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 ?-cells.
29	21139139	This resistance to apoptosis was associated with decreased abundance of the proapoptotic protein Bax and increases in abundance of the antiapoptotic proteins Bcl-2, Bcl-xL, XIAP, and Flip.
30	20363911	Diabetes of 2 months duration caused a significant decrease in expression of Bcl-2 in retina, upregulation of Bax in whole retina and isolated retinal microvessels, and increased generation of retinal superoxide and leukostasis.
31	20363911	Furthermore, overexpression of Bcl-2 in the vascular endothelium inhibited the diabetes-induced degeneration of retinal capillaries and aberrant superoxide generation, but had no effect on Bax expression or leukostasis.
32	20933054	Overexpression of mitochondrially located catalase (MitoCatalase) specifically increased basal Bcl-2 and decreased basal Bax expression, suppressed cytokine-mediated reduction of Bcl-2, and thereby prevented the release of cytochrome c, Smac/DIABLO and the activation of caspase-9 and -3.
33	20031167	Increased Bax, Daxx, and JNK mRNA expression and decreased Bcl X(L) expression in insulin-deficient rats, led to increased hepatocyte apoptosis than normal rats.
34	20676904	Activation of hypertrophic and cell signaling pathways was determined by assessing protein expression levels of atrial natriuretic peptide (ANP), ?-sarcomeric actin, p53, Bax and Bcl-2 and phosphorylation of p38, ERK and Akt.
35	21235725	Expression of phospho-Akt, phospho-Bad, Bcl-2, and concentrations of ATP and NAD+ were decreased in the DM group, whereas concentrations of MDA, expression of Bax, nuclear translocation of AIF, and caspase-3 activity were increased.
36	21500593	To explore the possible mechanism of nerve growth factor (NGF) mixed insulin on the angiogenesis of burn wounds and the effect on the expressions of Bcl-2 and Bax in diabetic rats.
37	21500593	A combination of NGF and insulin local application can enhance the angiogenesis of the burn wound in diabetic rats and accelerate wound healing by increasing the expression of Bcl-2 and decreasing the expression of Bax and restraining apoptosis of the wounds vascular endothelial cells of diabetic rats.
38	20798690	Knocking down Mcl-1 using small interference RNAs increased apoptosis and caspase-3 cleavage induced by cytokines, palmitate or thapsigargin, whereas Mcl-1 overexpression partly prevented Bax translocation to the mitochondria, cytochrome c release, caspase-3 cleavage and apoptosis induced by the ?-cell death effectors.
39	18506358	Antiapoptotic effect of fidarestat in high glucose-exposed retinal pericytes was not associated with the inhibition of Bax or increase in Bcl-2 expression.
40	20374430	This involved amelioration of elevated caspase 3 activity, down-regulation of pro-apoptotic Bax and up-regulation of anti-apoptotic Bcl-2 protein.
41	19662359	The results showed that in G1, G2 and G3 groups, insulin secretion was enhanced with the increase of glucose concentration, and the NF-kappaB expression was also increased (P<0.05), but Bax activity, Cyt C release and apoptosis rate showed no significant difference among them.
42	21625639	Further mechanistic study examined the expression of Bcl-2 family members, including Bcl-2, Mcl-1, Bax and Bim, in SPHK1-overexpressing glioma cells and revealed that only pro-apoptotic Bim was downregulated by SPHK1.
43	21730150	In pancreatic ? cells, c-Rel and p65 of the NF-?B family activated the mir21 gene promoter and increased miR-21 RNA levels; miR-21 in turn decreased the level of PDCD4, which is able to induce cell death through the Bax family of apoptotic proteins.
44	21320264	Furthermore, telmisartan also decreased Bax expression (4.45 � 1.24% vs. 10.25 � 0.96%, p < 0.01), number of TUNEL-positive cells (6.2 � 0.98% vs. 13.0 � 1.6, p < 0.01), inflammation, myonecrosis and increased Bcl-2 expression (5.45 � 0.15% vs. 1.24 � 0.3%, p < 0.01).
45	21614569	This effect was accompanied by a significant increase in insulin content and Pdx1 expression, and a significant decrease of apoptosis and Bax expression in pancreatic islets from db/db mice.
46	21753123	Consistent with these results, caspase-3 activity and BAX and sterol regulatory element binding protein-1c (SREBP-1c) mRNA levels were markedly increased in INS-1 cells co-administered palmitic acid and T0901317.
47	21773964	Furthermore, we found that glargine downregulated the level of Bax protein and upregulated that of Bcl-2 (p <0.05).
48	21798071	Furthermore, qRT-PCR assay demonstrated that rhNRG-1 treatment could decrease the expression of bax and caspase-3 and increase that of bcl-2.
49	18840766	Therefore, the purpose of this study was to determine whether palmitate-induced apoptosis in C(2)C(12) myotubes is dependent on Bax to Bcl-2 binding.
50	18840766	An additional purpose of this study was to determine whether the changes in Bax to Bcl-2 binding corresponded to decreases in Akt signaling in palmitate-treated myoblasts.
51	18840766	Bax to Bcl-2 binding was determined through a coimmunoprecipitation assay that was performed in myotubes after 2 h of serum starvation, followed by 10 min of serum reintroduction.
52	18840766	This experiment evaluated whether temporal Akt activity coincided with Bax to Bcl-2 binding.
53	18840766	In addition, there was a fourfold reduction in Bax to Bcl-2 binding with palmitate treatment, which mirrored the reduction in Akt(Ser473) phosphorylation.
54	22061042	Increased oxidative stress, mitochondrial membrane depolarization, activation of caspase-3, and PARP observed in diabetic groups indicated bax triggered mitochondrial mediated cellular apoptosis.
55	21984578	PTPN2 silencing and exposure to type I and II IFNs induced BAX translocation to the mitochondria, cytochrome c release, and caspase 3 activation.