Ignet

Gene Information

Gene symbol: BCL2

Gene name: B-cell CLL/lymphoma 2

HGNC ID: 990

Synonyms: Bcl-2, PPP1R50

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	ALB	1 hits
3	BAD	1 hits
4	BAX	1 hits
5	BCL2L1	1 hits
6	BIRC5	1 hits
7	BNIP3L	1 hits
8	CASP3	1 hits
9	CASP8	1 hits
10	CASP9	1 hits
11	CAT	1 hits
12	CREB1	1 hits
13	CXCR4	1 hits
14	CYCS	1 hits
15	DNTT	1 hits
16	EPO	1 hits
17	ESR2	1 hits
18	FAS	1 hits
19	FASLG	1 hits
20	FOXM1	1 hits
21	GCG	1 hits
22	HRK	1 hits
23	HSPA1A	1 hits
24	IFNG	1 hits
25	INS	1 hits
26	LEP	1 hits
27	MAPK1	1 hits
28	MAPK3	1 hits
29	MCL1	1 hits
30	NAMPT	1 hits
31	NFKB1	1 hits
32	NGF	1 hits
33	NOS2A	1 hits
34	NOS3	1 hits
35	NR1I2	1 hits
36	PDX1	1 hits
37	PPP2R4	1 hits
38	PRKAA2	1 hits
39	PRKAR2A	1 hits
40	PTGS2	1 hits
41	SLC2A2	1 hits
42	SOD1	1 hits
43	SPHK1	1 hits
44	SRC	1 hits
45	TNF	1 hits
46	TNFSF10	1 hits
47	TP53	1 hits
48	TSC2	1 hits
49	UCP2	1 hits

Related Sentences

#	PMID	Sentence
1	11899074	The delivery of transgenes capable of interfering with antigenic recognition and/or cell death [e.g., Fas ligand (FasL), Bcl-2, Bcl-XL] as well as imparting tolerance/immunoregulation [e.g., interleukin(IL)-4, IL-10, transforming growth factor (TGF)-beta], or cytoprotection [e.g., heme oxygenase-1 (HO-1), catalase, manganese superoxide dismutase (MnSOD)] may prevent recurrent type 1 diabetes in islet transplantation and offer a promising form of immunotherapy.
2	11812749	Cu/Zn-superoxide dismutase (SOD) and Mn-SOD were modestly induced, and Bcl-2 was modestly reduced; however, several other stress genes (catalase, heat shock protein 70, and p53) were unaltered.
3	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.
4	11978640	RT-PCR studies revealed no major change of iNOS and Bax mRNA expression and a marked decrease of Bcl-2 mRNA expression in the islets cultured with FFA.
5	12658358	The immunohistochemistry and RT-PCR assay showed a higher level of Fas expression and Fas mRNA in the cataracts with DR than in the senile cataracts, although there was no difference in the expression level of the Fas ligand, Bcl-2, and their mRNAs between both groups.
6	12663450	Our in silico screening strategy indicated that a hypoxia-inducible proapoptotic member of the Bcl-2 gene family called Nix is expressed during erythropoiesis.
7	15784465	To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction.
8	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.
9	15935144	The three principal objectives of this commentary are to: (i) review the existing evidence, which suggests regulation, by glucose and other insulin secretagogues, of PP2A in the beta cell; (ii) discuss the experimental evidence, which implicates PP2A-like enzymes in the dephosphorylation and inactivation of key beta cell phosphoprotein substrates (e.g., Akt and Bcl-2), which may be necessary for beta cell proliferation and survival, culminating in the loss of the beta cell mass; and (iii) highlight potential avenues for future research, including the development of specific pharmacological and therapeutic interventional modalities for the inhibition of specific PP2A-like phosphatases for the prevention of loss of beta cell mass leading to the onset of diabetes.
10	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.
11	16394503	MCTF treatment activated caspase-8, -9 and -3, and led to cleaved poly (ADP-ribose) polymerase and release of cytochrome c into cytosol in a concentration-dependent manner, while MCTF did not affect Bax or Bcl-2 protein levels as shown by Western blot analysis.
12	16243419	We investigated the apoptotic effects of polyphenols from red wine on human colon cancer cells SNU-C4 using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 4,6-diamidino-2-phenylindole (DAPI) staining, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, reverse transcription-polymerase chain reaction (RT-PCR) expressions of Bcl-2, Bax and Caspase-3 genes, and Caspase-3 enzyme activity.
13	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.
14	16873684	cAMP-responsive element-binding protein (CREB) is required for beta-cell survival by regulating expression of crucial genes such as bcl-2 and IRS-2.
15	16780994	After small and large dosage (1 or 10mg/kg/d) carvedilol-administrated for 5 weeks, hemodynamic parameters, the levels of malondialdehyde (MDA), the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and expression of Bcl-2 mRNA in the cardiac tissues of all six groups were measured.
16	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.
17	17318810	This study investigated the effects of leptin upon apoptosis induced by serum depletion and on expression of the apoptotic regulators B-cell leukaemia 2 gene product (BCL-2) and BCL2-associated X protein (Bax) in the glucose-responsive BRIN-BD11 beta-cell line.
18	17318810	At the protein level, leptin increased BCL-2 and decreased Bax, altering the BCL-2 : Bax ratio.
19	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.
20	17870134	Our findings suggest that streptozotocin-induced diabetes increases apoptotic cell death in testis tissue through the up-and down-regulation of Bcl-2 family proteins and the interaction of Bad and Bcl-X(L).
21	18252892	We isolated islets from mice lacking Bid, Bax, or Bak and those overexpressing Bcl-2 and exposed them to Fas ligand, tumor necrosis factor (TNF)-alpha, and proinflammatory cytokines or cytotoxic stimuli that activate the mitochondrial apoptotic pathway (staurosporine, etoposide, gamma-radiation, tunicamycin, and thapsigargin).
22	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.
23	19629134	We presently show that the cytokines IL-1beta+IFN-gamma and different ER stressors activate the Bcl-2 homology 3 (BH3)-only member death protein 5 (DP5)/harakiri (Hrk) resulting in beta-cell apoptosis.
24	19851988	Paradoxically in the face of such increased cell death, the expression of pro-apoptotic genes Casp3 and Casp9 was decreased by diabetes, while the anti-apoptotic gene Bcl2 was increased.
25	19706988	Interestingly, insulin I and II, anti-apoptotic bcl-2, and proliferation promoting ERK-1 gene expressions were significantly upregulated in db/m mice.
26	20382773	Finally, in STZ-treated animals, UAG and Ob up-regulated insulin and Pdx1 mRNA and increased the expression of BCL2 similarly to AG.
27	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.
28	20421300	Here, we demonstrate that the proinflammatory cytokine interleukin-1beta, combined with interferon-gamma, induces the expression of the Bcl-2 homology 3 (BH3)-only activator PUMA (p53 up-regulated modulator of apoptosis) in beta-cells.
29	20651283	Treatment with HNG significantly increased phosphorylation of AMPK and phosphorylation of endothelial nitric oxide synthase in the heart and attenuated Bcl-2-associated X protein and B-cell lymphoma-2 levels following myocardial ischemia and reperfusion.
30	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).
31	19758361	In addition, the expression of lipogenic genes and UCP-2 were upregulated, but AMPK, IRS-2, PDX-1, GLUT-2 and Bcl-2 were downregulated in the exposed cells.
32	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).
33	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.
34	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.
35	21048311	Interestingly, laccase balanced pro- (Bax) and anti-apoptotic (Bcl-2) proteins in terms of both the mRNA and protein levels with a downregulation of cytochrome c protein in RINm5f cells.
36	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.
37	20957341	Transfection of VSMC from non-diabetic patients with a plasmid containing COX-2 (also known as PTGS2) increased basal production of COX-2 and BCL2 and mimicked the resistance to apoptosis that occurs in diabetic patients.
38	20957341	However, inhibition of COX-2 production by small interfering RNA proved unable to reverse BCL2 production in diabetic VSMC.
39	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.
40	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.
41	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.
42	19114643	In vivo MR antagonist treatment promoted antiapoptotic effects by increasing phosphorylation of BAD serine(136) and expression of Bcl-2 and Bcl-xL, decreasing cytochrome c release and BAD expression, and suppressing caspase-3 activation.
43	20685070	Further, we found that EPO inhibited high glucose-induced renal tubular cell apoptosis and that this protective effect was dependent on reduction of Bax/caspase-3 expression as well as elevation of Bcl-2 expression.
44	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.
45	19463916	Twenty-three retinal genes, mainly from TNF ligand and receptor, caspase, Bcl-2 and death domain subfamilies that were upregulated by least a two-fold in PC rats remain upregulated after reversal of hyperglycemia.
46	21190961	BCL-6 decreased Fas and inducible nitric oxide synthase expression and nitric oxide production, but it inhibited the expression of the antiapoptotic proteins Bcl-2 and JunB while increasing the expression of the proapoptotic death protein 5.
47	21111711	GS treatment also decreased bcl-2 gene expression, followed by mitochondrial swelling, increased cytochrome c release, and caspase activation.
48	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.
49	21211384	Gastric bypass surgery can significantly reduce the blood glucose level and promote the secretion of GLP-1, and therefore inhibit the apoptosis of the islet ? cells in diabetic rats through the Bcl-2 pathway.
50	18524857	Under diabetic conditions, Bcl-2 protein expression was decreased, whereas cleaved caspase-3 protein expression was increased (P < 0.05), and these changes were inhibited by FR167653 treatment.
51	19144689	A role for the mitochondrial apoptotic pathway was unlikely as both caspase-9 activity (initiator caspase of this pathway) and expression of regulatory proteins such as Bax and Bcl-2 were unchanged.
52	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.
53	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.
54	21296063	Metoprolol induced a shift from protein kinase A to protein kinase B-mediated signaling, associated with a shift in the phosphorylation patterns of BCl-2 and Bad which favored BCl-2 action.
55	21289215	Induction of diabetes also increased phosphorylation of tuberin in association with mTOR activation (measured by p70S6K phosphorylation), inactivation of Bcl-2, increased cytosolic cytochrome c expression, activation of caspase 3, and cleavage of PARP; insulin treatment prevented these changes.
56	21289215	In vitro, exposure of PTE cells to HG increased phosphorylation of tuberin and p70S6K, phosphorylation of Bcl-2, expression of cytosolic cytochrome c, and caspase 3 activity.
57	20798690	All cytotoxic stresses rapidly and preferentially decreased Mcl-1 protein expression as compared with the late effect observed on the other antiapoptotic proteins, Bcl-2 and Bcl-xL.
58	21496888	The extent of oxidative stress and apoptosis, expression of poly(ADP-ribose) (PAR), NF-?B, phosphorylated inhibitor of NF-?B (I?B)-?, Bcl-2, and Bax in the bladder were also investigated.
59	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.
60	12697734	Bcl(XL) and Bcl-2 expression were reduced in Pdx1(+/-) islets.
61	20374430	This involved amelioration of elevated caspase 3 activity, down-regulation of pro-apoptotic Bax and up-regulation of anti-apoptotic Bcl-2 protein.
62	21521872	Bcl-2, Cdk4, and c-myc expression levels were increased in Pax4 islets while MafA, insulin, and GLUT2 transcript levels were suppressed in both animal models.
63	16951721	We found that ginseng suppresses UCP-2, down-regulates caspase-9 while increasing ATP and insulin production/secretion and up-regulates Bcl-2, reducing apoptosis.
64	16951721	These findings suggest that stimulation of insulin production and prevention of beta cell loss by American ginseng extracts can occur via the inhibition of mitochondrial UCP-2, resulting in increase in the ATP level and the anti-apoptotic factor Bcl-2, while down-regulation of pro-apoptotic factor caspase-9 occurs, lowering the occurrence of apoptosis, which support the hypothesis.
65	20233722	Concomitantly, AMPK activation increased the expression of both Bcl-2 and Survivin, two potent anti-apoptotic proteins.
66	20233722	Finally, we found that genetic deletion of the AMPKalpha1, but not AMPKalpha2, suppressed OGD-enhanced NF-kappaB activation, the expression of Bcl-2 and Survivin, and endothelial apoptosis.
67	20233722	Overall, our results suggest that AMPKalpha1, but not AMPKalpha2 activation, promotes cell survival by increasing NF-kappaB-mediated expression of anti-apoptotic proteins (Bcl-2 and Survivin) and intracellular ATP contents.
68	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.
69	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).
70	21773964	Furthermore, we found that glargine downregulated the level of Bax protein and upregulated that of Bcl-2 (p <0.05).
71	21667436	Immunohistochemical and Western blot analyses revealed the downregulation of Bcl-2, upregulation of Bax, and increased activation of caspase-9 and -3, in diabetic rats, indicating that the apoptosis of taste bud cells may be mediated via the intrinsic mitochondrial pathway in diabetics.
72	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.
73	21742976	T cell depletion induced by FNB anti-CD3 mAb was independent of the proapoptotic proteins Fas, caspase-3, and Bim and was not inhibited by overexpression of the anti-apoptotic protein, Bcl-2.
74	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.
75	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.
76	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.
77	18840766	This experiment evaluated whether temporal Akt activity coincided with Bax to Bcl-2 binding.
78	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.
79	21963730	Estrogen receptor beta was expressed in the cultured cells, and genistein protection was blocked by ICI-182780 administration as well as Bcl-2 siRNA transfection.
80	21471274	Visfatin significantly reduced the cell apoptosis induced by palmitate and caused a significant change in the expression of several proapoptotic proteins, including upregulation of Bcl-2 and a marked downregulation of cytochrome c and caspase 3.
81	11211190	We compared insulin secretion, islet cell death and survival, inducible nitric oxide synthase (iNOS) mRNA expression, nitrite production, and Bcl-2 and Bax mRNA expression in isolated human and large mammal (bovine) islets exposed to 50 U/ml recombinant human interleukin-1, 1,000 U/ml recombinant human tumor necrosis factor-alpha and 1,000 U/ml recombinant human interferon-gamma.
82	17878289	In MIN6 beta-cells, a CXCR4 antagonist (AMD3100) induces apoptosis, increases reactive oxygen species, decreases expression levels of the anti-apoptotic protein Bcl-2, and reduces phosphorylation of the proapoptotic protein Bad.