Browse our anti-BCL2 (BCL2) Antibodies

Human B-Cell CLL/lymphoma 2 (BCL2) interaction partners

1. BCL2 levels are elevated in breast cancer where they are marker of good prognosis. BCL2 and active caspase levels correlate negatively; yet, active caspases indicate good outcome. Low BCL2 and low caspase-7 are highly prognostic of unfavourable outcome across all breast cancers. BCL2 levels indicate molecular subtype and tumour proliferation status in breast cancer.

2. KPT-330 treatment increased binding of Bcl-2 to Bim but was overcome by ABT-199 treatment, demonstrating that KPT-330 and ABT-199 reciprocally overcome apoptosis resistance. Mcl-1 knockdown and overexpression confirmed its critical role in the antileukaemic activity of the combination

3. Mechanistic investigation demonstrated that FSTL5 promoted Hepatocellular carcinoma (HCC) cell apoptosis in a caspase-dependent manner and regulated Bcl-2 family proteins. These results indicate that FSTL5 may be a potential novel target for HCC treatment, and a biomarker for tumor prognosis.

4. These pore-forming effector proteins share four Bcl-2 homology (BH) domains.

5. Study results indicate that TRAF3, perhaps by promoting exacerbated B cell responses to certain antigens, and BCL2, presumably by supporting survival of these clones, cooperate to induce mature B cell neoplasms in transgenic mice expressing human proteins. TRAF3 upregulation favors the production of V(H)DJ(H) rearrangements producing HCDR3 sequences similar to those recognizing PAMPs and DAMPs.

6. Review focuses on the relevance of BCL-2 for apoptosis modulation at the mitochondrial level, its potential as therapeutic target for hematological malignancies, and the results obtained with selective inhibitors belonging to the BH3-mimetics, especially venetoclax used in monotherapy or in combination with other agents.

7. High BCL2 expression is associated with MYC-positive diffuse large B-cell lymphoma.

8. IL-17A-inhibited autophagy is related to Bcl2 degradation in hepatocellular carcinoma (HCC) cells. Bcl2 may be degraded via the autophagosome-lysosome pathway in HCC cells.

9. Information on molecular markers obtained from immunohistochemical staining of prostate tissue, included B cell lymphoma-2 (bcl-2), p53, and microvessel density.

10. miR-15a modulation has potential implications in controlling various biological and pathogenic processes in colon carcinogenesis via targeting its downstream proteins such as BCL2 and SOX2

11. Gray matter structural covariance networks (SCNs) analysis and covariance strength interactions support the genetic influences of the Bcl-2 rs956572 functional polymorphism on the SCN in the early stage of Alzheimer's disease. Results show a greater genetic influence in the A homozygotes on the executive control network.

12. Upregulation of Cyr61 significantly decreased IM-induced cellular apoptosis of K562 cells through nuclear factor kappa B/B-cell lymphoma 2 pathways.

13. The levels of expression of Bcl-2, CD95, and active caspase-3 in blasts of patients with Acute lymphoblastic leukemia, indicate that apoptosis is inhibited both in intrinsic and extrinsic pathways, mainly in patients with B-Acute lymphoblastic leukemia, B-Acute lymphoblastic leukemia/CD33+ and ambiguous lineage-lymphoblastic leukemia.

14. Levels of IL-1ss, IL-6, TNF-alpha, and BAX mRNA were negatively correlated with cardiac function, and BCL2 mRNA expression was positively associated with chronic heart failure.

15. Dysregulated gene expressions of MEX3D, FOS and BCL2 in human induced-neuronal (iN) cells from NF1 patients

16. The reduction in mitochondrial membrane potential favored mitochondrial apoptotic pathway which was further confirmed by determining the expression of Bax and Bcl-2. It was observed that MH downregulated the expression of Bax and upregulated the expression of MMP, ultimately leading to apoptosis of OSSC PE/CA-PJ41 cells. Additionally, MH also caused G2/M cell cycle arrest in a dose-dependent manner

17. In univariate time-to-event regression, diffuse large B cell lymphoma patients with either MYC or BCL2 expression and patients with concurrent overexpression of MYC and BCL2 had a 2.1-fold higher (P = 0.009) and 2.4-fold higher (P = 0.009) risk of progression or death within the first 5 years of follow-up than patients without DEL, respectively

18. Silencing of miR-19a significantly improved the sensitivity of SiHa cells to radiotherapy by reducing proliferation, increasing apoptosis, upregulating BAX, and downregulating Bcl-2. Overall, inhibiting miR-19a significantly improves the sensitivity of SiHa cells to radiotherapy, which could lead to new methods for the treatment of cervical cancer.

19. The results of the present work revealed that aesculetin exhibits selective anticancer effects in THP-1 human leukemia cells without causing much cytotoxicity in peripheral blood mono-nucleated cells. It also led to significant apoptosis induction, inhibition of cancer cell migration and decrease in Blc-2/Bax ratio.

20. Variable BCL2/BCL2L1 ratio in multiple myeloma with t(11;14).

Mouse (Murine) B-Cell CLL/lymphoma 2 (BCL2) interaction partners

1. Bcl2-associated athanogene 3 (BAG3) is a 575 amino acid protein that is found predominantly in the heart.

2. These results establish crucial residues in Bcl-2 required for Nur77/Nor-1-mediated apoptosis and point to potential new strategies for manipulating Bcl-2 function.

3. 6 months of aerobic exercise can effectively prevent cardiomyocyte apoptosis in mice. It is an important way to effectively regulate Bcl-2, Bax expression and Bcl-2/Bax level of cardiomyocytes.

4. data demonstrate that disruption of the beclin 1-BCL2 complex is an effective mechanism to increase autophagy, prevent premature ageing, improve healthspan and promote longevity in mammals

5. Results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of age-related hearing loss in the auditory cortex.

6. MiR-146a inhibits proliferation and induces apoptosis in murine osteoblastic MC3T3-E1 by regulating Bcl2

7. The data revealed that autophagy is an important regulator of osteoblastic apoptosis through its interaction with Bax/Bcl2, and maintains the osteoblastic function of MC3T3E1 cells following GC exposure. In addition, these results indicated that the suppression of autophagy in OBs under chronic GC therapy may increase the prevalence of GCinduced osteoporosis and fragility fractures.

8. 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.

9. The results suggest that SPK2 interacts with Bcl2 via its BH3 domain, thereby dissociating it from Beclin-1 and activating autophagy while protecting neurons against ischemic injury.

10. The findings support a model in which survival is determined by quantitative participation of multiple anti-apoptotic proteins, BCL2, Mcl1, and BCL2A1, rather than by a single anti-apoptotic protein.

11. Bcl-2 is strongly expressed in the inner hair cells and spiral ganglion neurons of young mice. In addition, moderate Bcl-2 expression is also detected in the outer hair cells and in the neurons of the auditory cortex. A significant reduction of Bcl-2 expression in the cochlea or auditory cortex is also associated with elevated hearing thresholds and hair cell loss during aging.

12. Bcl2 is the autophagy-related target of miR-449a.

13. anti-apoptotic molecules BclxL and Bcl-2 and the pro-apoptotic factors BAD and BID cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L.

14. Acute ethanol exposure induced autophagy-mediated heart toxicity and injury mainly through the ROS-JNK-Bcl-2 signaling pathway.

15. Th17 cells are resistant to glucocorticoid-induced apoptosis and cytokine suppression, at least in part due to high levels of BCL-2. These findings support a role of Th17 cells in glucocorticoid-resistant inflammatory conditions such as certain endotypes of asthma.

16. E2 protects skeletal myoblasts against apoptosis induced by H2 O2 modulating p53 and FoxO transcription factors and then their target genes Bcl-2, Bim, Puma, PERP, and MDM2, without affecting Noxa gene.

17. Bcl-2 expression has a significant impact on the mineralogical content of enamel crystals of tooth structure

18. The results suggest that CARP can protect against hypoxia-reperfusion induced cardiomyocyte apoptosis, possibly through increasing anti-apoptosis Bcl2 gene expression.

19. This study provides evidence from transgenic mouse models that Crebbp deletion results in deficits in B-cell development and can cooperate with Bcl2 overexpression to promote B-cell lymphoma.

20. an essential role for the binding of BCL2 to BIM in the survival of noncycling NK cells.

Zebrafish B-Cell CLL/lymphoma 2 (BCL2) interaction partners

1. upregulated in choriodecidua following labor

2. These results suggest a role for mitochondrial p53 activity in promoting hair cell death due to aminoglycosides, likely upstream of Bax and Bcl2.

3. Zebrafish gene expressions of P53, Bcl-2, Bax and caspase-3 were elevated after exposure with microcystin-LR under different ambient temperatures.

4. Analysis using clinical biopsy specimens revealed autophagy and increased levels of BCL2, S1P1, and ICAM1 in human T-lymphoblastic lymphoma compared with T-lymphoblastic leukemia.

5. Real-time RT-PCR revealed acetaminophen treatment of zebrafish embryos decreased the expression of cox2 and bcl2, but increased p53 expression.

6. Leukemia onset was dramatically accelerated in transgenic fish overexpressing human Notch1 and fish bcl-2, indicating synergy between the Notch pathway and the bcl2-mediated antiapoptotic pathway.

Cow (Bovine) B-Cell CLL/lymphoma 2 (BCL2) interaction partners

1. Over-expression of STC-1 up-regulated Bcl-2 protein expression and slightly down-regulated caspase-3 production in the damaged cells. Findings from this study suggest that STC-1 plays a protective role in intestinal cells through an antioxidant mechanism.

2. BoHV-5 replication apparently modulates BCL-2 expression and gene transcription, enhancing production of virus progeny, but does not increase Bax expression.

3. G3139, a BCL-2 antisesnse oligonucleotide is a promising candidate for treatment of patients with imatinib-resistant Ph-positive leukemia.

4. role of vascular endothelial growth factor receptor-1 in Bcl-2 expression

5. apoptosis-inducing factor was expressed in luminal alveolar cells and, in concert with a change in bax protein to bcl-2 protein ratio, might contribute to signalling of a change in the dynamic balance of the cell population as lactation progresses

6. mRNA expression of Bax, Bcl-2, caspase-3 and-7 cannot be used as a reliable apoptosis detection method.

7. These results propose an additional mechanism whereby resveratrol may exert its cardioprotective effects and suggest a key role for Bcl-2 in the resveratrol anti-apoptotic action, especially in disrupting peroxynitrite-triggered mitochondrial pathway.

Guinea Pig B-Cell CLL/lymphoma 2 (BCL2) interaction partners

1. bcl-2 and bax were expressed strongly in denervated guinea-pig facial muscle. [bcl-2; bax]

Rabbit B-Cell CLL/lymphoma 2 (BCL2) interaction partners

1. excessive apoptosis does occur in acetabular cartilage with developmental dislocations of the hip, and is positively correlated with high caspase-3 expression as well as low Bcl-2 expression.

2. These results indicate that RI-PostC can ameliorate myocardial ischemia-reperfusion injury and increase the Bcl-2/Bax ratio through a mechanism involving protein kinase C.

3. Cinobufagin can remarkably inhibit the proliferation and induce the apoptosis of lens epithelial cells by increasing expression of bax and decreasing expression of bcl2.

4. Elevated local temperature of the testis buried in the inguinal pocket increases the apoptosis of spermatogenic cells, and the spermatogenic cell apoptosis is highly correlated with the decreased expression of Bcl-2 and increased expression of Bax.

5. Our data indicate that exposure to rabbits to Pb(Ac)(2) caused a significant increase of apoptosis protein p53 and decrease in the antiapoptotic BCl2 proteins.

6. Isoflurane delayed preconditioning can inhibit the apoptosis of myocardium by up-regulating the expression of Bcl-2 and down-regulating the activation of caspase-3.

7. Data show that the damaged electron transport chain leads to bcl-2 depletion and MPT opening.