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Validated All-in-One™ qPCR Primer for BCL2L1(NM_001191.3) Search again
Product ID:
HQP016237
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BCL-XL/S, BCL2L, BCLX, Bcl-X, PPP1R52
Gene Description:
BCL2 like 1
Target Gene Accession:
NM_001191.3(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.
Summary
The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The proteins encoded by this gene are located at the outer mitochondrial membrane, and have been shown to regulate outer mitochondrial membrane channel (VDAC) opening. VDAC regulates mitochondrial membrane potential, and thus controls the production of reactive oxygen species and release of cytochrome C by mitochondria, both of which are the potent inducers of cell apoptosis. Two alternatively spliced transcript variants, which encode distinct isoforms, have been reported. The longer isoform acts as an apoptotic inhibitor and the shorter form acts as an apoptotic activator. [provided by RefSeq].
Gene References into function
- Jak-Stat and PI 3-kinase activation pathways regulate the TPO-induced survival of megakaryocytic cells via Bcl-xL gene expression.
- gene expression level of beta-TUB, Bcl-XL, and GSTpi was closely correlated with the IC50 for docetaxel
- regulation of alternative splicing in lung adenocarcinoma cells by de novo ceramide
- 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
- Bcl-X(L) may regulate Bax translocation through modulation of protein phosphatase or kinase signaling.
- Bcl-xL prevents TRAIL-induced apoptosis by abrogating caspase activation and cleavage of BH3 interacting domain death agonist protein in acute myelogenous leukemia HL-60 cells.
- Mature dendritic cells are protected from Fas/CD95-mediated apoptosis by upregulation of Bcl-X(L).
- Erythrocyte survival is suppressed by a Bak-derived BH3 peptide that interacts with membrane-associated Bcl-X(L).
- increased expression associated with low levels of apoptosis in renal cell carcinoma; may have role in progression of cancer and treatment resistance
- selective expression of Bcl-xL may be involved in the difference in the susceptibility to cell death between immature dendritic cells and mature dendritic cells .
- Antisense strategy shows that Mcl-1 rather than Bcl-2 or Bcl-x(L) is an essential survival protein of human myeloma cells.
- In Parkinson's disease patients, Bcl-xL mRNA expression per dopaminergic neuron is almost double that of controls, an effect that may be mediated by a redistribution of Bcl-xL from the cytosol to the outer mitochondrial membrane.
- role in modulating HIV-1/monocyte-derived macrophage-induced neuronal apoptosis
- Bcl-XL protects BimEL-induced Bax conformational change and cytochrome C release.
- In addition, B cell lymphoma leukemia (Bcl)-x(L), an antiapoptotic regulator, was also highly expressed in macrophages from smokers compared with nonsmokers and subjects with asthma.
- 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 endothelial cell apoptosis, Bcl-xl level showed no significant in HUVECs stimulated with TNF-alpha alone or in combination with IFN-gamma.
- Data suggest that Bcl-xl has a biochemical function that is capable of partially rescuing loss of function mutations in S. cerevisiae.
- Bcl-xL is deamidated in the cellular response to DNA damage and leads to apoptosis resistance
- treatment with an antisense oligonucleotide (5'Bcl-x AS) shifts the splicing pattern of Bcl-x pre-mRNA from the anti-apoptotic variant, Bcl-xL, to the pro-apoptotic variant, Bcl-xS
- role in inhibiting diamide-induced SM hydrolysis and ceramide accumulation but not the decrease in intracellular GSH
- A very low mRNA level was indicated at bax, bcl-2 and bcl-xL in hepatocellular carcinoma tissues in contrast to normal liver.
- Mitochondrial targeting of Bcl-x(L) requires the COOH-terminal transmembrane (TM) domain flanked at both ends by at least two basic amino acids
- Bcl-xl over-expression does not confer protection against cell death in U937 cells.
- BCL-xL levels decreased when H202 was greater than 250 micro M.
- findings indicate that the levels of XIAP and Bcl-X(L) are regulated by distinct pathways during monocytic differentiation, and that upregulation of these proteins contributes to the increased longevity of cells in the monocytic lineage
- Bcl-x(L) is a key target mediating the anti-apoptotic effects of glucocorticoids during fibrosarcoma development
- a novel role in cell fate decisions /during hematopoietic differentiation/ beyond cell survival
- Bcl-2 may not play a physiological role in antagonizing apoptosis signals pertinent to BAD activation in prostate cancer cells
- Following UV treatment, Mcl-1 protein synthesis is blocked, the existing pool of Mcl-1 protein is rapidly degraded by the proteasome, and cytosolic Bcl-xL translocates to the mitochondria
- Human Bcl-xL is deamidated at asparagines 52 and 66 & the rate of deamidation is significantly lower in hepatocellular carcinomas than in normal liver. Tumor cells may gain apoptosis resistance & a survival advantage by suppressing Bcl-xL deamidation.
- Bcl-xl has a role in suppressing a p53 and Bax-dependent apoptotic pathway in colorectal cancer cells
- Overexpression of bcl-2 and bcl-xL leading to prolonged survival of mast cells may contribute to the pathogenesis of mastocytosis.
- bcl-xL directly binds to Apaf-1.
- bcl-xL gene overexpression is linked to short overall survival times in follicular lymphoma.
- retinoic acid-induced apoptotic signals were transduced via downregulation of Bcl-xL and the decrease in the mitochondrial membrane function leading to caspase-3 activation
- Overexpression of bcl-xl is associated with colonic neoplasms
- BCL-XL is induced during rapamycin-resistant proliferation of CD8+ T cells
- Bcl-XL has a role in preventing Bax activation at the mitochondrial membrane
- Bcl-x was associated with increased survival in thymic neoplasms. Bcl-x:Bax ratio was also associated with survival.
- Transgenic mice crrossed with c-MYC transgenic mice develop multiple myeloma.
- results show a pivotal role for Bcl-XL in ALK-mediated oncogenicity
- the role of Bcl-x(L) in apoptosis in cardiomyocytes and discuss the potential use of Bcl-x(L) as a cardioprotective therapy for cardiac diseases.
- Bcl-xL inhibits p53- but not apoptin-induced apoptosis in head and neck neoplasms
- BCL-XL binds to Siva-1 putative amphipathic helical region which sensitizes cells to UV radiation induced apoptosis
- Bcl-xL and E1B-19K proteins inhibit p53-induced irreversible growth arrest and senescence by preventing reactive oxygen species-dependent p38 activation
- show that the Bcl-x(L) interaction surface on p53 involves the same region that is used by the protein to contact DNA. The p53-binding site on Bcl-x(L) is also defined.
- Bcl-x(L)-anti-apoptotic signal pathway seems to prevent mitochondrial multiple conductance channel opening, cytochrome c release and caspase-3 like activity following 6-OHDA treatment in the human neuroblastoma cell line SH-SY5Y
- Reduced levels of Bcl-xL may play an important role in the increased sensitivity to apoptosis of HIV-specific CD8+ T cells.
- CD28-stimulated T cells actively secrete IL-8, and Bcl-xL up-regulation protects T cells from radiation-induced apoptosis
- Bcl-XL was higher in plaques than in normal white and gray matter in multiple sclerosis
- Data show that Bcl-x(L) in the cytosol forms homodimers, and that the C-terminal hydrophobic tails of two Bcl-x(L) molecules are involved in homodimer formation.
- 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.
- Bcl-xL in hepatocellular carcinoma specimens. Bcl-xL may be significant prognostic factor for disease progression in human hepatocellular carcinoma.
- p38 MAPK and Bcl-XL expression play critical roles in the survival of UVA-irradiated HaCaT cells
- The amphipathic alpha 6 helix fragment of Bcl-xL inserts in membranes as part of the alpha 5-alpha 6 hairpins in a model chimeric system, showing direct potentiality for this Bcl-xL fragment to acquire a membrane inserted state.
- Anti-apoptotic factors, Bcl-2 and Bcl-xL, were significantly decreased in epithelial cells under a hypoxic condition as assessed by Western blotting
- Infection with OmpA+ E. coli induces the expression of Bcl(XL), an antiapoptotic protein, both at the mRNA level as assessed by gene array analysis and at the protein level
- Bcl-XL expression is induced by HIV-1 Nef in macrophages in an extracellular signal-regulated kinase-dependent manner
- the conformation of the BAX alpha9-helix plays a significant role in BAX/BCL-xL interaction
- The role of Bcl-xL in megakaryocyte (MK) differentiation was studied using siRNA to block its expression in essential thrombocythemia, chronic myeloid leukemia, & polycythemia vera cells. It is down-regulated early in MK differentiation of MKs from ET.
- The BCLX pre-mRNA is splicing by extracellular factors and their distinct requirements for pre-mRNA elements.
- There may be a dominance expression of proapoptotic proteins in optic nerve axons in glaucoma.
- c-erb-B2 and Bcl-xl expression can be useful for the histopatologic diagnosis of Barrett exophagux and correct interpretation of dysplasia.
- T cell blasts surviving activation-induced cell deathare memory CD44 high cells with increased Bcl-xL expression.
- 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 and Bcl-xl family members.
- The results of the current study suggest that the potential ability of 15d-PGJ(2) in regulation of cell cycle and inhibition of Bcl-xL expression might be beneficial in the development of novel pharmacological agents for chondrosarcoma.
- HER-2 overexpression is highly correlated with the expression of the apoptosis-suppressing gene bck-xL.
- ABL-MYC retroviral infection only elicits bone marrow plasma cell tumors in mice that ectopically express Bcl-X(L) in their B- and plasma cells.
- Bcl-XL has a role in suppressing proliferation of 5-fluorouracil-resistant human colon cancer cells
- Expression of Cx26, Bax and Bcl-xL in colorectal cancers. Association of Cx26, Bax and Bcl-xLwith histological G2 grade of tumors.
- Rapamycin induces apoptosis of tumor cells by increasing the ratio of Bax to Bcl-xL through mechanisms dependent and independent of its mTOR inhibitory activity
- androgen receptor silencing has a role in apoptotic cell death by disrupting the Bcl-xL-mediated survival signal in human prostate cancer cell lines
- hnRNP F/H proteins have a positive role in the production of the proapoptotic regulator Bcl-x(S)
- role in sequestering proapoptotic Bak
- Therefore, Bcl-X(L), a promising therapeutic candidate for ischemia and neurodegenerative diseases, is only of partial efficacy in preventing the direct neurotoxicity of pneumolysin.
- A novel molecular mechanism of T-cell apoptosis that contributes to the SARS-CoV-induced lymphopenia observed in most SARS patients is reported.
- Data show that stimulation of PAR1 results in increased DNA binding of the NFkappaB p65 subunit, and that activation of PAR1 attenuates docetaxel induced apoptosis through the upregulation of Bcl-xL.
- Stable Bcl-XL siRNA transfectants have an increased spontaneous apoptosis.
- Natural cytotoxic T cell-defined reactivity is detected against Bcl-xL in peripheral blood leukocytes from patients with breat cancer and melanoma.
- PXR expression is required for Bcl-2 and Bcl-xL up-regulation upon PXR activators treatment in human and rat hepatocytes.
- Bcl-xL/Bax ratio can block the apoptotic response in TNFalpha-stimulated cells but allows cell death initiation when it is altered by a crosstalk between IFNgamma presensitization and TNFalpha induced signaling.
- data demonstrate that OX40 and Bcl-x(L) can control survival of primed CD8 T cells and provide new insights into both regulation of CD8 immunity and control of tumors
- bcl-xl-mediated changes in metabolic pathways of breast cancer cells were studied from survival in the blood stream to organ-specific metastasis.
- catalase has a critical role in CSF-independent survival of human macrophages via regulation of the expression of BCL-2 and BCL-XL
- Overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation.ROS generation and Bax expression were also lower.These results provide insights into a new strategy for gene therapy of radiation-induced immune injury.
- Results describe the structure of BCL-X(L) homodimers as a 3D-domain swapped dimer.
- Pim phosphorylation of Bad was also found to promote the 14-3-3 binding of Bad and block its association with Bcl-XL
- Bcl-xL may have a role in underexpression of transcriptional regulators in metastatic breast cancer
- Significant correlation between Bcl-x(L) expression and number of inflammatory cells in subsynovium of rheumatoid arthritis and osteoarthritis patients. May play role in extended survival of synoviocytes and inflammatory cells in rheumatoid synovium.
- Role of bcl-xl protein on indomethacin-induced cell division inhibition in chronic myelogenous leukemia cells.
- the interaction of BAD with membranes is tied to binding of 14-3-3 protein and activation and membrane translocation of Bcl-XL
- PUMA initiates apoptosis in part by dissociating Bax and Bcl-X(L), thereby promoting Bax multimerization and mitochondrial translocation
- ligand engagement of uPAR promotes cell survival by activating Bcl-xL transcription through the MEK/ERK- and phosphatidylinositol 3-kinase/Akt-dependent pathways
- these data suggest the solution to membrane conformational change is controlled by an electrostatic mechanism
- Bcl-xL is capable of giving rise to Epo-independent erythroid colony formation.
- p21-mediated cytoprotection against hyperoxia involves regulation of Bcl-XL and is uncoupled from its ability to inhibit proliferation
- Expression of Bcl-x was strongly expression in both reactive astrocytes and astrocytomas. Expression of Bcl-x is more focal in oligodendrogliomas, with staining of mainly intervening astrocytic processes.
- identified SAP155 as an RNA trans-acting factor that binds to CRCE 1, functions to regulate the alternative 5' splice site selection of Bcl-x pre-mRNA, and is required for ceramide to induce the activation of the Bcl-x(s) 5' splice site
- Bcl-xL expression contributes to androgen resistance and progression of prostate cancer
- Radiation therapy for squamous cell carcinoma of cervix results in increased apoptosis with the up-regulation of Bax, a proapoptotic protein, the down-regulation of Bcl-XL, an antiapoptotic protein, and no significant change in the levels of Bcl-2.
- 1-Bromopropane inhibits nuclear factor kappa B activation to reduce Bcl-xL expression in astrocytes.
- Results describe the specific modulation of apoptosis and Bcl-xL phosphorylation in yeast by distinct mammalian protein kinase C isoforms.
- Downregulation of Bcl-xL (but not Bcl-2, Bax, or Bid) connects cathepsin D and the mitochondrial pathway during glucosamine sulfate-induced apoptosis.
- Bcl-XL is approximately ten times more active than Bcl-2 in repressing apoptosis induced by doxorubicin.
- These results suggest a relevant role for STAT5 and Bcl-xL as apoptosis-regulatory proteins in the pathogenesis of lung cancer, and overexpression of both Neu and activated STAT3, could be related with the proliferation rate in lung carcinoma cells.
- distal Bcl-X 1B promoter plays a critical role in driving constitutive expression-mediated via Ets family proteins in malignant B cells
- dissociation of Bad from Bcl-xL and an increase in the intracellular level of Bcl-xL are responsible for development of acquired TRAIL resistance
- Bcl-xL can bind to one or two VDAC1 molecules forming heterodimers and heterotrimers.
- GX15-070 induced apoptosis in vitro in MCL cell lines and primary cells from patients with MCL by releasing Bak from Mcl-1 and Bcl-X(L).
- Thus EPO promotes survival of endothelial cells through PI3K-dependent Bcl-x(L)-induction and BIM regulation, as well as through a separate mechanism involving the ERK pathway.
- Data show that Bcl-x(L) expression is increased in the pulmonary artery undergoing chronic pulmonary vascular remodeling.
- overexpression of Bcl-x(L) or Bcl-2 in PC12 cells markedly suppressed brefeldin A-induced activation of caspases and resulting cell death.
- recombinant GM-CSF-Bcl-XL binds the GM-CSF receptor on human monocyte/macrophage cells and bone marrow progenitors inducing differentiation and allowing Bcl-XL entry into cells
- xL is coupled to the stabilization of a cell-cycle checkpoint induced by DNA damage, and this effect is genetically distinct from its function on apoptosis
- 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.
- Significant coexpression of GLUT-1, Bcl-xL, and Bax points to cooperation of all three regulatory proteins in elimination due to irreversible injury, adaptation to hypoxia, reduction of further damage, and survival of colorectal cancer cells.
- Antiapoptotic proteins Bcl-2 and Bcl-X(L) bind and suppress NALP1, reducing caspase-1 activation and interleukin-1beta (IL-1beta) production.
- severe acute respiratory syndrome coronavirus 7a protein induction of apoptosis is dependent on its interaction with the Bcl-XL protein
- Bcl-xl RNA silencing in transfected HepG2 cells induced apoptosis and increased sensitivity of cells to 5-FU and 10-hydroxycamptothecin.
- Bcl-XL siRNA contributes to an increase of cisplatin-induced cell death in non-small-cell lung cancer and sensitizes cells to cisplatin
- We speculate that the TM1 helices of Bax may serve as 'structural antagonists' for BH3-Bcl-xL interactions.
- preformed Bim(EL)/Mcl-1 and Bim(EL)/Bcl-x(L) complexes can be rapidly dissociated following activation of ERK1/2 by survival factors
- our results support the feasibility of using adenovirus-mediated RNA interference therapy targeting Bcl-XL against colon cancers and warrant further studies of its safety and efficacy.
- Bcl-x(L) plays an important role in human RPE cell survival under normal conditions and when cells are exposed to oxidative stress
- Bcl-X(L) conferred complete resistance to apoptosis induced by fas ligation in atherosclerotic carotid artery.
- The structure of Bcl-xL in complex with the Beclin-1 BH3 domain was determined at high resolution by NMR spectroscopy.
- results indicate an action of Bcl-X(L) modulating human neural stem cell differentiation
- Bcl-x(L) interacts with the DNA binding site of p53, but Bak does not interact with this site
- activation of HSF1 and stabilization of Bcl-X(L) mediate a protective response that may contribute significantly to the cellular biology of lipid peroxidation
- 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.
- a caspase-9 signaling cascade induces feedback disruption of the mitochondrion through cleavage of anti-apoptotic Bcl-2, Bcl-xL, and Mcl-1
- low dose doxorubicin-induced cell death through mitotic catastrophe may provide an alternative therapeutic strategy for Bcl-xL-overexpressing hepatoma cells
- The protein kinase C (PKC) inhibitor and apoptotic inducer staurosporine switches the production of Bcl-x towards the x(S) mRNA isoform in 293 cells.
- Shp2E76K induces cytokine-independent survival of TF-1 cells by a novel mechanism involving up-regulation of Bcl-XL through the Erk1/2 pathway.
- IGF1 promotes resistance to apoptosis in melanoma cells through an increased expression of BCL2, BCL-X(L), and survivin
- while bcl-2 proteins are not required for ceramide to form protein-permeable channels in mitochondrial outer membranes, both recombinant human Bcl-x(L) and CED-9 disassemble ceramide channels in the mitochondrial outer membranes from rat liver and yeast
- The Bcl-X(L) chimeras that are targeted to the mitochondria and the wild type Bcl-X(L) provided same protection against cell death under several death inducing conditions.
- androgen stimulates Bcl-xL expression via the androgen receptor and that increased Bcl-xL expression plays a versatile role in castration-resistant progression of prostate cancer
- overexpression of Bcl-xL led to decreased cellular proliferation
- BCL-xL is itself responsible for the pre-senescence decline in the ability of a genotoxic stress to induce apoptosis
- VEGF, hTERT and Bcl-xl have roles in laryngeal squamous carcinoma
- BI-1 and Bcl-X(L) operate downstream of or parallel to Bax/Bak
- the present study is the first report of a negative prognostic value for Bcl-XL in bilharzial squamous cell carcinoma of the urinary bladder
- insulin-like growth factor 2 differentially regulated the intracellular translocation of Bcl-X(L)
- Bcl-xL plays an important role in carcinogenesis of human colorectal carcinoma and is associated with malignant biological behaviors of human colorectal carcinoma.
- Bcl-xL protein levels were significantly higher in tissue samples from nonemphysematous smokers than in those from nonemphysematous nonsmokers
- SRp30c stimulates splicing to the downstream 5' splice site of Bcl-x(L), thereby attenuating the repressive effect of upstream U1 snRNP binding sit
- Results indicate that HBSP interacts with Bcl-2/Bcl-xl in vitro and induces apoptosis in HepG2 cells.
- 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.
- Show that Bcl-XL was down-regulated and Bcl-XS was up-regulated in topotecan-induced apoptosis in HepG2 cells.
- preoperative chemoradiotherapy (CRT) reduced Bcl-X(L) expression, and this decrease closely correlated with the prolonged survival of advanced esophageal cancer patients treated with preoperative CRT
- Therefore, over-expression of Bcl-x(L) has a potential for amelioration of SMA, and Bcl-x(L) may be another attractive therapeutic target other than survival motor neuron (SMN) protein for use in future drug screening for SMA.
- Expressed in most dysmorphic neurons in focal cortical dysplasia type II.
- Bcl-x(L) and, to a lower extent, Mcl-1, are important anti-apoptotic factors in colorectal carcinoma.
- Bcl-xL and UVRAG cause a monomer-dimer switch in Beclin1
- IL-3 up-regulates the expression of the antiapoptotic proteins cIAP2, Mcl-1, and Bcl-X(L) and induces a rapid and sustained de novo expression of the serine/threonine kinase Pim1 that closely correlates with cytokine-enhanced survival.
- JAK2 promotes cell survival by signaling through the Pim/BAD/BCL-xL pathway
- our results demonstrate the role of NF-kB as the mediator of bcl-xL-induced CXCL8 up-regulation in glioblastoma cells.
- Bcl-Xl deamidation and methylation has a role in protein isoaspartate methyltransferase prevention of apoptosis induced by oxidative stress in endothelial cells
- the anti-apoptotic protein Bcl-xL is phosphorylated by benzylisothiocyanate treatment
- BCL2 and BCL-xL facilitation of G0 quiescence requires BAX, BAK, and p27 phosphorylation by Mirk
- These observations suggest that Plk1 is a regulator of Bcl-x(L) phosphorylation and controls the anti-apoptotic activity of Bcl-x(L) during pironetin-induced apoptosis.
- Results show that 072RB, a novel BH3-Bim-derived peptide inhibitor of Bcl-XL, inhibits leukemic cell growth.
- Bcl-xL phosphorylation induced by microtubule inhibitors plays a key pro-apoptotic role at least in part by disabling the ability of Bcl-xL to bind Bax.
- Bcl-2 and bcl-xL have roles in cell death rates in transitional cell carcinoma cell lines