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Validated All-in-One™ qPCR Primer for BCL2(NM_000633.2) Search again
Product ID:
HQP016211
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
Bcl-2, PPP1R50
Gene Description:
BCL2 apoptosis regulator
Target Gene Accession:
NM_000633.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants, produced by alternate splicing, differ in their C-terminal ends. [provided by RefSeq].
Gene References into function
- Review. Regulation of BCL2 phosphorylation and its role in leukemic cell apoptosis and drug resistance.
- expression is related to apoptosis in thymus
- an elevated bcl-2/bax ratio in rectal carcinoma tissue specimens suggests increased tumor resistance to adjuvant radiotherapy
- BCL2 antisense transcripts decrease intracellular Bcl-2 expression and sensitize LNCaP prostate cancer cells to apoptosis-inducing agents.
- Cells of JM1 human cell line treated with sanguinarine expressed BCL2 protein in apoptosis and cell death.
- OVEREXPRESSION OF BCL-2 IS ASSOCIATED WITH POOR SURVIVAL IN PRIMARY CENTRAL NERVOUS SYSTEM LYMPHOMA PATIENTS
- overexpression appears to be an early event in lung tumorigenesis; may function as a potential biomarker for the development of NSCLC
- Fibroblast growth factor-2 induces translational regulation of Bcl-XL and Bcl-2 via a MEK-dependent pathway: correlation with resistance to etoposide-induced apoptosis
- Protein kinase A RIalpha antisense inhibition of PC3M prostate cancer cell growth: Bcl-2 hyperphosphorylation, Bax up-regulation, and Bad-hypophosphorylation
- GM-CSF-driven apoptosis, but not TNF-driven apoptosis was reversibly associated with bcl-2-expression (bcl-2-dependent mechanism)in acute lymphoblastic leukaemia and non-Hodgkin's lymphoma in children.
- AUF1 binds in vitro to bcl-2 mRNA; involvement of AUF1 in the ARE/AUBP-mediated modulation of bcl-2 mRNA decay during apoptosis
- overexpression in regulatory volume decrease. Enhancing swelling-activated Ca(2+) entry and Cl(-) channel activity
- The over-expression of bcl-2 in the lens epithelium of fetus and children suggests that bcl-2 might be related to the development of cataract.
- analyzed expression in leiomyomas and myometrium from fertile and menopausal women
- Using a recombinant vaccinia virus expressing protooncogene Bcl-2, we demonstrate opposite effects of the expressed Bcl-2 in two cell lines: apoptosis induction in BSC-40 cells and apoptosis prevention in HeLa G cells.
- Dysregulated bcl-2 expression does not play a significant pathogenetic role in most pediatric follicular lymphomas, but does identify a subset of patients in whom disease is often disseminated and more refractory to combination chemotherapy.
- the first report of partial trisomy 3 and Bcl-2 overexpression in type II cryoglobulinemic vasculitis associated with HCV infection
- Bcl-2 expression is upregulated by VEGF in neuroblastoma cells.
- Bcl-2 expression is upregulated by IGF-I in neuroblastoma cells, which are thereby protected from starvation-induced apoptosis.
- REVIEW: gene expression regulation and role of bcl-2 in cell survival and cell cycle control in early hematopoiesis
- Bcl-2 upregulation by HIV-1 Tat during infection of primary human macrophages in culture.
- A functional role for the B56 alpha-subunit of protein phosphatase 2A in ceramide-mediated regulation of Bcl2 phosphorylation status and function
- Apoptotic index (includes nick-end labeling) and bcl-2 do not correlate with key clinical data (prognosis and blood counts at diagnosis) in patients with myelodysplastic syndrome, whie p53 protein levels do.
- expression of apoptosis-regulating proteins p53, Bcl-2, and Bax in primary resected esophageal squamous cell carcinoma
- Expression of p53 and bcl-2 proteins in acute leukemias: an immunocytochemical study
- expression in pelvic lymph nodes and primary tumors in early stage cervical carcinomas
- Bcl-2 overexpression prevents apoptosis induced by ceramidase inhibitors in malignant melanoma and HaCaT keratinocytes.
- Synergistic induction of apoptosis by simultaneous disruption of the Bcl-2 and MEK/MAPK pathways in acute myelogenous leukemia.
- IGFBP-3 inactivates Bcl-2 through serine phosphorylation.
- bcl-2 overexpression promotes myocyte proliferation
- The coexpression of the apoptosis-related genes bcl-2 and wt1 in predicting survival in adult acute myeloid leukemia.
- conformational change of Bcl2 due to association with peptidyl prolyl isomerase can contribute to irreversible apoptotic signaling.
- BCL-2 overexpression was noted in 29.4% cases of T-cell lymphoblastic lymphoma cases but was not correlated with higher rate of relapse
- ionomycin-induced calpain activation promotes decrease of Bcl-2 proteins thereby triggering the intrinsic apoptotic pathway
- Bcl-2 expression in lymphocytes infiltrating into the liver was investigated by immunohistochemistry
- increased expression in renal cell carcinoma associated with minimal apoptosis levels; may play role in progression of renal cell carcinomas and resistance to treatment
- overexpressed in acute myeloid luekemia while translocations associated with this gene are absent
- NF-kappaB activates Bcl-2 expression in t(14;18) lymphoma cells.
- Involvement of nuclear factor-kappa B, Bax and Bcl-2 in induction of cell cycle arrest and apoptosis by apigenin in human prostate carcinoma cells
- compared rates of bcl-2 translocation in follicular lymphoma across geographic regions
- Expression levels of apoptosis-related proteins caspase 3, Bcl-2, and PI9 predict clinical outcome in anaplastic large cell lymphoma.
- Changes of NF-kB, p53, Bcl-2 and caspase in apoptosis induced by JTE-522 in human gastric adenocarcinoma cell line AGS cells: role of reactive oxygen species.
- TNF alpha dramatically reduced intracellular levels of Bcl-2, while Dex abrogated this reduction.
- Increased cytosol Ca(2+) and type 1 programmed cell death in Bcl-2-positive U937 but not in Bcl-2-negative PC-3 and Panc-1 cells induced by the 5-lipoxygenase inhibitor MK 886.
- Antisense strategy shows that Mcl-1 rather than Bcl-2 or Bcl-x(L) is an essential survival protein of human myeloma cells.
- Bcl2 regulation by the melanocyte master regulator Mitf modulates lineage survival and melanoma cell viability
- Bcl-2-dependent modulation of Ca(2+) homeostasis and store-operated channels in prostate cancer cells
- N-cadherin signal transduction upregulates Bcl-2
- photoactivated hypericin does not cause Bcl-2 degradation but induces Bcl-2 phosphorylation in a dose- and time-dependent manner; Bcl-2 phosphorylation may be a signal to delay apoptosis in G(2)/M phase-arrested cells
- Bcl-2 protein expression in breast cancer
- Failure of up-regulation in proximal tubular epithelial cells of donor kidney biopsy specimens is associated with apoptosis and delayed graft function
- Association between Bcl-2 gene polymorphism with systemic lupus erythematosus(Bcl-2)
- Regulation of bcl-2 gene expression in human breast cancer cells by prolactin and its antagonist, hPRL-G129R.
- Inactivation of p21WAF1 sensitizes cells to apoptosis via an increase of both p14ARF and p53 levels and an alteration of bax and this protein ratio
- Depletion of Bcl-2 by an antisense oligonucleotide induces apoptosis accompanied by oxidation and externalization of phosphatidylserine in NCI-H226 lung carcinoma cells
- Fibroblast-like synoviocytes from rheumatoid arthritis patients express functional IL-15 receptor complex: endogenous IL-15 in autocrine fashion enhances cell proliferation and expression of Bcl-x(L) and Bcl-2.
- Expression of Bcl-2 eliminates selective advantages for p53-deficient cells in the tumor.
- REVIEW: Bcl-2 family members as prognostic indicators in AML.
- The lack of Bcl2 accompanied by p53 overexpression affects the distribution of cells among the cell cycle phases and modifies the sensitivity to cytotoxic drugs and the type of cell death.
- role in modulating HIV-1/monocyte-derived macrophage-induced neuronal apoptosis
- Retinoids cause apoptosis in pancreatic cancer cells via activation of RAR-gamma and altered expression of Bcl-2/Bax.
- increased expression of bcl-2 protein plays an important role in acquiring tolerance for testosterone ablation in mouse mammary carcinoma cells
- Lipotropes regulate gene expression in the human breast cancer cell line, MCF-7
- Overexpression affects mitochondrial structure and function
- REVIEW: The Bcl2 family: regulators of the cellular life-or-death switch
- overexpression of the Bcl-2 or Bcl-x(L) associated with the loss of apoptosis in breast cancer cells in vivo may account for their metastatic behavior
- During vascular endothelial cell apoptosis, high initial expression of Bcl-2 protein was significantly downregulated by IFN-gamma, but less so by TNF-alpha.
- Nitric oxide may be involved in the endometrial apoptotic process, whose control may be related predominantly to the changes of Bcl-2 expression
- bcl-2/Jh lymphomas show molecular heterogeneity and that bcl-6 and p53 mutations may be acquired during the evolution of such lymphomas
- Bcl-2-mediates regulation of CD69-induced apoptosis of human eosinophils.
- Immunohistochemical expression of this protein in squamous cell carcinomas from immunosuppressed renal transplant recipients and immunocompetent individuals.
- Forced expression of STAT5a in human cord blood-derived CD34+ cells enhanced expression Bcl-2 and p21(WAF/Cip1), suggesting they may be important in STAT5a-mediated eosinophil differentiation.
- levels of Bcl-2 were higher in the metastatic sublines than in parental breast cancer cells, which correlated with the activation of Stat3, but not with the expression/activation of bcl-2 transcription factors (CREB and WT1).
- 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.
- Improves oxidative phosphorylation and modulates adenine nucleotide translocation in mitochondria of cells harboring mutant mtDNA.
- A very low mRNA level was indicated at bax, bcl-2 and bcl-xL in hepatocellular carcinoma tissues in contrast to normal liver.
- Bcl-2 expression, especially in preinvasive cervical lesions may play a role in the apoptotic process and be regarded as a marker for disease progression
- expression of telomerase genes (hTR, hTRT) and apoptosis related genes (p53, bcl-2) in mammary atypical ductal hyperplasia
- This protein, via its BH4 domain, blocks apoptotic signaling mediated by mitochondrial Ras.
- This gene on the endoplasmic reticulum regulates Bax activity by binding to BH3-only proteins.
- Bcl-2 controls caspase activation following a p53-dependent cyclin D1-induced death signal
- BCL2 expression is not dependent upon the level of BAX epxression; reduction of BCL2 level activates p53-dependent apoptototic pathway.
- The relationships and interactions between p53, Rb and bcl-2 immunostaining, clinical parameters and response to cisplatin-based chemotherapy were evaluated in the present study.
- BCL-2 has a role in prostate carcinogenesis and cancer progression [review]
- Bcl-2 may be involved in protecting against CD95-mediated apoptosis of cord blood CD34(+) cell.
- Bcl-2 lacks a signal for the mitochondrial outer membrane and therefore localizes to several intracellular membranes
- Bcl-2 protein expression in developing human brain
- Bcl-2 staining was not observed in gastric carcinoma cells without E-cadherin mutations, but was detectable in 5 of 16 tumors with E-cadherin mutations (31.3%), a difference that was not statistically significant (p = 0.13).
- Chemotherapy induced Bcl-2 cleavage was blunted by inhibition of caspase activity in leukemia cells; however, coculture with bone marrow stromal cells resulted in reduced levels of 23 kDa Bcl-2.
- H. pylori-induced ERK1/2 activation, especially by the cagA(+) H. pylori strain, may play a protective role against gastric epithelial cell apoptosis partially through maintenance of bcl-2 gene expression
- BCL2 expression was determined in doxorubicin resistant gastric carcinoma lines.
- In adenocarcinoma, the expression of bcl-2 is associated with improved survival compared with bcl-2 negative patients.
- Bax, Bcl-2, fas and Fas-L antigen expression in human seminoma: correlation with the apoptotic index.
- Abnormally migrating bands on SSCP gels were identified only in 4/24 samples, providing strong support for the notion that in FL the translocated bcl-2 coding region is not targeted by somatic hypermutation.
- This study suggest that Bcl-2 modulates neuroprotective effects of calcineurin and that calcineurin inhibitors increase ischemic neuronal damage.
- Regulation of Bcl-2 expression by dihydrotestosterone in hormone sensitive LNCaP-FGC prostate cancer cells.
- SCF up-regulates Bcl-2 and Bcl-X L in erythroid precursors and exogenous expression of these proteins protects erythroblasts from caspase activation and death induced by chemotherapeutic agents.
- This gene constitutively suppresses p53-dependent apoptosis in colorectal cancer cells.
- over-expression of BCL2 is associated with muscle invasive transitional cell carcinoma of the bladder.
- role in counterregulating mitochondrial protassium transport
- Patients having radical prostatectomy after radiotherapy had significantly higher Bcl-2 overexpression than patients having surgery as the initial treatment. Changes in the apoptotic pathway may be important in local recurrence after radiotherapy.
- results showed that Fas and/or Fas-Ligand, Bcl-2, and tissue transglutaminase may be involved in apoptotic pathways leading to mucosal atrophy in children with coeliac disease
- biochemical and functional mechanisms regulating the ARE-dependent degradation of bcl-2 mRNA
- results suggest that the expression of Bcl-2 protein and of adrenomedullin in invasive squamous carcinoma may play crucial roles in selecting carcinoma cells resistant to apoptosis and in promoting malignant progression
- a novel role in cell fate decisions /during hematopoietic differentiation/ beyond cell survival
- High levels of Bcl-2 prevent accumulation of (99m)Tc-MIBI in breast tumour cells.
- BCL2 antiproliferative effect in E1A + c-Ha-ras-transformants was not associated with alterations in Cdk2, cyclins E and A content.
- Data show that overexpression of Bcl-2 in human Ms-1 cells inhibited not only the release of cytochrome c from mitochondria but also de novo ceramide synthesis induced by inostamycin.
- Bcl-2 should be considered as independent biologic prognostic parameter in diffuse large B-cell lymphoma, thereby aiding in the identification of patient risk groups.
- Role in polyclonal proliferation and apoptosis of CCR5-positive T-lymphocytes in patients with HIV type-1 infection.
- p53 gene and msh2 expression in recurrent glioblastoma multiforme
- The detected pattern of the p53/ bcl-2 ratio in hypertrophic actinic keratosis suggests important role for another gene: the proapoptotic gene bax.
- results demonstrated significant positive staining of Bcl-2 in the salivary tumorigenic tissue, but not in the surrounding non-tumorigenic tissue, pointing to a biological role in the tumorigenic process
- Importance of Bcl-2 as anti-apoptotic protein and mechanisms underlying its cytoprotective effects on pancreatic islets.
- p50 and p52 homodimers can transactivate the bcl-2 promoter through association with Bcl-3; in breast cancer and leukemic cells (CLL), high NF-kappaB2/p100 expression was associated with high Bcl-2 expression
- bcl-2 and bcl-6 proteins may play a role in the pathogenesis of transitional cell carcinoma, and bcl-6 expression reflects histopathologic grade.
- Bcl-2 decreases the level of functional E-cadherin thereby interfering with junction formation.
- Expression of BCR/ABL and BCL-2 in myeloid progenitors leads to myeloid leukemias.
- BNIPL-2, a novel homologue of BNIP-2, interacts with Bcl-2 and Cdc42GAP in apoptosis.
- Overexpression of bcl-2 and bcl-xL leading to prolonged survival of mast cells may contribute to the pathogenesis of mastocytosis.
- Results show that shear stress-induced nitric oxide is associated with decreased expression of bcl-2.
- These data indicate that As(2)O(3) induces apoptosis in T cells by enhancing oxidative stress and that Bcl-2 appears to play a major role in As(2)O(3)-induced apoptosis.
- Transgenic mice over-expressing human Bcl-2 in myeloid cells exhibit markedly increased neutrophil accumulation and reduced bacteria counts in peritoneum following cecal ligation and puncture, consistent with an increased host response.
- We conclude that C/EBPalpha and C/EBPbeta contribute to the deregulated expression of Bcl-2 in t(14;18) lymphoma cells
- Sustained reduction of bcl-2 protein causes glioma cells to undergo marked morphological change, reduced in vitro growth, complete loss of tumorigenicity, and increased sensitivity to cisplatin.
- Protects from apoptosis. when transfected into T cell from renal cell carcinoma.
- The immunodetection of both p53 and bcl-2 proteins in squamous cell carcinoma of the uterine cervix can be used as an independent diagnostic marker for cervical cancer associated with HPV infection.
- upregulation protects against apoptosis effected by live rabies virus vaccine strain in Jurkat T-cells and results in the establishment of long-term, persistently infected cultures that continue to produce rabies virus
- bcl-2 transcriptional regulation is mediated by the sonic hedgehog signaling pathway through gli-1
- Bcl-2 phosphorylated at serine-70 plays a critial role in the translocation of Bax from the cytosol to the mitochondria in nitric oxide-induced neuronal apoptosis.
- pancreatic carcinoma expressed a high positivity for bcl-2; findings suggested that the overexpression of bcl-2 is related to the carcinogenesis and progression of human pancreatic carcinoma.
- possible deregulation of the mechanisms that control bcl-2 expression in high-grade and advanced-stage colorectal carcinomas.
- Abnormal Bcl-2 and Bax protein bands after induction therapy in AML patients may be considered as factors associated with unfavorable clinical outcome.
- Bcl-2 expression was determined in thymic neuroendocrine tumors.
- Human prolactin-G129R-induced breast cancer cell and/or mammary gland apoptosis which is mediated, at least in part, through the regulation of Bax and Bcl-2 gene expression.
- bcl-2 may inhibit cell death at multiple points downstream of p53 activation
- up-regulation of uPAR expression by Bcl-2 in hypoxia is modulated by Sp1 DNA binding activity through the ERK signaling pathway
- bcl-2 mRNA contains an AU-rich element that functions in regulating bcl-2 stability
- bcl-2 protein positivity did not affect significantly the AgNOR distribution either in p53 protein positive or p53-negative cases of leukemia patients.
- The expression of estrogen receptor alpha, progesterone receptor and of Bcl-2 protein changed parallel with that of Akt protein in leiomyoma and myometrium.
- interaction of bcl-2 with paxillin plays an important role during nephrogenesis
- Bcl-2 overexpression is associated with B-cell leukemia and lymphoma
- determination of divergent sequences to facilitate design of specific inhibitors
- Bcl-2 level in asthmatic children is higher than control.
- a selective decrease in Bcl-2 expression was seen in myeloid progenitor cells of pateients with Kostmann syndrome: severe congenital neutropenia.
- Bax and Bcl-2 proteins are elevated after treatment with cladribine, cyclophosphamide, mitoxantrone, and combination chemotherapy
- Levels of Bcl-2 are decreased in three important brain tissues, i.e. frontal, parietal, and cerebellar cortices of autistic subjects, alluding to impaired apoptotic mechanisms in autism.
- the Ca(2+) spike, mitochondrial Bcl-2 presensitization, and subsequent Delta psi(m) transition, Bax translocation, and ROS generation are important upstream signals for cytochrome c release upon stimulation by a Bcl-2 inhibitor.
- Bcl-2 and bax molecules play a role in the regulation of apoptotic mechanisms in pituitary adenomas.
- the role of BCL-2 depends on its interaction with nuclear orphan receptor Nur77/TR3
- a stable non-B-DNA structure in the human genome appears to be the basis for the fragility of the Bcl-2 major breakpoint region, and the RAG complex is able to cleave this structure
- normal, hyperplastic and neoplastic breast epithelial cells expressing the anti-apoptotic protein Bcl-2 are immature cells that form part of the stem-cell subpopulation
- Bcl-2 downregulation has a role in cisplatin resistance in human small cell lung cancer cells
- Reduced gastric Bcl-2 level may be the main pathogenic mechanism of H. pylori-induced apoptosis in gastric epithelial cells.
- Expression of this apoptosis-related protein may be a useful marker in cervix cancer development.
- Expression of bcl(2) was present in only 5 cases or rectal cancer with the postchemotherapy changes being not significant.
- Reduced levels of Bcl-2 may play an important role in the increased sensitivity to apoptosis of HIV-specific CD8+ T cells.
- Bcl-2 protein was expressed more frequently and more strongly in uterine leiomyomas compared with leiomyosarcomas and smooth muscle tumors of uncertain malignant potential (STUMP)
- SRF-regulated Bcl-2 expression as a novel mechanism that is important for cell survival during early murine embryogenesis
- Patients with BCL2 overexpression showed significantly inferior disease free survival rate
- Increased bcl-2 protein expression in cells of 5-8 wk human embryos was found.
- Data suggest that the internal ribosome entry site-mediated translation of BCL-2 may enable the cell to replenish levels of this critical protein during cell stress, when cap-dependent translation is repressed.
- both Bak and Bcl-2 were found to be increased in correlation with an immune marker (beta2-microglobulin) in white and gray matter and plaque compared with corresponding cortical regions.
- mechanisms other than p53 may play a role in the regulation of bcl-2 expression in endometrial carcinoma
- survivin, p53, and bcl-2 are elevated in breast carcinoma but not ductal intraepithelial neoplasia
- Overexpression of antiapoptotic proteins Bcl-2 and Bcl-X(L) and down-regulation of caspase-3 activity may be associated with cisplatin resistance in human ovarian cancer.
- downregulation assists GD3 synthase's apoptotic effect on ECV304 cells
- Assessment of Bcl-2 and Fas expression at diagnosis in acute leukemia (1) could predict responsiveness to induction chemotherapy in ALL but not in AML
- Extracellular signal related kinase and protein phosphatase 2A are physiological regulators of Bcl-2 phosphorylation, and these enzymes exert an influence on the anti-apoptotic function of Bcl-2.
- Down regulation in Hep3B cell line in the presence of Ni(2+).
- bcl-2 oncogene has not shown to be a prognostic factor for laryngeal squamous cell carcinoma of the supraglottic larynx.
- direct interaction of Bcl-2 with SERCA may be involved in the regulation of apoptotic processes in vivo through modulation of cytoplasmic and/or endoplasmic reticulum calcium levels required for the execution of apoptosis
- This review focuses on the mechanisms by which anti-apoptotic Bcl-2 family members control the permeability of the mitochondrial membrane and influence other aspects of mitochondrial function after brain ischemia.
- Bcl-2 and InsP3Rs were detected together in macromolecular complexes, inhibiting InsP3R activation and thereby regulating InsP3-induced calcium release from the ER.
- Advanced stage non-small cell lung tumors or tumors with lymph node metastasis were analyzed, a more favorable survival was noted in patients with bcl-2-positive tumors than those with bcl-2-negative tumors.
- Bcl-2 overexpression led to reduced cytochrome c-mediated caspase-9-dependent cardiomyocyte apoptosis and local inflammation in cardiac allografts during ischemia-reperfusion injury and also led to reduced immune responses
- Bcl-2 interacts with activated Bax during apoptosis in an effective manner to neutralize the proapoptotic activity of Bax.
- bcl-2 expression is low in large non-polypoid colonic neoplasms
- The apoptotic effect of 11-hydroxy-15-oxokaur-16-en-19-olic acid could be significantly offset by over-expression of Bcl-2 in colon cancer cells.
- Down Regulation of BCL2 protein is associated with benign prostatic hyperplasia
- Bcl-2 is significantly expressed in squamous cell carcinoma compared to those with transitional cell carcinoma type in the presence of schistosomiasis.
- Bcl-2 is over-expressed in CD34+ acute myeloid leukemia (AML); conversely, MDR1 is over-expressed in CD34- AML.
- We made an NG108-15 transfectant, Bcl-2(P2), that stably expressed human Bcl-2, and used it to test Bcl-2's effect on the serum-starvation-induced apoptosis in NG108-15 cells.
- Mouse hearts overexpressing transgenic human BCL2 have a slower rate of decline in ATP during ischemia & reduced acidification. Oligomycin & Bcl-2 affect a common pathway. Bcl-2 modulates mitochondrial physiology & function.
- evaluated the expression of Bcl-2, Bax and Bak in patients with Graves Disease (GD); findings suggest that the differential expression of Bcl-2 family proteins in both thyrocytes and lymphoid follicles may be involved in the pathology of GD
- spontaneous T-cell reactivity against Bcl-2 in peripheral blood from patients suffering from unrelated tumor types
- Anti-apoptotic factors, Bcl-2 and Bcl-xL, were significantly decreased in epithelial cells under a hypoxic condition as assessed by Western blotting
- Downregulation of Bcl-2 protein is associated with breast disease
- These data show that JNK activation provides a molecular linkage from microtubule damages to the mitochondrial apoptotic machinery
- Results describe the expression of Bak and Bcl-2 in primary human breast cancers.
- aberrant ratio of bcl-2 to bax protein expression may be involved in the course of tumorigenesis of cholangiocellular carcinoma
- overexpression does not affect apoptotic pathway triggered by the Fhit protein in lung cancer cell lines
- Retinoic acid-induced apoptosis is a consequence of cellular differentiation, which leads to nucleolin down-regulation and bcl-2 mRNA instability.
- Bcl-2 expression markedly enhanced spontaneous lung metastasis from orthotopically implanted primary tumors.
- Bcl-2 transgene promotes B cell accumulation in signaling-deficient B-cell maturation defect 1 (bcmd-1) mice, but formation of white pulp areas of the spleen and follicles in the lymph nodes is severely impaired.
- BCL2 expression is important for maintenance of hair follicle epithelial stem cells and formation of secondary hair germ
- annexin I is regulated by an anti-apoptotic Bcl-2 protein in TNF-alpha-induced renal apoptotic events
- p53, bcl-2 and telomerase have roles in progression of Egyptian breast cancer patients
- Bcl-2 overexpression leads to the induction of activated signal transducer and activator of transcription 3 (STAT3) and to the induction of SOCS3, which may contribute to the pathogenesis of follicular lymphoma.
- PCNA expression induces apoptosis by up-regulating cleaved caspase-3 and poly adp ribose polymerase expression and down-regulating Bcl-2 protein expression in leiomyoma cells.
- Increase in serum bcl-2 is associated with melanoma
- HGF and BCL-2 family proteins use a furin-dependent pathway to promote invasion via TGF-beta and MMP in human malignant glioma cells and the pro-invasive properties of TGF-beta require furin- dependent MMP activity.
- colocalization of Human papillomavirus type 16 E5 protein with the Bcl-2 antiapoptotic protein on intracellular membranes was established
- Skp2 in tumor cells suppresses apoptosis through Bcl-2 expression
- Here we demonstrate that the Bcl-2-mediated suppression of hMSH2 expression results in a reduced cellular capacity to repair mismatches.
- NS-398 significantly inhibits the proliferation and induces apoptosis of hepatoma cells, which may involve decrease of BCL-2 expression.
- Apoptosis is blocked by human Bcl-2 in a mouse macrophage cell line and in primary mouse macrophages.
- The optic nerve axons in glaucomatous eyeballs showed statistically significant higher Bax protein expressions than those of Bcl-2 proteins.
- 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 and Bcl-X(L.)
- Gossypol is a potent and novel therapeutic able to overcome apoptosis resistance by specifically targeting the activity of antiapoptotic Bcl-2 family members.
- frequency and chromosomal features of this der(8)t(8;14;18) in a series of acute leukaemias and malignant lymphomas
- Expression of bcl-2 expression has no prognostic value for gastrointestinal stromal tumours.
- Bcl-2 positivity identified a subgroup with invariably fatal disease in the high-risk IPI (International Prognostic Index) patients.
- Bcl-2 interacts with FKBP38 through the unstructured loop, and the interaction appears to regulate phosphorylation in the loop of Bcl-2
- Arsenic trioxide might exert cell killing in part by inducing Bax activation through a Bcl-2-suppressible pathway in hematopoietic cells that is caspase independent and intracellular ROS regulated
- COX-2 may regulate expression of apoptosis suppressor gene (bcl-2) through interaction of tumor cells and stromal cells
- BCL2-mediated apoptosis appears to play a significant role in pathogenesis of laminin alpha2 deficiency
- expression of ESRA, bcl-2 and c-myc gene expression in fibroadenomas and adjacent normal breast is related to nodule size, hormonal and reproductive features
- The weak immunoreactive expression of p53, combined with a relatively strong expression of bcl-2 contributes to the characteristic slow progression of parathyroid adenoma
- The c-bcl-2 presence will have less mutations at A and T in B cells mutating their immunoglobulin genes.
- Bcl-2-positive dendritic cells in epidermis of inverted follicular keratoses. Keratinocyte bcl-2 staining was significantly higher in seborrheic keratoses(SKs). Bcl-2 may be increased in SKs as anti-apoptotic mechanism.
- Blockage of the mitochondrial permeability transition pore and caspase-9 demonstrated that Bcl-2-modulated caspase-2 activity occurred upstream of mitochondria
- Inhibition of bcl-2 expression may be an attractive therapeutic strategy in RCC tumors with high bcl-2 expression.
- Expression of Bcl-2 is significantly higher in squamous cell carcinomas than in verrucous penile carcinomas.
- p53, Bax, Bcl-2 and Mdm2 mRNA expression levels correlate with the malignant transformation of the uterine cervix
- Transplantation with mouse embryo stem (ES) cells overexpressing human Bcl-2 increases the survival of transplanted ES cells, neuronal differentiation, and functional outcome in ES-transplanted rats after severe focal ischemia.
- an imperfect purine/purine/pyrimidine triplex likely forms at the bcl-2 major breakpoint region of the t(14;18) translocation
- Pak1-dependent Raf-1 phosphorylation regulates its mitochondrial localization, phosphorylation of BAD, and Bcl-2 association
- in cells synchronized at the onset of mitosis, Bcl-2 is present in a complex with nucleolin, cdc2 kinase and PP1 phosphatase
- role of COX-2 in regulating the degree of apoptosis by modulating bcl-2 protein in benign and malignant parotid gland tumors
- Bax but not Bcl-2 expression is increased after exposure to prostaglandin A2 and 2-methoxyestradiol in Hela cells
- lack of role in sequestering proapoptotic Bak
- Maspin overexpression modulates tumor cell apoptosis through the regulation of Bcl2 family proteins
- Bcl-2 provided Purkinje cell protection from SV40 Tag-induced cell death. Interestingly, RotaRod behavioral analysis demonstrated that 'rescued' Purkinje cells degrade cerebellar function.
- Apoptosis-associated bcl-2 oncogene is abnormally expressed in gastric precancerous lesions
- Significantly higher Bcl-2 levels were associated with advanced lung cancer patients
- in the germinal centers, most T cells are Bcl-2(-); most CD4(+) T cells are Bcl-2(-), while nearly 100% of the CD8(+)T cells are Bcl-2(+). The Bcl-2 downregulation by both B and CD4(+) T cells suggests these two subsets may undergo a selection process
- Expression of Bcl-2 in osteoblasts is important in regulating bone mass in development and in the normal aging process of bone.
- Bcl-2 is antagonized by dynamin-related protein (Drp1) and mitochondrial fission protein (hFis1).
- overexpressing an antioxidant gene such as GPX1 in endothelial cells is able to change the basal mRNA and protein Bax levels without affecting those of p53 and Bcl-2
- During tuberculosis, predisposition of CD4 T-cell subsets to apoptosis may involve both low expression of Bcl-2 and excessive expression of transforming growth factor (TGF)-beta, tumor necrosis factor(TNF)-alpha, and Fas ligand (FasL).
- Spontaneous apoptosis is reduced in the endometrium of unexplained-infertile women, and is associated with the changed Bcl-2:Bax ratio
- Bax, Bad, and Bim are upregulated, while Bcl-2 is downregulated in human neuroblastoma cells treated with propargylamine
- BCL2 repression by miR-15 and miR-16 microRNAs induces apoptopsis in a leukemic cell line model.
- overall survival of post-surgical pancreatic adenocarcinoma patients seemed to be improved with Bcl-2 and Bax expression
- Transducible loop deleted Bcl-2 increases survival of cortical neurons after trophic factor withdrawal and also rescues neural cell lines from staurosporine-induced death. Supports concept of protein transduction of Bcl-2 constructs for neuroprotection.
- Data evaluate and compare the bcl2, bax, and nestin patterns in the frontal cortices of Alzheimer and multiple-infarct dementia patients, and in normal aging.
- Oct-2, therefore, acts as a cell survival factor in t(14;18) lymphoma cells by directly activating the antiapoptotic gene bcl-2.
- We present here a case of Follicular Lymphoma with leukemic presentation and a complex translocation involving the IgH, BCL2 and BCL6 loci
- IL-1Ra, Bcl-2, and iNOS are upregulated and counter the proinflammatory and proapoptotic effects of ischemia-reperfusion
- studies suggested that acetylsalicylic acid -promoted Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) cytotoxicity is mediated through down-regulating BCL-2
- catalase has a critical role in CSF-independent survival of human macrophages via regulation of the expression of BCL-2 and BCL-XL
- These findings imply that some of the biological functions of Bcl-2 may be attributed to their ability to inhibit anticancer agents-induced apoptosis through the sustained Akt activation.
- The low frequency of BCL-2/IgH translocation in healthy Chinese individuals of Han nationality located in Zhejiang area may be one of the reasons for the difference in the incidence of follicular lymphoma between China and Western countries.
- Bcl-2-mediated apoptosis resistance in human colon cancer cells.
- Bcl-2 has a role in cell death, apoptosis, and cytochrome c release independent of p53
- Loss of pSer70 Bcl-2 expression is closely linked to biological aggressiveness in colorectal tumors and represents a statistically significant molecular index for prognosis of patients with these tumors.
- Suppression of Bax and overexpression of Bcl-2 protein is an early event in gastric tumorigenesis, before gastric dysplastic
- Bcl-2 expression was associated with better overall survival and appears to be the key biological factor influencing clinical behaviour.
- We aimed to investigate the expression pattern of p53, Bcl-2 and C-Myc in colorectal cancer(CRC)tissues obtained from Egyptian colorectal cancer patients divided in two different groups, associated with and without Schistosoma mansoni.
- The expression of bcl-2 and p53 represent biological characteristics of colorectal carcinomas.
- This study aims to evaluate the expression of bcl-2, which is an antidote of apoptosis, and aims to evaluate the value of bcl-2 as a prognostic marker in papillary thyroid cancer
- WT p53, but not tumor-derived mutants, bind to BCL2 via the DNA binding domain and induce mitochondrial permeabilization.
- results indicate that GATA4 positively regulates cardiac Bcl2 gene expression in vitro and in vivo
- beta amyloid-induced neurotoxicity occurs via apoptosis regulator BAX over-expression, bcl-2 down-regulation, and caspase-3 activation, first indicating that methionine 35 redox state may alter this cell death pathway
- The expression rate of bcl-2 was relatively high in small cell lung cancer without any prognostic significance.
- BCL-2-overexpressing cells are sensitized to apoptosis by a pyrimidine-2,4,6-trione derivative
- Data suggest that prolaction-mediated induction of ornithine decarboxylase activity enhances expression of Bcl-2 strongly enough to bring about prolactin's anti-apoptotic function.
- Bcl-2 expression appears significantly (p<0.005) more often in cases of mild colonic dysplasia (61.1%) compared to inflammatory-regenerative mucosa (14.8%).
- AP-2alpha induces apoptosis by down-regulating Bcl-2 and utilizing a bax/cytochrome c/Apaf1/caspase 9-dependent mitochondrial pathway
- Data suggest that 2-methoxyestradiol 2 inhibits estradiol-stimulated proliferation and induces apoptosis in ovarian carcinoma cells, and that activation of p38 and phosphorylation of Bcl-2 plays a critical role in the mechanism.
- BCL2 has a role in growth of breast cancers with reduced capability of distant colonization
- Overexpression of Bcl-2 protected primary fibroblasts against oxidative stress-mediated reduction in cell proliferation, but did not prevent premature senescence.
- Expression of both bcl-2 and cyclooxygenase-2 were increased in non-dysplastic Barr
- Bcl2, in addition to its survival function, may also suppress DNA repair in a novel mechanism involving c-Myc and APE1, which may lead to an accumulation of DNA damage in living cells, genetic instability, and tumorigenesis
- Results suggest that Ubc9 might regulate bcl-2 expression through the ER signaling pathway, which ultimately contributes to the alterations of drug responsiveness and tumor growth.
- overexpression of Bcl-2 is one of the key mechanisms to give neuroblastoma cells the resistance against ATRA-mediated apoptosis
- the ratio of Bax:Bcl-2 in the human oviduct increases significantly in the luteal phase consistent with cells undergoing apoptosis
- Bcl-2 expression in MCF7 cells stabilizes p53, induces phosphorylation of p53 serine 15 (p53pSer15) and inhibits MCF7 cell growth
- Bcl-2 is an independent predictor of breast cancer outcome and seems to be useful as a prognostic adjunct to the Nottingham Prognostic Index (NPI), particularly in the first 5 years after diagnosis.
- Data suggest that Bcl-2 functions as an inhibitor of mitochondrial permeabilization by changing conformation in the mitochondrial membrane to bind membrane-inserted Bax monomers and prevent productive oligomerization of Bax.
- Finds a statistical significance for Bcl-2, Bax, and apoptosis with H. pylori status in gastric cancer patients in Egypt
- Clusterin and bcl-2 are upregulated in laryngeal carcinomas and their expression is related to invasiveness of these tumors.
- in diffuse large B-cell lymphoma, molecular alterations in ice, bcl-2, c-myc and p53 are present in hematopoietic cells from bone marrow as well as in primitive hematopoietic progenitors
- This study reveals a compartment-specific toxicity of PrP misfolding that involves coaggregation of Bcl-2 and indicates a protective role of molecular chaperones.
- down regulation of MAD2 could promote the drug resistance of gastric cancer cells and inhibit anticancer drugs induced-apoptosis by upregulating Bcl-2 and interfering the mitochondrion apoptosis pathway
- PP2A-mediated dephosphorylation of BCL-2 is required to protect BCL-2 from proteasome-dependent degradation, affecting resistance to ER stress
- BCL-2 variants may be associated with a decrease in prostate cancer susceptibility.
- We analysed the ability of human Bcl-2 to interact with and regulate the activity of nematode apoptosis proteins, and hypothesise that Bcl-2 might suppress nematode cell death by preventing EGL-1 from antagonising CED-9, rather than by inhibiting CED-4.
- bcl2 and ROS1 oncogene expression in meningiomas are not concurrent and neither can be ascribed to any histologic subtype or grade of tumor.
- the bcl-2 mbr possessed regulatory function that was related to special AT-rich sequence-binding protein 1 (SATB1).
- An analysis of clinical outcome in 23 PIOL (primary intraocular lymphoma) patients revealed no significant association between bcl-2 t(14;18) translocations and survival or relapse.
- lysosomal damage by ATX-s10-PDT can initiate apoptotic response and this apoptotic pathway can be regulated by photodamage to Bcl-2 via mitochondrial damage
- The Bcl-2 protein expression has a close correlation with p27 and p53 protein expressions and the proliferation activity determined by MIB-1 counts in invasive ductal carcinoma of the breast.
- up-regulation of bcl-2 has a role in preferential survival of acute lymphoblastic leukemia cells at 33 degrees C
- STAT3 activation by IL-6 provides an antiapoptotic advantage in human cord blood cells CD34+ cells, essentially owing to the expression of bcl-2.
- Asbestos may affect the human immune system through STAT3 activation and Bcl-2 overexpression.
- anti-beta-2 glycoprotein I antibodies react with trophoblast cells and reduce the Bcl-2/Bax ratio, but without any clear apoptotic effect
- Bcl-2 by competing with IP3R1 for the binding of PP1 can reduce the inositol trisphosphate-mediated calcium signal and protect cells from mitochondrial dysfunction and cell death.
- The high expression of bcl-2 in Hodgkin and Reed-Sternberg cells in most classical Hodgkin's lymphomas (HLs)indicates that this protein may play predominant role in the regulation of apoptosis in classical HLs.
- Bcl-2 expression acts as a regulator of HSV-2 replication.
- BCL2-938AA genotype is associated with increased Bcl-2 expression and a novel unfavorable genetic marker in patients with B-CLL.
- Increased serum levels of Bcl-2 is associated with advanced stage non-small cell lung cancer
- The cooperative effects of phenotypes determined by mdm-2, p53, and bcl-2 expression may predict survival in patients with muscle-invasive TCC of the bladder
- Bcl-2 is a common mediator of early apoptotic and necrotic events occurring at rates that are dependent on cellular factors accumulating over time
- Molecular model of the major G-quadruplex structure formed in the BCL2 promoter provides insights for its loop conformations and interactions with the core tetrad structures.
- down-regulation of the neuropilin-1 transcripts by short interfering RNA caused spontaneous synoviocyte apoptosis, which was associated with both the decrease in Bcl-2 expression and the increase in Bax translocation to mitochondria.
- Bcl-2 induced by functional regulation of G-protein coupled receptors protects from oxidative glutamate toxicity by increasing glutathione
- Patients carrying BCL2 gene rearrangements showed longer telomere length (4.19 +/- 0.14 kb) than those without (3.51 +/- 0.14 kb; P = 0.05).
- repression of BCL2 transcription is the single essential consequence of targeting the MIZ-1 pathway during apoptosis induction, which explains a copperative interaction between c-MYC and BCL2
- The expression of p53, Bcl-2 and Bax was altered in lung cancer tissue compared to histologically normal bronchial epithelium.
- In CD19+ B-cell chronic lymphocytic leukemia (B-CLL) cells of untreated patients, Bcl-2 showed over expression compared with CD19+ cells of healthy donors.
- The Bcl-2 expression was low and showed no significant difference between laryngeal papillomatosis and normal larynxes.
- p53 and Ki-67 were expressed with increasing frequency, and bcl-2, p21, and mdm-2 with decreasing frequency in thyroid carcinoma progression. p27 and cyclin D1 were expressed in <15% of cases, with a trend toward decreasing expression.
- These findings indicate that RTN3 is directly involved in the endoplasmic reticulum-constituents trafficking events through dually acting as an essential and important ER-stress sensor, and a trigger for the Bcl-2 translocation.
- Activator BH3-only occupation of BCL2 may prime cancer cells for death, offering a potential explanation for the marked chemosensitivity of certain cancers.
- pro-apoptotic Bax/Bcl-2 are upregulated in human leukemic HL-60 cells after treatment with ethyl acetate extract of Chinese medicinal herb Sarcandra glabra
- These findings suggest that neuroprotection by simvastatin is dependent on the drug's previously unexplored and important effect of up-regulating Bcl-2.
- Data suggest that cytoplasmic mutant p53 increases Bcl-2 expression in estrogen receptor-positive breast cancer cells.
- Bcl2 suppression of MMR may occur in a novel mechanism by directly regulating the heterodimeric hMSH2-hMSH6 complex, which potentially contributes to genetic instability and carcinogenesis
- Kringle 5 of human plasminogen has a role in autophagic survival by up-regulating Beclin 1 and complexing Bcl-2 to Beclin 1
- These results suggest that failure of stress-induced downregulation of Bcl-2 underlies resistance of senescent human diploid fibroblasts to apoptosis.
- The delay of tumor progression is apparently determined by the ability of Bcl-2-expressing tumor cells to extinguish the cell-damaging environmental stress signals and Bax activation, while its acceleration correlates with Bcl-2 loss.
- overexpression of Bcl-x(L) or Bcl-2 in PC12 cells markedly suppressed brefeldin A-induced activation of caspases and resulting cell death.
- Siatistically significant value in assocation with survival or event-free survival in head and neck squamous cell carcinoma.
- BCL-2 expression was investigated depending on the site of the tissue material sample and the final histopathological result.
- HIV Tat protein increases Bcl-2 expression in monocytes which inhibited apoptosis induced by TRAIL.
- Researchers found increased Bcl-2 positive identification after neoadjuvant therapy in patients with colorectal cancer.
- in breast cancer, Bcl2 protein expression parallels its mRNA level, and it has a highly significant and independent prognostic relevance.
- In normal HeLa cells, ectopic overexpressed Bcl-2 reduced cell apoptosis induced by overexpressed RTN3. results suggest that RTN3 could bind with Bcl-2 and mediate its accumulation in mitochondria, which modulate the anti-apoptotic activity of Bcl-2.
- This study is the first to show a clear dissociation between changes in Bcl-2 expression (downregulation) and Bcl-XL, Mcl-1 expression (upregulation) during progression of melanoma.
- The level of bcl-2 expression could be a valuable predictor of tumor behavior and disease outcome.
- Antiapoptotic proteins Bcl-2 and Bcl-X(L) bind and suppress NALP1, reducing caspase-1 activation and interleukin-1beta (IL-1beta) production.
- 18q21-23 copy number will be a clinically relevant predictor for sensitivity of SCLC to Bcl-2 family inhibitors. The 18q21-23 genomic marker may have a broader application in cancer because Bcl-2 is associated with apoptosis evasion and chemoresistance.
- Cells over-expressing Bcl-2 showed evidence of increased genomic instability, consistent with the impairment of apoptosis in damaged cells.
- BH3-only proeins and BH3 mimetics induce autophagy by competitively disrupting the interqction between BECN1 and Bcl-2/Bcl-X(L).
- Bcl-2 RNA silencing in transfected HepG2 cells induced apoptosis and increased sensitivity of cells to 5-FU and 10-hydroxycamptothecin.
- Bcl-2 expression was up-regulated in cervical carcinoma (both adenocarcinomas and squamous cell cancers) associated with humanpapillomavirus (HPV) infection
- Upregulation of bcl-2 may play a major role in therapy resistance.
- Rho inactivation allows the activity of Rac to become dominant leading to stimulation of the phosphoinositide 3-kinase/Akt/IkappaB kinase/nuclear factor-kappaB prosurvival pathway.
- CDK11(p58) down-regulates Bcl-2 in pro-apoptosis pathway depending on its kinase activity, which elicits survival signal in hepatocarcinoma cells.
- Patients with active and inactive juvenile-onset systemic lupus erythematosis have a different profile of Fas and Bcl-2 expression.
- immunoreactivity of p53, MDM2, WAF1, and BCL-2 were measured in soft tissue sarcomas cases consisting of 54 low-grade, 40 intermediate-grade, and 58 high-grade sarcomas
- There appears to be an influence of BCL2 ala43ala genotypes on esophageal cancer phenotype, particularly with regard to tumor location, which supports the theory of prevalence of site-specific genetic alterations
- These data suggest that long-term androgen deprivation + radiotherapy should be used when either Bcl-2 or Bax is abnormally expressed.
- BCL2 repression by the tumor suppressor activity of the lysyl oxidase propeptide inhibits transformed phenotype of lung and pancreatic cancer cells
- High Bcl-2 expression is associated with osteosarcoma
- Correlation of breakpoints with histology showed that major breakpoint region occur more frequently in grade 2 lymphomas.
- Impaifred kinetics of Bax-GFP and Smac/DIABLO-GFP in caspase 8 and bid-silenced and Bcl-2-overexpressed breast cancer cells exposed to camptothecin.
- a novel role for BAD in cell cycle regulation dependent upon its phosphorylation state and independent of the BAD/BCL2 interaction and apoptosis.
- Bcl-2 up-regulation is a homeostatic survival mechanism necessary for the manifestation of immunomodulatory effect of estrogen on human macrophages.
- Risk for head and neck squamous cell carcinoma may be assocated with single-nucleotide polymorphism in the promoter region.
- bcl-2 and p53 expression in neuroblastoma is related to DNA fragmentation
- p53 expression may have a role in the carcinogenesis of squamous cell cervical carcinoma whereas Bcl-2 expression has no role. Ki-67 expression can not be used in determining the aggressiveness of CIN lesions
- progesterone via progesterone receptor interacts with the bcl-2 promoter to induce its expression in leiomyoma tissue
- Study demonstrates that PKCepsilon forms a signaling complex and acts co-operatively with Akt to protect human vascular endothelial cells against apoptosis through induction of the anti-apoptotic protein Bcl-2 and inhibition of caspase-3 cleavage.
- Therefore, these data support the hypothesis that CREB plays a critical role in the regulation of Bcl-2 expression in TCS-induced Hela cell death.
- p53 and Ki-67, but not bcl-2, cyclin D1 or HER-2 may have roles in the process of tumor genesis in non-small cell lung carcinoma
- overexpression of Bcl-2 may result in "oncogene addiction" of the cancer cell
- IFN-alpha sensitivity of B-cell lymphomas depends on the presence or absence of BCL
- We conclude that alteration in the expression of proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins on surface of thyroid follicular cells may play a role in the pathogenesis of thyroid autoimmune disorders.
- p38 is necessary for Bcl-2-induced inhibition of apoptosis, induction of cell cycle arrest and accelerated senescence after DNA damage and serum starvation, but not after nocodazole treatment.
- a caspase-9 signaling cascade induces feedback disruption of the mitochondrion through cleavage of anti-apoptotic Bcl-2, Bcl-xL, and Mcl-1
- Epo has a role in reducing expression of apoptosis-related proteins Bcl-2 and Bcl-10 in ovarian cancer cells
- Report modulation of the BCL-2/BAX ratio by interferon-gamma and hypoxia in human peritoneal and adhesion fibroblasts.
- the AA genotype of the BCL2 (-938C>A) single-nucleotide polymorphism may play a role in increased survival in lymph node-negative breast cancer patients
- a novel link between TLR4 and a calcium-dependent signaling cascade comprising CaMKIV-CREB-Bcl-2 that is essential for DC survival.
- This study aimed to explore, whether polymorphisms in BCL2, Cyclin D1, FAS, EGF and EGFR genes affect survival in a cohort of patients with squamous cell esophageal cancer treated with CT+RT with a view to identify the potential therapeutic targets.
- These data suggest that P1 promoter is the main driving force for transcribing the bcl-2 gene and P1 activity is modulated by M and P2 in a p53-dependent and -independent manner.
- COX-2 and Bcl-2 may promote phaeochromocytoma malignancy, and these oncoproteins may be valuable surrogate markers of an aggressive tumour phenotype.
- Bcl-2 over-expression prevented a number of DENSPM-induced apoptotic effects.
- Gastrins activate members of Rho family G proteins which in turn regulate different proteins of the Bcl-2 family leading to changes in caspase 3 activity.
- interaction between the catalytic FKBP38 domain and the N-terminal CaM domain activates FKBP38 and, as a consequence, also regulates Bcl-2.
- study concludes that the nuclear and mitochondrial intracellular pools of Bcl-2 are regulated through different mechanisms & only the cytokine-mediated regulation of the mitochondrial pool is relevant to the control of the initiation of apoptosis
- BCL2 protein levels in CLL reflect a complex interplay of transcriptional and posttranscriptional controls, but do not appear to be associated with the -938C>A promoter SNP.
- BCL2 functions as an activator of the AKT signaling pathway in pancreatic cancer.
- Diabetic human conjunctiva, with its inflammatory and cicatricial phenomena, is a privileged target for BCL2 protein apoptotic cell death.
- bcl2 and Caspase-3 have roles in Shikonin analogue (SA) 93/637 induced apoptosis of human U937 cells
- After the addition of 20 microg/ml DDP or 100 microM DADS, siRNA targeting of the Bcl-2 gene specifically down-regulated gene expression in A549/DDP cells, increased spontaneous apoptosis, and sensitized cells to DDP and DADS.
- silencing of PrPc facilitates the activation of proapoptotic Bax by down-regulation of Bcl-2 expression, thereby abolishing the resistance of breast cancer cells to TRAIL-induced apoptosis
- Expression of antiapoptotic Bcl-2 protein occurs during the entire heart posttransplant period, being probably a preservative and adaptative response.
- IL-10 modulated the pro-apoptotic capacity of TNF-alpha in chondrocytes as shown by the decrease in caspase activities and bax/bcl-2 ratio
- BP1 may regulate bcl-2 and c-myc expression
- sHA 14-1 antagonizes anti-apoptotic Bcl-2 proteins and may represent a promising candidate for the treatment of drug-resistant cancers.
- Alterations in the expression of p53, survivn, and bcl-2 take place in a concerted fashion, implying that many of these cases may share common abnormalities.
- our data do not support the use of the (-938C>A) BCL-2 polymorphism as a prognostic marker in CLL and argue against its postulated role in modulating Bcl-2 levels.
- GCs induce both pro- and anti-apoptotic BCL2 family member-dependent pathways, with the outcome depending on cellular context and additional signals feeding into the BCL2 rheostat.
- In human K562 cells, induction of apoptosis by sorbitol involves pro- and anti-apoptotic Bcl-2 family proteins.
- BCL2 translocation is essential for the pathogenesis of follicular lymphoma in Thai patients
- These findings suggest that downregulating CIAPIN1 could sensitize leukemia cells to chemotherapeutic drugs by downregulating MDR-1 and Bcl-2 and by upregulating Bax.
- data indicate that in early and advanced gastric tumors, p53 and bcl-2 protein accumulation is more intense in gastric mucosa adjacent to advanced tumors and p53 immunoreactivity peaks in advanced carcinomas
- In T lymphoma cells, STS induces the expression of the pro-apoptotic orphan receptor Nur77 that overcomes the anti-apoptotic effect of Bcl-2, thus enabling GCinduced apoptosis.
- IGF1 promotes resistance to apoptosis in melanoma cells through an increased expression of BCL2, BCL-X(L), and survivin
- study shows bcl-2 is occasionally expressed in pancreatic endocrine tumors
- genetic variation due to ethnicity may influence prognostic value in chronic lymphocytic leukemia
- Id-1 regulates Bcl-2 and Bax expression through p53 and NF-kappaB in MCF-7 breast cancer cells
- cancer mutations induce APC mitochondrial localization and that APC regulation of Bcl-2 at mitochondria may contribute to tumor cell survival.
- In thyroid glands of patients with Graves disease the regulation of Fas/Fas ligand/Bcl-2 favors apoptosis of infiltrating lymphocytes.
- distinctions in the behaviors of Bcl-B and Mcl-1 relative to the other anti-apoptotic Bcl-2 family members, where Bcl-B and Mcl-1 display reciprocal abilities to bind and neutralize Bax and Bak.
- substitution of C-terminal tail or tail & adjacent loop of Bcl-2 with equivalent regions from Bak or Bax mutant resulted in association with mitochondria. change in subcellular localization of Bcl-2 chimeras triggered cells to undergo apoptotis
- Sanguinarine-mediated apoptosis is blocked by ectopic expression of Bcl-2 and cFLIPs
- t-Darpp promotes cancer cell survival by up-regulation of Bcl2 through Akt-dependent mechanism.
- Clinical and histological differences between BCL2-/BCL6+ and BCL2+/BCL6+ tumours could reflect an interplay between both translocations.
- data reveal that high cellular concentrations of Bcl-2 lead to a calcium- and ROS-dependent induction of death.
- CD34+ leukemic subpopulation predominantly displays lower spontaneous apoptosis and has higher expression levels of Bcl-2(B-cell CLL/lymphoma 2) genes than CD34- cells in childhood AML
- Results describe the interrelationship between H pylori and Epstein-Barr virus infection in gastric carcinogenesis, focusing on p53 mutation and c-Myc, Bcl-2 and Bax expression.
- overexpression acts as a strong antiapoptotic in both squamous cells and adenocystic carcinoma
- Bcl2 inhibition of AP site repair may occur in a novel mechanism by down-regulating APE1 endonuclease activity, which may promote genetic instability and tumorigenesis.
- TAT-IkappaBalphaSR reduced NF-kappaB dependent transcription, Bcl-2 expression and promoted Jun-N-terminal kinase-dependent apoptosis in human and rat hepatic myofibroblasts.
- Data show that Bcl2 suppresses DNA double-strand-break (DSB) repair and V(D)J recombination by downregulating Ku DNA binding activity, which is associated with increased genetic instability.
- BCL-2 proteins induce mitochondrial outer membrane permeabilization
- Hyperexpression of BCL2 is associated with gliomas
- this study has found bcl-2 of no value as a prognostic marker in this group of serous ovarian tumors
- this is another negative report on the prognostic value of bcl-2 in bilharzial bladder tumors.
- important mechanistic insights related to Bcl-2-mediated resistance to SP600125-induced apoptosis, and induction of G2/M phase arrest and endoreduplication.
- Our current study demonstrated that Bcl-2 siRNA significantly augmented taxol mediated apoptosis in different human glioblastoma cells through induction of calpain and caspase proteolytic activities.
- our study demonstrates increased concentrations of VEGF and Bcl-2, but not MMP-3, in serum of melanoma patients
- chromosome region 18q21 gain including the MALT1 gene is associated with the activated B-cell-like gene expression subtype and increased BCL2 gene dosage and protein expression in diffuse large B-cell lymphoma
- Overexpression of bcl-2 is associated with mantle cell lymphoma
- EBV is not related to the overexpression of Bcl-2 and c-Myc (nuclear) in gastric carcinomas.
- in endometrial carcinoma Bcl-2 (B-cell lymphoma protein 2) expression was related with younger age, favorable grade and Progesterone receptor expression by tumor cells
- BCL-2 expression was not correlated with any known histological factors in endometrial carcinoma
- the presence of Bcl-2 in the proteome of cells has multiple effects on agonist-mediated Ca2+ signals, and can abrogate responses to submaximal levels of stimulation through direct control of inositol 1,4,5-trisphosphate receptors.
- Bcl-2 is expressed in dermal lymphocytes in lichen planus and psoriasis vulgaris.
- accumulation of bcl-2 in the syncytiotrophoblast may reflect its high resistance to detrimental factors.
- It is concluded that P. aeruginosa can induce apoptosis with an up-regulated expression of Bax and a down-regulated expression of Bcl-2, which resulted in increased levels of cytochrome c release and increased caspase-3 and -9 in human U937 cells.
- The distribution of the bcl-2, bax and caspase-3 proteins was investigated in the cells of developing human spinal ganglia.
- we found a substantial number of primary diffuse large B-cell lymphomas (DLBCLs) of bone cases with a rearrangement of BCL2 and c -MYC
- insulin-like growth factor 2 differentially regulated the intracellular translocation of Bcl-2
- Bcl-2 expression in breast tumors is associated with improved outcome and steroid receptor positivity.
- Bcl-2 was better expressed in MCF-7 cells, while it was almost undetectable in T47D cells.
- Data show that DAP5 promotes cap-independent translation of Bcl-2 and CDK1 to facilitate cell survival during mitosis.
- The role of Bcl-2 in the sustained phosphorylation of c-Jun-N-terminal kinase mediating melanoma apoptosis induced by 2-acetyl furanonapthaquinone is reported.
- p53 was not associated with survival after radiotherapy in high-risk breast cancer, but BCL2 might be.
- Bcl-2 augmentation protected renal tubular epithelial cells from ischemia reperfusion injury, and subsequent interstitial injury by inhibiting tubular apoptosis
- Prolonged hypoxia-reoxygenation caused the most severe villous apoptotic changes, increased the expression of Bax and Bak mRNA and protein and reduced the expression of Bcl-2 mRNA.
- s-NITROSYLATION OF BLC2 AND FLIP PRECLUDES THEIR UBIQUINATION AND DEGRADATION, ACCENTUATING THEIR ANTI-APOPTOTIC EFFECT
- Compared to published adult DLBCL studies, pediatric DLBCL demonstrated increased c-Myc protein expression (84%)and decreased Bcl2 protein expression (28%)
- Apolipoprotein L1 is a novel Bcl-2 homology domain 3-only lipid-binding protein, induces autophagic cell death
- meta-analysis strongly supports the prognostic role of BCL2 in breast cancer & shows this effect is independent of lymph node status, tumour size & tumour grade as well as a range of other biological variables on multi-variate analysis [meta-analysis]
- Bcl-2 cannot be considered a predictive factor in colorectal adenocarcinoma.
- in patients with chronic myeloid leukemia, Antiapoptotic bcl-2(B-cell lymphoma protein 2) protein increased significantly with the progression of the disease
- BCL-2 was detected from week 12 to 17 and became undetectable thereafter in the developing human ovary.
- among gastrointestinal MALT lymphomas, t(14;18)-(IgH;Bcl-2) translocation clusters in hepatitis C-positive patients sustaining the role of HCV infection in the lymphoma development
- Results indicate that HBSP interacts with Bcl-2/Bcl-xl in vitro and induces apoptosis in HepG2 cells.
- Progression of neoplasia in the uterine cervix is accompanied by an increase of antiapoptotic protein, bcl-2 as well as cellular proliferation.
- Data show that the worm protein EGL-1 binds mammalian pro-survival proteins very poorly, but can be converted into a high-affinity ligand for Bcl-2 and Bcl-x(L) by mutation of the cysteine residue at position 62 within the BH3 domain.
- was no difference in the expression of EGFR, p185(erbB-2) or Bcl-2, or in nuclear accumulation of p53 in these IDC from pre- vs. post-menopausal women.
- Report correlation between expression of Bcl-2 and drug resistance in glioblastomas.
- Antiapoptotic activities of BCL2 correlate with vascular maturation and transcriptional modulation of endothelial cells.
- Bcl-2, binds to Beclin 1 during nonstarvation conditions and inhibits its autophagy function by phosphorylation of cellular Bcl-2 at residues T69, S70, and S87 of the nonstructured loop.
- Report relationship of Ki67, TP53, MDM-2 and BCL-2 expressions with WHO 1973 and WHO/ISUP grades, tumor category and overall patient survival in urothelial tumors of the bladder.
- Methyl jasmonate suppressed the radiation-induced Bcl-2 expression and enhanced the radiation sensitivity of human prostate cancer cells.
- Sometimes expressed in dysmorphic neurons in focal cortical dysplasia type II.
- A novel fusion 5'AFF3/3'BCL2 originated from a t(2;18)(q11.2;q21.33) translocation in follicular lymphoma.
- We show that Bcl-2 can position on the outer cell surface membrane of B cells from patients with chronic lymphocytic leukemia (B-CLL) and certain other leukemias that do not classically possess the chromosomal breakpoint t(14;18).
- Bcl-2 expressions decreased immediately after marathon running, but increased in the 24 h later.
- GATA-4 influences granulosa cell fate by transactivating Bcl-2.
- The interaction of Bcl-2 with IP3Rs contributes to the regulation of proapoptotic Ca2+ signals by Bcl-2.
- Data show that caspase-8 participates in an anoikis-inducing process in MG-63 cells at an early time, and overexpression of Bcl-2 blocks activation of caspase-8 making MG-63 cells anoikis resistant.
- There is a strong correlation between Bcl-2 levels and resistance to Fas-mediated apoptosis.
- The survival-promoting effect of CXCL12 was mediated by the up-regulation of Bcl-2 protein expression and the concomitant down-regulation of Bax protein expression
- Oct-2 and its cofactor Bob-1 have an important function in mediating the IgH enhancer-bcl-2 promoter region interactions
- Data show that overexpression of anti-apoptotic Bcl-2 significantly increases the level of endogenous reduced glutathione, thus presrving cytoskeletal stability after metabolic stress in cells with defective respiratory complex I.
- expression & distribution of Bax & Bcl-2 molecules in term, pre-term & post-term placentas; Bax/Bcl-2 ratio was higher in both pre-term & post-term placental samples compared with term placentas
- Describe bcl-2 expression in developing pituitary gland.
- identifies the interaction sites of Bcl-2 and its homologues with ASPP2
- Aberration tends to have an adverse effect on survival of adult diffuse large B-cell lymphoma patients.
- These data indicate that, in cell culture models, autophagy occurs but is not required for entrance into quiescence or for the G(0) function of BCL-2 or BCL-x(L).
- A direct relation between the rise of tumoral proliferation index expressions of Bcl-2 and progression of the disease.
- A speculative model for understanding the interrelationship between autophagy and apoptosis regulated by JNK1-mediated Bcl-2 phosphorylation was proposed.
- Higher expression of BCL2 is associated with minimal residual disease.
- Immunohistochemistry using antibodies to determine the protein expression of Fas, Fas-L, Bax, Bcl-2, p53 and c-Myc in skin of venous ulcer patients.
- BCL2 and BCL-xL facilitation of G0 quiescence requires BAX, BAK, and p27 phosphorylation by Mirk
- Report the identification of a Nur77-derived Bcl-2-converting peptide with 9 amino acids (NuBCP-9) and its enantiomer, which induce apoptosis of cancer cells in vitro and in animals.
- slow growth of BCL2 overexpressing immortalized breast cell line, with expression of CDC25A and CDC42 protein.
- BCL2 or BCL3 are recurrent translocation partners of the IGH locus in cHL (classical Hodgkin lymphomas).
- microsatellite instability Colorectal cancer patients with low Bcl-2 and hMLH1 and hMSH2 demonstrate a significantly shorter disease-free survival.
- PKR regulates B56(alpha)-mediated BCL2 phosphatase activity in acute lymphoblastic leukemia-derived REH cells.
- The resistance of E-cadherin over-expressing cells to staurosporine may due to the up-regulation of Bcl-2/Bax ratio. When E-cadherin interference plasmids were transfected into MCF-7 cells, Bcl-2 expression was down-regulated.
- No significant association of bcl-2 expression with either overall survival or disease free survival was found in women with breast cancer.
- Bcl-2 and bcl-xL have roles in cell death rates in transitional cell carcinoma cell lines
- Serum bcl-2 was significantly higher in patients with ovarian cancer.
- Bcl-2 can regulate tumoral angiogenesis and lymphangiogenesis in human prostate cancer cells.
- Trends suggested down-modulation of cyclooxygenase-2 and Ki-67 in some tissues, increased pAKT-Ser473 expression, and an inverse relationship between PGE(2) and BCL2 expression.
- Bcl-2 negative germinal centre patients had the most favourable prognosis among patients with diffuse large B cell lymphoma that received R-CHOP