Bcl 2

Summary

Gene Symbol: Bcl 2
Description: BCL2, apoptosis regulator
Alias: Bcl-2, PPP1R50, apoptosis regulator Bcl-2, B-cell CLL/lymphoma 2, protein phosphatase 1, regulatory subunit 50
Species: human
Products:     Bcl 2

Top Publications

  1. Kaufmann T, Schlipf S, Sanz J, Neubert K, Stein R, Borner C. Characterization of the signal that directs Bcl-x(L), but not Bcl-2, to the mitochondrial outer membrane. J Cell Biol. 2003;160:53-64 pubmed
    ..These data define a new targeting sequence for the MOM and propose that Bcl-2 acts on several intracellular membranes whereas Bcl-x(L) specifically functions on the MOM. ..
  2. Machado Vieira R, Pivovarova N, Stanika R, Yuan P, Wang Y, Zhou R, et al. The Bcl-2 gene polymorphism rs956572AA increases inositol 1,4,5-trisphosphate receptor-mediated endoplasmic reticulum calcium release in subjects with bipolar disorder. Biol Psychiatry. 2011;69:344-52 pubmed publisher
    ..These results demonstrate that, in patients with BPD, abnormal Bcl-2 gene expression in the AA variant contributes to dysfunctional Ca(2+) homeostasis through a specific ER inositol 1,4,5-trisphosphate receptor-dependent mechanism. ..
  3. Johnson N, Slack G, Savage K, Connors J, Ben Neriah S, Rogic S, et al. Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone. J Clin Oncol. 2012;30:3452-9 pubmed
    ..Assessment of MYC and BCL2 expression by IHC represents a robust, rapid, and inexpensive approach to risk-stratify patients with DLBCL at diagnosis. ..
  4. Edlich F, Banerjee S, Suzuki M, Cleland M, Arnoult D, Wang C, et al. Bcl-x(L) retrotranslocates Bax from the mitochondria into the cytosol. Cell. 2011;145:104-16 pubmed publisher
    ..We propose that Bcl-x(L) inhibits and maintains Bax in the cytosol by constant retrotranslocation of mitochondrial Bax. ..
  5. Salvadore G, Nugent A, Chen G, Akula N, Yuan P, Cannon D, et al. Bcl-2 polymorphism influences gray matter volume in the ventral striatum in healthy humans. Biol Psychiatry. 2009;66:804-7 pubmed publisher
    ..Thus, the findings from the current study are noteworthy insofar as they converge with preclinical findings that Bcl-2 functions to enhance neuronal viability and might indirectly extend this evidence to humans. ..
  6. Heubner M, Wimberger P, Otterbach F, Kasimir Bauer S, Siffert W, Kimmig R, et al. Association of the AA genotype of the BCL2 (-938C>A) promoter polymorphism with better survival in ovarian cancer. Int J Biol Markers. 2009;24:223-9 pubmed
    ..Recently, a novel regulatory single nucleotide polymorphism (-938C>A) in the inhibitory P2 BCL2 promoter was described. In this study we investigated its potential association with survival in epithelial ovarian cancer...
  7. Berndt S, Skibola C, Joseph V, Camp N, Nieters A, Wang Z, et al. Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia. Nat Genet. 2013;45:868-76 pubmed publisher
    ..3 (ODF1, P=5.40×10(-8)) and 5p15.33 (TERT, P=1.92×10(-7)). Although further studies are required, the proximity of several of these loci to genes involved in apoptosis suggests a plausible underlying biological mechanism. ..
  8. Koh Y, Park C, Yoon D, Suh C, Huh J. Prognostic significance of COX-2 expression and correlation with Bcl-2 and VEGF expression, microvessel density, and clinical variables in classical Hodgkin lymphoma. Am J Surg Pathol. 2013;37:1242-51 pubmed publisher
    ..013). COX-2 and VEGF correlated with angiogenesis and tumor progression in cHL. The findings support targeting COX-2 as a potential new therapeutic approach in cHL. ..
  9. Renault T, Chipuk J. Getting away with murder: how does the BCL-2 family of proteins kill with immunity?. Ann N Y Acad Sci. 2013;1285:59-79 pubmed publisher
    ..From lethal mechanisms to more gentle ones, the final portion of the review discusses the nonapoptotic functions of the BCL-2 family and how they pertain to the control of immunity. ..

More Information

Publications135 found, 100 shown here

  1. Lamy L, Ngo V, Emre N, Shaffer A, Yang Y, Tian E, et al. Control of autophagic cell death by caspase-10 in multiple myeloma. Cancer Cell. 2013;23:435-49 pubmed publisher
    ..While myeloma cells require a basal level of autophagy for survival, caspase-10 tempers this response to avoid cell death. Drugs that disrupt this vital balance may have therapeutic potential in myeloma. ..
  2. Vaillant F, Merino D, Lee L, Breslin K, Pal B, Ritchie M, et al. Targeting BCL-2 with the BH3 mimetic ABT-199 in estrogen receptor-positive breast cancer. Cancer Cell. 2013;24:120-9 pubmed publisher
    ..Importantly, these two classes of inhibitor further enhanced tumor response in combination therapy with tamoxifen. Collectively, our findings provide a rationale for the clinical evaluation of BH3 mimetics in therapy for breast cancer. ..
  3. Guo S, Zhi Y, Yang H, Yu Y, Wang Y, Zhang J, et al. Bcl-2 expression is associated with poor prognosis of solitary plasmacytoma of bone. Ann Hematol. 2014;93:471-7 pubmed publisher
    ..In conclusion, results showed Bcl-2 expression to be a clinically significant prognostic indicator for SPB patients and constitutive activated STAT3 may not be the sole primary regulatory mechanism. ..
  4. Geng M, Wang L, Li P. Correlation between chemosensitivity to anticancer drugs and Bcl-2 expression in gastric cancer. Int J Clin Exp Pathol. 2013;6:2554-9 pubmed
    ..009). Overexpression of Bcl-2 may predict a loss of the efficacy of the chemotherapy drugs 5-FU, ADM and MMC in patients with gastric cancer. ..
  5. Hu S, Xu Monette Z, Tzankov A, Green T, Wu L, Balasubramanyam A, et al. MYC/BCL2 protein coexpression contributes to the inferior survival of activated B-cell subtype of diffuse large B-cell lymphoma and demonstrates high-risk gene expression signatures: a report from The International DLBCL Rituximab-CHOP Consortium Pro. Blood. 2013;121:4021-31; quiz 4250 pubmed publisher
    ..In conclusion, the data suggest that MYC/BCL2 coexpression, rather than cell-of-origin classification, is a better predictor of prognosis in patients with DLBCL treated with R-CHOP. ..
  6. Lin J, Wu Y, Yang D, Zhao Y. Induction of apoptosis and antitumor effects of a small molecule inhibitor of Bcl-2 and Bcl-xl, gossypol acetate, in multiple myeloma in vitro and in vivo. Oncol Rep. 2013;30:731-8 pubmed publisher
  7. Ferreira A, Suriano G, Mendes N, Gomes B, Wen X, Carneiro F, et al. E-cadherin impairment increases cell survival through Notch-dependent upregulation of Bcl-2. Hum Mol Genet. 2012;21:334-43 pubmed publisher
    ..These findings highlight the possibility of new targeted therapeutical strategies for the treatment of tumours associated with E-cadherin inactivation. ..
  8. Ciechomska I, Goemans G, Skepper J, Tolkovsky A. Bcl-2 complexed with Beclin-1 maintains full anti-apoptotic function. Oncogene. 2009;28:2128-41 pubmed publisher
    ..Hence, although Beclin-1 contains a BH3-only motif typical of pro-apoptotic proteins, it is a negligible modulator of Bcl-2's anti-apoptotic function. ..
  9. Tagami S, Eguchi Y, Kinoshita M, Takeda M, Tsujimoto Y. A novel protein, RTN-XS, interacts with both Bcl-XL and Bcl-2 on endoplasmic reticulum and reduces their anti-apoptotic activity. Oncogene. 2000;19:5736-46 pubmed
    ..These results suggest that RTN family proteins can modulate the anti-apoptotic activity of Bcl-XL and Bcl-2 by binding with them and can change their localization to the ER. ..
  10. Muthumani K, Choo A, PremKumar A, Hwang D, Thieu K, Desai B, et al. Human immunodeficiency virus type 1 (HIV-1) Vpr-regulated cell death: insights into mechanism. Cell Death Differ. 2005;12 Suppl 1:962-70 pubmed
    ..Further, we also discuss caveats and future directions for investigation of the interesting biology of this HIV accessory gene. ..
  11. Bigelow R, Chari N, Unden A, Spurgers K, Lee S, Roop D, et al. Transcriptional regulation of bcl-2 mediated by the sonic hedgehog signaling pathway through gli-1. J Biol Chem. 2004;279:1197-205 pubmed
    ..These studies further suggest that one consequence of the deregulation of shh signaling in BCC is the up-regulation of bcl-2. ..
  12. Del Gaizo Moore V, Brown J, Certo M, Love T, Novina C, Letai A. Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737. J Clin Invest. 2007;117:112-21 pubmed
    ..Indeed, activator BH3-only occupation of BCL2 may prime cancer cells for death, offering a potential explanation for the marked chemosensitivity of certain cancers that express abundant BCL2, such as CLL and follicular lymphoma. ..
  13. Liang X, Kleeman L, Jiang H, Gordon G, Goldman J, Berry G, et al. Protection against fatal Sindbis virus encephalitis by beclin, a novel Bcl-2-interacting protein. J Virol. 1998;72:8586-96 pubmed
    ..These findings demonstrate that Beclin is a novel Bcl-2-interacting cellular protein that may play a role in antiviral host defense. ..
  14. Hirata H, Hinoda Y, Kikuno N, Suehiro Y, Shahryari V, Ahmad A, et al. Bcl2 -938C/A polymorphism carries increased risk of biochemical recurrence after radical prostatectomy. J Urol. 2009;181:1907-12 pubmed publisher
    ..To our knowledge this is the first report documenting that bcl2 promoter region -938 C/C genotype carriers more frequently show biochemical recurrence than -938C/A+A/A carriers. ..
  15. Azad N, Iyer A, Vallyathan V, Wang L, Castranova V, Stehlik C, et al. Role of oxidative/nitrosative stress-mediated Bcl-2 regulation in apoptosis and malignant transformation. Ann N Y Acad Sci. 2010;1203:1-6 pubmed publisher
    ..We describe a novel mechanism of Bcl-2 regulation by *O(2)(-) and NO, providing a new dimension to reactive species-mediated Bcl-2 stability, apoptotic cell death, and cancer development. ..
  16. Ku B, Liang C, Jung J, Oh B. Evidence that inhibition of BAX activation by BCL-2 involves its tight and preferential interaction with the BH3 domain of BAX. Cell Res. 2011;21:627-41 pubmed publisher
  17. Huang F, Yang Z, Yu D, Wang J, Li R, Ding G. Sepia ink oligopeptide induces apoptosis in prostate cancer cell lines via caspase-3 activation and elevation of Bax/Bcl-2 ratio. Mar Drugs. 2012;10:2153-65 pubmed publisher
    ..Moreover, the Bax/Bcl-2expression ratio was increased. Concurrently, the expression of caspase-3 was upregulated. These data support our hypothesis that SIO has anticarcinogenic properties. ..
  18. McGill G, Horstmann M, Widlund H, Du J, Motyckova G, Nishimura E, et al. Bcl2 regulation by the melanocyte master regulator Mitf modulates lineage survival and melanoma cell viability. Cell. 2002;109:707-18 pubmed
    ..This linkage helps explain the vital roles of both Mitf and Bcl2 in the melanocyte lineage and the well-known treatment resistance of melanoma. ..
  19. Zalckvar E, Berissi H, Mizrachy L, Idelchuk Y, Koren I, Eisenstein M, et al. DAP-kinase-mediated phosphorylation on the BH3 domain of beclin 1 promotes dissociation of beclin 1 from Bcl-XL and induction of autophagy. EMBO Rep. 2009;10:285-92 pubmed publisher
  20. Lam M, Dubyak G, Chen L, Nunez G, Miesfeld R, Distelhorst C. Evidence that BCL-2 represses apoptosis by regulating endoplasmic reticulum-associated Ca2+ fluxes. Proc Natl Acad Sci U S A. 1994;91:6569-73 pubmed
    ..These findings suggest that BCL-2 either directly or indirectly regulates the flux of Ca2+ across the ER membrane, thereby abrogating Ca2+ signaling of apoptosis. ..
  21. Lehnerdt G, Franz P, Bankfalvi A, Grehl S, Kelava A, Nuckel H, et al. The regulatory BCL2 promoter polymorphism (-938C>A) is associated with relapse and survival of patients with oropharyngeal squamous cell carcinoma. Ann Oncol. 2009;20:1094-9 pubmed publisher
    ..897, P = 0.013). The (-938C>A) SNP represents a potential novel prognostic marker in patients with OSCC that could help to identify a group of patients at high risk for relapse and death. ..
  22. Porichi O, Nikolaidou M, Apostolaki A, Tserkezoglou A, Arnogiannaki N, Kassanos D, et al. BCL-2, BAX and P53 expression profiles in endometrial carcinoma as studied by real-time PCR and immunohistochemistry. Anticancer Res. 2009;29:3977-82 pubmed
    ..7). The Bcl-2/bax ratio is increased in grade 3 tumors. Bax protein shows a strong tendency for expression in the third group of clinical staging (stage IIb, III and IV). Poorly differentiated tumors highly expressed mutated p53. ..
  23. Yang J, Liu X, Bhalla K, Kim C, Ibrado A, Cai J, et al. Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked. Science. 1997;275:1129-32 pubmed
    ..Overexpression of Bcl-2 prevented the efflux of cytochrome c from the mitochondria and the initiation of apoptosis. Thus, one possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria. ..
  24. Cheng E, Wei M, Weiler S, Flavell R, Mak T, Lindsten T, et al. BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis. Mol Cell. 2001;8:705-11 pubmed
    ..Thus, in mammals, BH3 domain-only molecules activate multidomain proapoptotic members to trigger a mitochondrial pathway, which both releases cytochrome c to activate caspases and initiates caspase-independent mitochondrial dysfunction. ..
  25. Cartron P, Gallenne T, Bougras G, Gautier F, Manero F, Vusio P, et al. The first alpha helix of Bax plays a necessary role in its ligand-induced activation by the BH3-only proteins Bid and PUMA. Mol Cell. 2004;16:807-18 pubmed
    ..Thus, a specific interaction between Bax Halpha1 and their BH3 domains allows Bid and PUMA to function as "death agonists" of Bax, whereas Bad recruits Bax activity through a distinct pathway. ..
  26. Noble C, Dong J, Manser E, Song H. Bcl-xL and UVRAG cause a monomer-dimer switch in Beclin1. J Biol Chem. 2008;283:26274-82 pubmed publisher
    ..Furthermore, our data suggest that an alternative strategy for developing anti-cancer compounds would be to disrupt the Beclin1-dimer interface. ..
  27. Fletcher J, Meusburger S, Hawkins C, Riglar D, Lee E, Fairlie W, et al. Apoptosis is triggered when prosurvival Bcl-2 proteins cannot restrain Bax. Proc Natl Acad Sci U S A. 2008;105:18081-7 pubmed publisher
  28. Portier B, Taglialatela G. Bcl-2 localized at the nuclear compartment induces apoptosis after transient overexpression. J Biol Chem. 2006;281:40493-502 pubmed
    ..These results indicate that Bcl-2 has a dual role as both a protector and a killer and that the ability to switch roles depends on Bcl-2 subcellular localization. ..
  29. Azad N, Iyer A, Wang L, Lu Y, Medan D, Castranova V, et al. Nitric oxide-mediated bcl-2 stabilization potentiates malignant transformation of human lung epithelial cells. Am J Respir Cell Mol Biol. 2010;42:578-85 pubmed publisher
  30. El Hindy N, Bachmann H, Lambertz N, Adamzik M, Nuckel H, Worm K, et al. Association of the CC genotype of the regulatory BCL2 promoter polymorphism (-938C>A) with better 2-year survival in patients with glioblastoma multiforme. J Neurosurg. 2011;114:1631-9 pubmed publisher
    ..50, 95% CI 1.14-5.48, p = 0.022). These results suggested that the (-938C>A) polymorphism is a survival prognosticator as well as a marker for a high-risk group among patients with GBM who underwent GTR. ..
  31. Rebollo A, Perez Sala D, Martinez A C. Bcl-2 differentially targets K-, N-, and H-Ras to mitochondria in IL-2 supplemented or deprived cells: implications in prevention of apoptosis. Oncogene. 1999;18:4930-9 pubmed
    ..These results evidence a distinct behavior among the three Ras proteins in TS1alphabeta cells, depending on IL-2 supply, and suggest homologue-specific roles for Ras proteins in IL-2-dependent events. ..
  32. Niture S, Jaiswal A. Nrf2 protein up-regulates antiapoptotic protein Bcl-2 and prevents cellular apoptosis. J Biol Chem. 2012;287:9873-86 pubmed publisher
    ..These data provide the first evidence of Nrf2 in control of Bcl-2 expression and apoptotic cell death with implications in antioxidant protection, survival of cancer cells, and drug resistance. ..
  33. Sakurikar N, Eichhorn J, Chambers T. Cyclin-dependent kinase-1 (Cdk1)/cyclin B1 dictates cell fate after mitotic arrest via phosphoregulation of antiapoptotic Bcl-2 proteins. J Biol Chem. 2012;287:39193-204 pubmed publisher
  34. Broome H, Dargan C, Krajewski S, Reed J. Expression of Bcl-2, Bcl-x, and Bax after T cell activation and IL-2 withdrawal. J Immunol. 1995;155:2311-7 pubmed
    ..These findings suggest that a decrease in Bcl-x protein levels precedes apoptosis after IL-2 withdrawal in T cells and that transfected bcl-2 promotes survival after IL-2 withdrawal by functionally masking this drop in Bcl-x. ..
  35. Boyd J, Malstrom S, Subramanian T, Venkatesh L, Schaeper U, Elangovan B, et al. Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a common set of cellular proteins. Cell. 1994;79:341-51 pubmed
    ..Our results suggest that two diverse proteins, the E1B 19 kDa and the Bcl-2 proteins, promote cell survival through interaction with a common set of cellular proteins. ..
  36. Ng F, Nguyen M, Kwan T, Branton P, Nicholson D, Cromlish J, et al. p28 Bap31, a Bcl-2/Bcl-XL- and procaspase-8-associated protein in the endoplasmic reticulum. J Cell Biol. 1997;139:327-38 pubmed
    ..This raises the possibility that the p28 complex contributes to the regulation of procaspase-8 or a related caspase in response to E1A, dependent on the status of the Bcl-2 setpoint within the complex. ..
  37. Lin B, Kolluri S, Lin F, Liu W, Han Y, Cao X, et al. Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3. Cell. 2004;116:527-40 pubmed
  38. Bachmann H, Otterbach F, Callies R, Nuckel H, Bau M, Schmid K, et al. The AA genotype of the regulatory BCL2 promoter polymorphism ( 938C>A) is associated with a favorable outcome in lymph node negative invasive breast cancer patients. Clin Cancer Res. 2007;13:5790-7 pubmed
    ..006). These results suggest the (-938C>A) polymorphism as a survival prognosticator as well as indicator of a high-risk group within patients with lymph node-negative breast cancer. ..
  39. Derenne S, Monia B, Dean N, Taylor J, Rapp M, Harousseau J, et al. Antisense strategy shows that Mcl-1 rather than Bcl-2 or Bcl-x(L) is an essential survival protein of human myeloma cells. Blood. 2002;100:194-9 pubmed
    ..As MM remains an incurable disease despite intensive chemotherapy, these results suggest that Mcl-1 antisense strategy rather than Bcl-2 antisense strategy could be of considerable importance in the treatment of MM. ..
  40. Abdulkader I, Sanchez L, Cameselle Teijeiro J, Gude F, Chavez J, Lopez Lopez R, et al. Cell-cycle-associated markers and clinical outcome in human epithelial cancers: a tissue microarray study. Oncol Rep. 2005;14:1527-31 pubmed
    ..We found that in most common epithelial cancers, regardless of origin, Bcl-2 appears to be the key biological factor influencing clinical behaviour. ..
  41. Yoon S, Jeon Y, Paik J, Kim W, Kim Y, Kim J, et al. MYC translocation and an increased copy number predict poor prognosis in adult diffuse large B-cell lymphoma (DLBCL), especially in germinal centre-like B cell (GCB) type. Histopathology. 2008;53:205-17 pubmed publisher
    ..Analyses of MYC and Bcl-2 status, i.e. translocation and ICN, in the context of DLBCL phenotype might help predict prognosis and determine therapeutic strategies. ..
  42. Strack P, Frey M, Rizzo C, Cordova B, George H, Meade R, et al. Apoptosis mediated by HIV protease is preceded by cleavage of Bcl-2. Proc Natl Acad Sci U S A. 1996;93:9571-6 pubmed
    ..Purified bcl-2 is cleaved by HIV protease between phenylalanine 112 and alanine 113. The results suggest a new option for HIV gene therapy; bcl-2 muteins that have noncleavable alterations surrounding the HIV protease cleavage site. ..
  43. Willis S, Fletcher J, Kaufmann T, van Delft M, Chen L, Czabotar P, et al. Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak. Science. 2007;315:856-9 pubmed
    ..Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak. ..
  44. Ishimaru D, Zuraw L, Ramalingam S, Sengupta T, Bandyopadhyay S, Reuben A, et al. Mechanism of regulation of bcl-2 mRNA by nucleolin and A+U-rich element-binding factor 1 (AUF1). J Biol Chem. 2010;285:27182-91 pubmed publisher
    ..Based on our findings, we propose a model that illustrates the opposing roles of nucleolin and AUF1 in regulating bcl-2 mRNA stability. ..
  45. Protrka Z, Djuric J, Protrka O, Arsenijevic S. The possible role of Bcl-2 expression of tumors of the uterine cervix. J BUON. 2010;15:323-9 pubmed
    ..Our results indicate that overexpression of Bcl-2 may play an important role in cervical carcinogenesis. However, more extensive series of samples is required to establish the prognostic significance of Bcl-2 in cervical carcinogenesis. ..
  46. Yu J, Zhang L, Hwang P, Kinzler K, Vogelstein B. PUMA induces the rapid apoptosis of colorectal cancer cells. Mol Cell. 2001;7:673-82 pubmed
    ..Based on its unique expression patterns, p53 dependence, and biochemical properties, PUMA may be a direct mediator of p53-associated apoptosis. ..
  47. Real P, Cao Y, Wang R, Nikolovska Coleska Z, Sanz Ortiz J, Wang S, et al. Breast cancer cells can evade apoptosis-mediated selective killing by a novel small molecule inhibitor of Bcl-2. Cancer Res. 2004;64:7947-53 pubmed
    ..Consistently, HER2 blockade led to YC137 resistance. These data provide evidence for the selective killing of tumor cells by YC137 and represent the first example of in vitro selection of cancer cells refractory to a Bcl-2 inhibitor. ..
  48. Nuckel H, Frey U, Bau M, Sellmann L, Stanelle J, Dürig J, et al. Association of a novel regulatory polymorphism (-938C>A) in the BCL2 gene promoter with disease progression and survival in chronic lymphocytic leukemia. Blood. 2007;109:290-7 pubmed
    ..034) together with disease stage at diagnosis (HR 2.5; P = .004) and ZAP-70 status (HR 3.0; P = .001). The BCL2-938AA genotype is associated with increased Bcl-2 expression and a novel unfavorable genetic marker in patients with B-CLL. ..
  49. Hirata H, Hinoda Y, Nakajima K, Kikuno N, Suehiro Y, Tabatabai Z, et al. The bcl2 -938CC genotype has poor prognosis and lower survival in renal cancer. J Urol. 2009;182:721-7 pubmed publisher
    ..In addition, the bcl2 -938C/A single nucleotide polymorphism was shown to be an independent adverse prognostic factor for renal cell carcinoma. ..
  50. Masood A, Chitta K, Paulus A, Khan A, Sher T, Ersing N, et al. Downregulation of BCL2 by AT-101 enhances the antileukaemic effect of lenalidomide both by an immune dependant and independent manner. Br J Haematol. 2012;157:59-66 pubmed publisher
    ..Our data suggest that AT-101 in combination with lenalidomide can potentially be an effective therapeutic regimen for CLL. ..
  51. Korant B, Strack P, Frey M, Rizzo C. A cellular anti-apoptosis protein is cleaved by the HIV-1 protease. Adv Exp Med Biol. 1998;436:27-9 pubmed
    ..The loss of bcl-2 has biological consequences, leading to enhanced HIV replication and programmed death of the host cell. A strategy is proposed to suppress HIV with non-cleavable mutants of bcl-2. ..
  52. Molto L, Rayman P, Paszkiewicz Kozik E, Thornton M, Reese L, Thomas J, et al. The Bcl-2 transgene protects T cells from renal cell carcinoma-mediated apoptosis. Clin Cancer Res. 2003;9:4060-8 pubmed
    ..Overexpression of Bcl-2 protected Jurkat cells from tumor-mediated killing. Bcl-2 inhibition is a mechanism by which tumors may render lymphocytes sensitive to other tumor-derived, proapoptotic stimuli. ..
  53. Tamura Y, Simizu S, Osada H. The phosphorylation status and anti-apoptotic activity of Bcl-2 are regulated by ERK and protein phosphatase 2A on the mitochondria. FEBS Lett. 2004;569:249-55 pubmed
    ..Thus, the present findings suggest that ERK and PP2A are physiological regulators of Bcl-2 phosphorylation, and these enzymes exert an influence on the anti-apoptotic function of Bcl-2. ..
  54. Bachmann H, Heukamp L, Schmitz K, Hilburn C, Kahl P, Buettner R, et al. Regulatory BCL2 promoter polymorphism (-938C>A) is associated with adverse outcome in patients with prostate carcinoma. Int J Cancer. 2011;129:2390-9 pubmed publisher
    ..The BCL2 -938C>A polymorphism should be evaluated prospectively and may also have promise in assisting optimal patient choice for treatment with BCL2-targeted drugs already in evaluation for prostate cancer treatment. ..
  55. Deng J, Carlson N, Takeyama K, Dal Cin P, Shipp M, Letai A. BH3 profiling identifies three distinct classes of apoptotic blocks to predict response to ABT-737 and conventional chemotherapeutic agents. Cancer Cell. 2007;12:171-85 pubmed
    ..BCL-2 dependence correlates with high levels of proapoptotic BIM sequestered by BCL-2. Strikingly, BH3 profiling can also predict sensitivity to conventional chemotherapeutic agents like etoposide, vincristine, and adriamycin. ..
  56. Chen K, Hu Z, Wang L, Sturgis E, El Naggar A, Zhang W, et al. Single-nucleotide polymorphisms at the TP53-binding or responsive promoter regions of BAX and BCL2 genes and risk of squamous cell carcinoma of the head and neck. Carcinogenesis. 2007;28:2008-12 pubmed
    ..Our data suggest that the risk of SCCHN may be associated with these two SNPs of BAX and BCL2 promoter regions, particularly among TP53 heterozygotes. Larger studies are needed to validate these findings. ..
  57. Priault M, Hue E, Marhuenda F, Pilet P, Oliver L, Vallette F. Differential dependence on Beclin 1 for the regulation of pro-survival autophagy by Bcl-2 and Bcl-xL in HCT116 colorectal cancer cells. PLoS ONE. 2010;5:e8755 pubmed publisher
  58. Biagi J, Seymour J. Insights into the molecular pathogenesis of follicular lymphoma arising from analysis of geographic variation. Blood. 2002;99:4265-75 pubmed
    ..If these findings were confirmed in prospective studies, it would imply that different etiologic or genetic factors might influence the development of FL across separate regions. ..
  59. Kang C, Tai J, Chia J, Yoon H. The flexible loop of Bcl-2 is required for molecular interaction with immunosuppressant FK-506 binding protein 38 (FKBP38). FEBS Lett. 2005;579:1469-76 pubmed
    ..Here, we investigated the molecular interaction between FKBP38 and Bcl-2, and demonstrated that Bcl-2 interacts with FKBP38 through the unstructured loop, and the interaction appears to regulate phosphorylation in the loop of Bcl-2. ..
  60. Jain M, Kumar S, Lal P, Tiwari A, Ghoshal U, Mittal B. Role of BCL2 (ala43thr), CCND1 (G870A) and FAS (A-670G) polymorphisms in modulating the risk of developing esophageal cancer. Cancer Detect Prev. 2007;31:225-32 pubmed
    ..FAS A-670G was not associated with the risk of developing esophageal cancer. Gene-environment interaction analysis showed cancer susceptibility in CCND1 870AA and FAS -670AA genotype to be influenced by quantity of tobacco. ..
  61. Kolluri S, Zhu X, Zhou X, Lin B, Chen Y, Sun K, et al. A short Nur77-derived peptide converts Bcl-2 from a protector to a killer. Cancer Cell. 2008;14:285-98 pubmed publisher
    ..NuBCP-9s act as molecular switches to dislodge the Bcl-2 BH4 domain, exposing its BH3 domain, which in turn blocks the activity of antiapoptotic Bcl-X(L). ..
  62. Sacconi A, Biagioni F, Canu V, Mori F, Di Benedetto A, Lorenzon L, et al. miR-204 targets Bcl-2 expression and enhances responsiveness of gastric cancer. Cell Death Dis. 2012;3:e423 pubmed publisher
    ..Altogether, these findings suggest that modulation of aberrant expression of miR-204, which in turn releases oncogenic Bcl-2 protein activity might hold promise for preventive and therapeutic strategies of GC. ..
  63. Enyedy I, Ling Y, Nacro K, Tomita Y, Wu X, Cao Y, et al. Discovery of small-molecule inhibitors of Bcl-2 through structure-based computer screening. J Med Chem. 2001;44:4313-24 pubmed
    ..Our results suggest that the structure-based computer screening strategy employed in the study is effective for identifying novel, structurally diverse, nonpeptide small-molecule inhibitors that target the BH3 binding site of Bcl-2. ..
  64. Greider C, Chattopadhyay A, Parkhurst C, Yang E. BCL-x(L) and BCL2 delay Myc-induced cell cycle entry through elevation of p27 and inhibition of G1 cyclin-dependent kinases. Oncogene. 2002;21:7765-75 pubmed
    ..Our results suggest that one possible mechanism by which BCL-x(L) and BCL2 delay cell cycle entry may be the inhibition of Myc activity through the elevation of p27. ..
  65. Sultana R, Banks W, Butterfield D. Decreased levels of PSD95 and two associated proteins and increased levels of BCl2 and caspase 3 in hippocampus from subjects with amnestic mild cognitive impairment: Insights into their potential roles for loss of synapses and memory, accumulation o. J Neurosci Res. 2010;88:469-77 pubmed publisher
    ..The data obtained from the current study suggest a possible involvement of these proteins in synaptic alterations, apoptosis and consequent decrements in learning and memory associated with the progression of MCI to AD. ..
  66. Lopez H, Zhang L, George N, Liu X, Pang X, Evans J, et al. Perturbation of the Bcl-2 network and an induced Noxa/Bcl-xL interaction trigger mitochondrial dysfunction after DNA damage. J Biol Chem. 2010;285:15016-26 pubmed publisher
    ..These results suggest that the loss/inactivation of Mcl-1 in conjunction with an induced Noxa/Bcl-xL interaction may serve as a trigger for mitochondrial dysfunction during DNA damage-induced apoptosis. ..
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