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Validated All-in-One™ qPCR Primer for TNFSF10(NM_003810.3) Search again
Product ID:
HQP114978
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
APO2L, Apo-2L, CD253, TANCR, TL2, TNLG6A, TRAIL
Gene Description:
TNF superfamily member 10
Target Gene Accession:
NM_003810.3(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.
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
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein preferentially induces apoptosis in transformed and tumor cells, but does not appear to kill normal cells although it is expressed at a significant level in most normal tissues. This protein binds to several members of TNF receptor superfamily including TNFRSF10A/TRAILR1, TNFRSF10B/TRAILR2, TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4, and possibly also to TNFRSF11B/OPG. The activity of this protein may be modulated by binding to the decoy receptors TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4, and TNFRSF11B/OPG that cannot induce apoptosis. The binding of this protein to its receptors has been shown to trigger the activation of MAPK8/JNK, caspase 8, and caspase 3. [provided by RefSeq].
Gene References into function
- crystal structure at 2.2 A resolution of a complex between TRAIL and the extracellular region of DR5
- Apo2 ligand mRNA levels increase following irradiation of human T lineage-derived tumor cells. Recombinant soluble Apo2L enhanced the lethality of therapeutic doses of irradiation, indicating their possible use in combination for clinical therapy.
- The Apo2L gene spans ~ 20 kb and is composed of 5 exons. The 1.2-kb Apo2L promoter region upstream of the translation initiation codon was cloned, its transcription start site defined, and several putative transcription factor binding sites identified.
- TNF-related apoptosis-inducing ligand (TRAIL) enhances T cell proliferation following T cell receptor engagement and signals the augmentation of IFN-gamma secretion via a p38 mitogen-activated protein kinase-dependent pathway.
- Interferon-alpha and -beta, but not -gamma, induce apoptosis through Apo2 ligand transcriptional induction in multiple myeloma tumor cells and freshly derived primary cells.
- Differential secretion of APO2 ligand microvesicles during activation-induced death of T cells
- Up-regulation in highly malignant multiple myeloma plasma cells negatively regulates erythroblast maturation; a major pathogenetic mechanism of anemia in multiple myeloma.
- TNF-related apoptosis-inducing ligand (TRAIL) is not constitutively expressed in the human brain, whereas both apoptosis-mediating and apoptosis-blocking TRAIL receptors are found on neurons, astrocytes, and oligodendrocytes
- TRAIL/Apo2L-induced apoptosis is mediated by ROS-activated p38 MAP kinase followed by caspase activation in HeLa cells.
- signaling pathway and intracellular regulation of TRAIL-induced apoptosis in multiple myeloma cells
- Results suggest that IFN-gamma facilitates TRAIL-induced activation of mitochondria-regulated as well as mitochondria-independent apoptotic pathways in breast tumour cells.
- An inducible pathway for degradation of FLIP protein sensitizes tumor cells to TRAIL-induced apoptosis
- Histone deacetylase inhibitors sensitize human colonic adenocarcinoma cell lines to TNF-related apoptosis inducing ligand-mediated apoptosis.
- Apo-2L-induced processing of caspase-3,caspase-8, and Bid is significantly increased by overexpression of Smac/DIABLO.
- Although it does not contribute to mechanisms of peripheral T cell tolerance such as clonal anergy or deletion by apoptosis, TRAIL can directly inhibit activation of human T cells via blockade of calcium influx.
- XAF1 augments TRAIL-induced apoptosis
- Stimulation of the mitogen-activated protein kinase pathway antagonizes TRAIL-induced apoptosis downstream of BID cleavage in human breast cancer MCF-7 cells.
- TRAIL induced translocation of Bax after cleavage of Bid in parental cells but not mitochondrial-DNA-deficient cells.
- APO2L/TRAIL, specifically induced by autologous tumor and up-regulated by IFN-alpha, is a key mediator of tumor-specific CD4+ cytotoxic T lymphocyte-mediated cell death.
- TRAIL/Apo2L in combination with interferon-beta synergistically induces apoptosis and inhibits melanoma cell proliferation in vitro, at least in part by cleavage of the X-linked inhibitor of apoptosis (XIAP).
- Data show that transfer of the gene encoding Smac sensitized tumor and malignant glioma cells for apoptosis, and that Smac peptides enhanced the antitumor activity of Apo-2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
- TRAIL gene expression regulation by PI3 kinase, Akt and GSK-3 in tumor cells
- Caspase-10 is recruited to and activated at the native TRAIL death-inducing signalling complex in a FADD-dependent manner.
- TRAIL is a direct target of FKHRL1
- induces apoptosis independently of the mitochondrial apoptosis mediator DAP3
- osteoblasts are resistant to Apo2L/TRAIL-mediated apoptosis
- These results provide new insights into the mechanisms of bile acid cytotoxicity and the proapoptotic effects of cFLIP phosphorylation in TRAIL signaling.
- The human papillomavirus type 16 E5 protein impairs TRAIL- and FasL-mediated apoptosis in HaCaT cells by different mechanisms.
- Plasma cells synthesize TRAIL and are subject to TRAIL-mediated apoptosis, which correlates with inactivation of the CD40-NF-kappa B survival pathway.
- Enhanced expression of TRAIL promotes peripheral blood eosinophil survival in the airways of allergic asthmatics following segmental antigen challenge.
- T cells from systemic lupus erythematosus patients kill autologous monocytes through apoptotic pathways involving the ligand TRAIL.
- Trail protein sensitivity and cell cycle phase; TRAIL preferentially induces apoptosis in tumor cells over normal cells.
- soluble TRAIL in the HBV infected people may participate in the liver damage
- The apoptosis-inducing TRAIL gene caused significant changes in the biomechanics properties of Jurkat cells.
- NF-kappaB prevents TRAIL-induced apoptosis in human hepatoma through a TRAIL-activated TRAF2-NIK-IKK pathway.
- TRAIL death pathway is present and can function in human islet beta cells.
- TRAIL protein binds and induces oligomerization of its cell-membrane death receptors (DR4 and DR5). These trigger the activity of CASP8 and apoptosis through DISC.
- The susceptibility of neutrophils to TRAIL-mediated apoptosis suggests a role for TRAIL in the regulation of inflammation and may provide a mechanism for clearance of neutrophils from sites of inflammation.
- Localization of TRAIL/TRAILR in fetal pancreas.
- c-FLIP(L) and c-FLIP(S) potently control TRAIL responses, both by distinct regulatory features, and further imply that the differentiation state of malignant cells determines their sensitivity to death receptor signals.
- TRAIL is the main effector molecule responsible for the in vitro tumoricidal activity of Newcastle disease virus-stimulated human monocytes.
- high expression of this protein is associated with favorable ovarian cancer survival
- Akt1 may be an important regulator of TRAIL sensitivity in HL60 cells through the activation of NF-kappaB and up-regulation of cFLIP(L) synthesis
- loss of expression of pro-apoptotic proteins (Bax, Bak and Bcl-Xs) in Burkitt's lymphomas resistant to Fas did not compromise sensitivity to TRAIL.
- sensitization hepatoma cells to TRAIL induced apoptosis through DR5 upregulation and NF-kappa B inactivation is sensitized by interferon-alpha
- activation of JNK is required for sensitization of PC3 cells to TRAIL-induced apoptosis by translation inhibitors in cells that are otherwise TRAIL-resistant.
- TRAIL and JNK1 combine with DNA damage and mediate signals independent of p53 leading to apoptosis
- results suggest involvement in the induction of neuronal apoptosis in HIV-1 infected brain
- bystander effect of the TRAIL gene is mainly mediated by membrane-bound TRAIL on the surface of transduced cells
- TRAIL signaling pathway circumvents caspase-8 activation of Bid upstream of the mitochondria; TRAIL acts in mitochondria via a mechanism that may involve components of the sphingomyelin cycle.
- produced by Tat protein-stimulated monocytes and provides a mechanism by which HIV infection can destroy uninfected CD4-positive t-lymphocytes
- This review focuses on the apoptosis signaling pathways stimulated by Apo2L/TRAIL, summarize what is known to date about the physiological role of this cell death ligand and the potential for its application to cancer therapy.
- likely to be involved in chronic pancreatitis; pancreatic stellate cells may directly contribute to acinar regression by inducing apoptosis of parenchymal cells in a TRAIL-dependent manner
- The data describe the biological significance of TRAIL-mediated activation of NF-kappaB in cancer cells resistant to TRAIL-mediated apoptosis: TRAIL leads to an increase in tumor cell count by a prosurvival and possibly mitogenic function.
- beside its potent pro-apoptotic role, leucine zipper-TRAIL leads to pro-inflammatory responses that are mainly mediated by TRAIL receptor 1 in HaCaT keratinocytes.
- Recombinant human TRAIL can both injure and activate human endothelial cells in vitro and in vivo; compared with TNF, TRAIL is potent at causing injury but less effective at stimulating inflammation.
- Apo2L/TRAIL exhibits enhanced apoptotic activity in prostate carcinoma cells cultured in vitro and xenografted tumors in vivo through differential regulation of Bcl-2 family proteins when combined with the topoisomerase I inhibitor CPT-11 (irinotecan)
- Respiratory syncytial virus-infected cells in vivo are susceptible to killing through the TRAIL pathway.
- osteoprotegerin is abundant in gestational membranes and, in concert with TRAIL decoy receptors, may protect resident cells of membranes against the proapoptotic effects of TRAIL during pregnancy
- results show that protein kinase C activation specifically inhibits the recruitment of TRAIL receptors 1 and 2 complexes, thereby modulating tumor necrosis-related apoptosis-inducing ligand(TRAIL)-induced apoptosis
- TRAIL-induced apoptosis is enhanced by level of HBV replication in human hepatocytes, in part, by HBV-encoded X antigen-dependent upregulation of TRAIL-R1/DR4.
- Apoptosis induced by the combination of Apo2L/TRAIL and PG490 warrants evaluation as a treatment for lung cancer
- biologic activity of on human erythropoiesis
- TRAIL-induced apoptosis of glioma tumors in vivo were studied by real-time imaging.
- Cocotreatment with TRAIL/Apo2L and VP16 provides an attractive approach for selective killing of tumour cells while leaving unaffected normal cells.
- Our data suggest that Akt is an endogenous inhibitor during TRAIL-mediated synovial cell apoptotic pathway.
- sensitization to TRAIL requires p53
- Bak is a regulatory molecule involved in IFNgamma-facilitated TRAIL-mediated apoptosis in thyroid cancer cells
- TRAIL activates a caspase 9/7-dependent pathway in caspase 8/10-defective tumor cell lines
- TRAIL appears to cause apoptosis in dividing, but not differentiating keratinocytes, while internucleosomal DNA fragmentation does not take place.
- MG132 upregulates death receptor-5 and cooperates with APO2L to induce apoptosis in Bax-proficient and -deficient cells.
- Our data suggest a cross-talk between HDAC inhibition and TRAIL that results in modulation of expression of specific apoptotic mediators.
- IFNalpha stimulates the expression of high levels of TRAIL mRNA and the release of elevated amounts of a soluble bioactive form of TRAIL (sTRAIL) in both human neutrophils and monocytes
- Results suggest that human placenta may not only produce TRAIL but also be a TRAIL target organ, and that the TRAIL/TRAIL receptor system could take part in the homeostasis of placenta during gestation.
- Localization of tumour necrosis factor-alpha-related apoptosis-inducing ligand in adult human testes.
- TRAIL expression was down regulated during liver regeneration in organ donors
- Cell-cell-associated and secreted TRAIL contribute to the triggering of Ewing cell apoptosis induced by IFN gamma alone or combinaed with TNF.
- Glucose deprivation enhances TRAIL-induced apoptotic death as well as caspase activation (caspase-3, -9, and -8) in human prostate adenocarcinoma
- OPG blocks endothelial cell apoptosis through binding tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and preventing its interaction with death-inducing TRAIL-receptors.
- Interferon/cytokine combinations are able to induce TRAIL gene expression and TRAIL protein in Ewing tumor cells.
- TRAIL expression and secretion were nalyzed in melanoma cells in culture. The secretion was associated with microvesicles upon melanoma activation with phytohemagglutinins or alpha-MSH.
- TRAIL is present in the brain of Alzheimer's disease patients but absent in the brain of normal patients. TRAIL was localized in AD affected regions, such as cerebral cortex, often in the proximity of Congo-red-positive amyloid plaques.
- Low-dose UV-radiation sensitizes keratinocytes to TRAIL-induced apoptosis.
- 8-Cloroadenosine can promote TRAIL killing activity in a hepatoma cell line in a dose- and time-dependent manner in vitro.
- once activated the major cytotoxic effector cells are potentially sensitive to TRAIL but are physiologically protected from its apoptotic action by intracellular level of c-FLIP
- a novel TRAIL-mediated tumor suppressor activity of interferon regulatory factor 1 and suggest a mechanistic basis for the synergistic antitumor activities of certain retinoids and interferons
- TRAIL can induce apoptosis of DR4/DR5-expressing cells and its receptors may participate in renal graft rejection.
- TRAIL may play an unexpected role in promoting angiogenesis in tumor angiogenesis.
- endotoxin increases sTRAIL where the p38 MAP kinase signaling pathway is involved
- Infiltrating lymphocytes were isolated from H pylori-infected gastric mucosa, and expression of TRAIL in T cells was analyzed by flow cytometry.
- New antitumor activity of parthenolide, which can be exploited to reverse resistance of breast cancer cells to TRAIL.
- Enhanced apoptosis adjacent to vascular calcification and concurrent expression of regulators of apoptosis and osteoclastic differentiation, TNF-related apoptosis-inducing ligand and OPG. May be involved in pathogenesis of vascular calcification.
- results highlight that MM T cells support OC formation and survival, possibly involving OPG/TRAIL interaction and unbalanced OC expression of TRAIL death and decoy receptors
- TRAIL-induced cell death is magnified by all-trans retinoic acid treatment, independently of telomerase activity on telomeres
- CD40-activated CLL cells also express DR5, a receptor for tumor-necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) that is expressed by CD4+ T-cells
- Triggering triggering the mitochondrial pathway by betulinic acid may enhance TRAIL-based therapy in cancer.
- TRAIL plays important roles in interferon-induced apoptosis.
- cFLIP(L) is not only a central antiapoptotic modulator of TRAIL-mediated apoptosis but also an inhibitor of TRAIL-induced NF-kappaB activation and subsequent proinflammatory target gene expression
- The bility of decoy receptor 3 to promote TRAIL-triggered death may be used to potentiate TRAIL efficacy during treatment tumors overexpressing DcR3.
- TRAIL effects on mitochondrial NF-kappaB-DNA binding
- TRAIL can induce apoptosis in premalignant cells
- IFN-gamma enhances TRAIL-induced apoptosis through IRF-1
- The DR4-selective Apo2L/TRAIL variants examined in this study showed a markedly reduced ability to trigger apoptosis, whereas the DR5-selective variants had minimally decreased or slightly increased apoptosis-inducing activity
- Rottlerin contribute to amplification of caspase cascades, thereby overcoming resistance of glioma cells to TRAIL-mediated apoptosis.
- TRAIL expression was mediated by increased transcriptional activity of the TRAIL promoter, suggesting lineage-specific regulation of TRAIL during megakaryocyte differentiation
- Fas and TRAIL play an important role in the H. pylori-mediated apoptosis of gastric epithelial cells.
- Amiloride enhances TRAIL-induced cytotoxicity by inhibiting phosphorylation of the PI 3-Kinase-Akt pathway-associated kinases and phosphatases.
- G(1) cell cycle arrest sensitizes breast cancer cells to TRAIL at least in part by reducing levels of the anti-apoptotic protein survivin: ectopic expression of survivin partially suppresses apoptosis induced by TRAIL
- These data suggest that amiloride sensitizes both tumor cells to TRAIL-induced apoptosis by promoting Akt dephosphorylation and caspase-8 activation via the intracellular acidification.
- Bid mediates apoptotic synergy between TRAIL and DNA damage
- DAP kinase is involved in TRAIL-mediated cell apoptosis and a demethylating agent may have a role in enhancing TRAIL-mediated apoptosis in some NSCLC cells by reactivation of DAP kinase
- removal of N-terminal domains of Bid by caspase-8 and Mcl-1 by caspase-3 enables the maximal mitochondrial perturbation that potentiates TRAIL-induced apoptosis
- expression induced by Tax protein through the NF-kB pathway in HTLV-1 infected T-cell lines and adult T cell leukemia cells
- Supernatants from T cell blasts, pulse-stimulated with phytohemagglutinin contained TRAIL expressed on microvesicles .
- in patients infected with cagA+/vacAs1+ H. pylori strains, expression of TRAIL and TRAIL-R1 and -R2 was down-regulated; down-regulation may limit apoptosis of gastric epithelial cells & destruction of tissue and may enable H. pylori to maintain its niche
- Results suggest that the intracellular TRAIL mRNA expression in PBMC is up-regulated in MCNS patients during the nephrosis phase.
- TRAIL has a role in the anemia of myelodysplastic syndromes
- Casein kinase II plays a critical antiapoptotic role by conferring resistance to TRAIL in colonic carcinoma.
- RAS-MEK-ERK1/2 signaling pathway can sensitize cells to TRAIL-induced apoptosis by up-regulating DR4 and DR5
- c-FLIP(L) functions primarily as an inhibitor of death receptor-mediated apoptosis through TRAIL and caspase-8 activation
- Bik and Bim have roles in bortezomib sensitization of cells to killing by death receptor ligand TRAIL
- apoptosis of glioma cells induced by TRAIL is protected from by protein kinase C delta
- Dengue virus infection promotes apoptosis in hepatic cells partly through the induction of Apo2L/TRAIL expression
- hypoxia or low glucose-augmented TRAIL cytotoxicity is mediated through the mitochondria-independent or -dependent pathway
- roles for Bax and Bak in linking the TRAIL death receptor pathway to the mitochondrial apoptosis signaling cascade upon DNA damage by ionizing radiation.
- TRAIL expressed on the surface of hepatocellular carcinoma cells by cytokines or cytostatic drugs might contribute to an alternative mechanism that enables tumors to evade immune surveillance by inducing apoptosis of activated human lymphocytes
- data suggests a role of TRAIL as a regulator of megakaryocytopoiesis
- APO2L/TRAIL plays a role in the regulation of human T cell activation.
- TRAIL is aberrantly expressed in mononuclear leukocytes from patients with B chronic lymphocytic leukemia.
- TRAIL-R4 but not TRAIL-R3 is the decoy receptor which appeared to influence TRAIL sensitivity in breast cancer cells
- We identified the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as a mediator of TGF-beta-induced apoptosis in hepatoma cells.
- Upregulaationof TRAIL expression may be induced by virus antigen and inflammatory cytokine IFN-gamma in chronic hepatitis B.
- TRAIL does not seem to influence leukocyte and platelet production but has an important relationship to erythropoiesis in healthy adults.
- the effects of TRAIL on apoptosis are associated with changes in mitochondrial functions and expressions of cell cycle regulatory genes in multiple myeloma
- Chemotherapy-resistant tumor cells can be sensitized for TRAIL-induced apoptosis at the death inducing signaing complex by proteasome inhibitor treatment.
- The results indicate that the presence of the CC genotype at position 1595 in exon 5 represents a higher risk of MS.
- Pigs expressing biologically active human TRAIL will be used for future xenotransplantation experiments to modulate primate anti-pig cellular immune responses.
- TRAIL expression from a viral vector activated the Caspase-3 enzymatic capacity, and hepatocellular carcinoma cells were sensitive to TRAIL.
- Blocking the proteasome may be a way to sensitize hepatcellular carcinoma cells to TRAIL.
- TRAIL promotes cell migration and invasion via a NF-kappaB-dependent pathway in human cholangiocarcinoma cell lines, an observation that has a potential negative implication for TRAIL in cancer therapy.
- HIV-1 induces TRAIL expression on primary CD4+ T cells.
- description of TRAIL (CD253) [review]
- TRAIL receptor 2 is highly expressed on human NPCs derived from fetal cortex, yet TRAIL induces only minimal levels of apoptosis in neural progenitor cells.
- studies suggested that acetylsalicylic acid -promoted Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) cytotoxicity is mediated through down-regulating BCL-2
- jun NH2-terminal kinase pathway is critically involved in human oligodendrocyte death induced by Tumor necrosis-related apoptosis-inducing ligand
- Apo2L/TRAIL, combined with the BH3 mimetic, Bcl-xL inhibitor BH3I-2', induced apoptosis synergistically in prostate cancer cells through activation of Caspase-8 and Bid, resulting in activation of Caspase-3 and PARP cleavage.
- TRAIL apoptotic pathway plays an important role in hepatic cell death during viral infection.
- Nocodazole treatment inhibited TRAIL-increased NOS activity, indicating that, on cultured HUVEC, TRAIL ability to affect NO production by regulating eNOS sub-cellular distribution is mediated by cytoskeleton and Golgi complex modifications.
- these data suggest that TRAIL might act as a paracrine trophic cytokine on intestinal epithelium, promoting intestinal cell differentiation
- systemic upregulation of TRAIL in dilated cardiomyopathy patients and concomitant local upregulation of osteoprotegerin in the myocardium
- In an immortalized human KC cell line (HaCaT cells with both p53 alleles mutated) enhanced apoptotic susceptibility to interferon exposure was also observed and the mechanism for this enhanced apoptosis involved induction of TRAIL
- Apo2L/TRAIL has a role in apoptosis [review]
- bortezomib (Velcade) sensitizes some human tumor cells to Apo2L/TRAIL-mediated apoptosis
- This study identified primary osteoblasts as additional potential targets for myeloma cell-mediated suppression which was partly dependent on the death receptor ligand TRAIL.
- Retinoic acid induction of the TRAIL pathway is also operative in leukemia cells
- Results suggest that TRAIL-mediated mast cell (MC) survival in vivo and, potentially, for down-regulating MC hyperplasia in pathologic conditions
- Gene expression incresed in multiple sclerosis patients treated with interferon-beta.
- Mcl-1 may serve as a direct substrate for TRAIL-activated caspases implying the existence of a novel TRAIL/caspase-8/Mcl-1/Bim communication mechanism between the extrinsic and the intrinsic apoptotic pathways
- complex pattern of synergistic interaction between TRAIL and cisplatin is related to the cleavage of CASP8 and FADD-like apoptosis regulating protein
- significant up-regulation of TRAIL was detected in monocyte-derived macrophages infected with avian influenza viruses A/Hong Kong/483/97 (H5N1/97) or its precursor, A/Quail/Hong Kong/G1/97
- Review. Neutrophils produce in a finely regulated manner TRAIL, a TNF superfamily member involved in apoptosis, tumor cell killing and autoimmunity.
- Decitabine and IFN-gamma at relatively low individual concentrations cooperate to restore caspase-8 expression and sensitize resistant neuroblastoma and medulloblastoma cells to TRAIL-induced apoptosis.
- The combined delivery of CYLD and TRAIL may be a new useful strategy for hepatocellular carcinoma or other tumor cells with enhanced NF-kappaB activity.
- Both addition of IGFBP-3 protein to cell cultures or enforced expression of IGFBP-3 in the HT29 colon carcinoma cell line inhibited nuclear factor kappa B (NF-kappaB) activation in response to the induction of apoptosis by TRAIL.
- DR5-selective TRAIL variants do not induce apoptosis in DR4-responsive cell lines but show a large increase in biological activity in DR5-responsive cancer cell lines.
- TRAIL strongly induces the expression of the proinflammatory cytokines interleukin-8 and monocyte chemoattractant protein 1 and enhances the invasion of apoptosis-resistant pancreatic ductal adenocarcinoma cells in vitro
- is a mediator of cell death that preferentially targets cancer cells
- IFN-gamma modulates the expression of TRAIL in astrocytes, which may enhance cytotoxic sensitivity of infiltrating immune cells or brain cells other than astrocytes during inflammation of brain
- Apo2L/TRAIL has a role in valproic acid-induced cytotoxicity in cultured thoracic cancer cells through mitochondria-dependent caspase activation
- Persistence of osteoclastogenesis can be related to the formation of the osteoprogerin/TRAIL complex.
- TRAIL has a role in inducing apoptosis in human colorectal adenoma
- TRAIL induces apoptotic cell death in neuroblastoma and survivin inhibits TRAIL induced apoptosis. Neuroblastoma cell sensitivity to TRAIL is governed by the ratio of TRAIL-R to survivin expression.
- Preferentially provokes apoptosis of HIV-1-infected monocyte-derived macrophages, by a mechanism reliant upon the inhibition of Akt-1 phosphorylation.
- upregulation of TRAIL in astroglial cells may abrogate immune cell effector functions
- TRAIL down-regulation of Ste20-related proline-alanine-rich kinase is an important event that enhances its apoptotic effects
- Flavopiridol sensitizes breast cancer cells to TRAIL-induced apoptosis by facilitating early events in the apoptotic pathway.
- photochemically mediated delivery of TRAIL allows a selective enhancement in cell killing in a colorectal cancer cell line.
- In the present study, we observed strong effects of sodium arsenite treatment on upregulation of TRAIL-mediated apoptosis in human and mouse melanomas.
- a recombinant form of the extracellular domain of the TRAIL (sTRAIL) was expressed in Escherichia coli BL21(DE3) under the control of a T7 promoter. A rapid and simple on-column refolding procedure was developed.
- dissociation of Bad from Bcl-xL and an increase in the intracellular level of Bcl-xL are responsible for development of acquired TRAIL resistance
- Flavopiridol synergizes TRAIL cytotoxicity by downregulation of FLIP(L) and this synergistic effect is Bcl-2 family independent.
- Data show that histone deacetylase inhibition leads to decreased protein kinase casein kinase 2 activity, caspase-2 activation and partial cleavage of caspase-8 that sensitizes the tumor cell to TRAIL.
- These findings suggest that in tumors retaining functional p53 and expressing high levels of Hsp70, TRAIL may be an effective therapy.
- MADD has a role in the control of cancer cell survival/death as a negative regulator of caspase-8 and confers significant resistance to TRAIL-induced apoptosis
- The effect of hyperinsulinemia on TRAIL expression in diabetic and normal rats and in humans with type 2 diabetes mellitus is reported.
- HIV Tat protein increases Bcl-2 expression in monocytes which inhibited apoptosis induced by TRAIL.
- A mutant of p68 RNA helicase at the phosphorylation sites (Y593/595F) dramatically sensitizes TRAIL-resistant cells to TRAIL-induced apoptosis, suggesting a potential therapeutic strategy to overcome TRAIL resistance.
- GAL-3 mediates TRAIL signaling by regulating PTEN in human breast carcinoma cells
- Apo2L/TRAIL, in combination with low-dose CPT-11 or aphidicolin, induces apoptosis in human prostate cancer cells. Combinations with S-phase arrest-inducing drugs may represent promising avenues for its clinical development.
- findings suggest that TRAIL activates apoptosis pathway dependent on Bid, but largely independent of FADD and caspase-8, in U2OS cells
- Fluorocytosine together with TRAIL dramatically decreased tumor growth and eradicated a neuroblastoma tumor.
- Cutaneous T-cell lymphoma (CTCL) cell lines revealed pronounced resistance to death ligands (TRAIL and TNF-alpha) as compared to cell lines of T-cell acute lymphoblastic leukemia (T-ALL).
- 5-Aminoimidazole-4-carboxamide riboside sensitizes TRAIL- and TNF{alpha}-induced cytotoxicity in colon cancer cells through AMP-activated protein kinase signaling
- Data suggest that interferon-gamma sensitizes resistant Ewing's sarcoma cells to TRAIL-induced apoptosis by up-regulation of caspase-8 without altering chemosensitivity.
- Nitric oxide-mediated S-nitrosylation of GAPDH and subsequent nuclear translocation of GAPDH might function as a mediator of TNF-related apoptosis-inducing ligand (TRAIL) induced cell death in thyroid cancer cells.
- Wnt3A treatment significantly suppressed TRAIL-induced apoptosis in control hepatic stellate cells versus sFRP1 over-expressing cells.
- The potentiation of TRAIL-induced cell death could be implicated in lung cancer therapy and prevention
- We showed that DR5, upregulated by TRAIL, could be the mediator of TRAIL-induced OC apoptosis. intracellular pathway induced by TRAIL in OCs involves caspase-8 and Bid activation.
- ability of TRAIL to modify inflammatory responses and to reduce neuronal cell death in meningitis suggests that it may be used as a novel antiinflammatory agent in invasive infections
- analysis of certain carotenoids that sensitize cancer cells to TRAIL-induced apoptosis
- We demonstrated that TRAIL alters gene expression through mRNA splicing and may change proapoptotic potential in response to cytokine stimulation.
- IFNalpha induces TRAIL expression via a STAT-1/IRF-1-dependent mechanism in human bladder cancer cells
- RIP and c-FLIP-mediated assembly of the death-inducing signaling complex in nonrafts is a critical upstream event in TRAIL resistance
- increased expression of TRAIL mRNA in PBMC closely correlates with SLE activity and suggest an important role for TRAIL in the pathogenesis of SLE.
- TRAIL can trigger an apoptotic pathway that involves JNK-dependent activation of Bim, which in turn induces Bax-mediated permeabilization of lysosomes.
- VPA significantly increased sensitivity of leukemic cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and led to downregulation of c-FLIP (L) expression.
- These results establish that unlike HBx, MHBs(t) enhances TRAIL-induced hepatocyte apoptosis through a novel mechanism that involves ERK2.
- Data suggest that OPG can bind both to RANKL and TRAIL and that the affinity of OPG for these two ligands is of a similar order of magnitude.
- Variants of human TRAIL (hTRAIL) and human CD95L (hCD95L), encompassing the TNF homology domain (THD), interact with the corresponding receptors and stimulate CD95 and TRAILR2 signaling after cross-linking.
- the homotrimerization and apoptotic activity of zinc-free TRAIL is enhanced by a more rigid local structure around the zinc-binding region
- New link between death-receptor O-glycosylation and apoptotic signaling provides a potential predictive biomarkers for Apo2L/TRAIL-based cancer therapy.
- data provide a novel link between hypoxia, TRAIL and BRCA1, and suggest that this relationship may be especially relevant to the potential use of TRAIL as a chemotherapeutic agent
- c-Myc activates DR4 transcription through E-box DNA-response elements located in the DR4 promoter, thereby increasing the expression of cell-surface pro-apoptotic death receptors in TRAIL-resistant cell lines
- However, neither sTRAIL nor chemokine levels allowed prediction of one- and two-year clinical treatment response in 30 RRMS patients, prospectively followed by blinded investigators.
- Incubation in the presence of TRAIL enhanced the caspase-dependent and chymotrypsin-like-protease-dependent apoptotic cell death in A549 cells exposed to X rays.
- *matinib-resistant tumor cell lines undergo apoptosis after transfection with full-length TRAIL cDNA.
- This review focuses on recent advances in the understanding of TRAIL signal transduction and discusses the existing and future challenges of TRAIL-based cancer therapy development.
- These data suggest that TRAIL plays an important role in the antiviral response to dengue virus (DV) infection and is a candidate for antiviral interventions against DV.
- Activated protein C may provide cytoprotective activity by activating the ERK pathway, which upregulates EGR-1 thereby suppressing the expression of TRAIL by PAR-1/S1p1 dependent but EPCR independent mechanism.
- TRAIL may induce endothelial activation in concert with endothelial apoptosis.
- nuclear factor kappaB pathway inhibition blocks myeloma cell growth and induces apoptosis in strong synergy with TRAIL
- IFN-alpha produced after HIV-induced Toll-like receptor 7 stimulation was responsible for TRAIL expression and the down-regulation of both CXCR4 and CCR5 by IKpDC
- CK2 regulates endometrial carcinoma cell sensitivity to TRAIL and Fas by regulating FLIP levels.
- Human hepatoma cells mount an intact innate antiviral defense through induction of interferon, Trail, death receptor 4 and 5, and triggering apoptosis of infected cells.
- CDK4 is a modulator of TRAIL-induced apoptosis pathway
- cathepsin E plays a substantial role in host defense against tumor cells through TRAIL-dependent apoptosis and/or tumor-associated macrophage-mediated cytotoxicity
- 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
- TRAIL induced a slight, but consistent, decrease in viability for granulosa tumor cell lines, and inhibition of proteasome activity synergistically enhanced TRAIL-induced loss of viability.
- expression of TRAIL and its receptors in peripheral T-cells at both protein and mRNA levels are significantly increased in type 1 diabetic patients
- TRAIL is expressed throughout neutrophil development, resulting in a broad distribution among different granule subtypes.
- Ioniing radiation signaling in a lung tumor cell line is due to release of TRAIL-associatted nuclear translocation of PAR-4 protein.
- TRAIL may play an important role in atherosclerosis by regulating IGF1R expression in VSMC in an NF-kappaB-dependent manner.
- the role of triptolide as a sensitizer to TRAIL-induced apoptosis in part by independent modulation of XIAP expression and p53 signaling.
- Describe a novel p53 rescue compound that induces p53-dependent growth arrest and sensitises glioma cells to Apo2L/TRAIL-induced apoptosis.
- This paper demonstrates that CD1c-positive myeloid DCs, but not BDCA-4-positive plasmacytoid DCs, are able to kill different target cells mainly via tumour necrosis factor-related apoptosis-inducing ligand.
- The Wnt pathway substantially contributes to TRAIL-related neurotoxicity in SH-SY5Y human neuroblastoma cells.
- Soluble TRAIL does not impair the anti-osteoclastic activity of osteoprotegerin.
- These results establish that besides HBx, preS2 viral proteins are also involved in enhancing TRAIL-induced hepatocyte apoptosis.
- TRAIL-induced cell death could play an important role in the progression of human diabetic nephropathy
- primary SzS lymphocytes reveal frequent resistance to apoptosis induced by FasL and TRAIL
- Data suggest a role of caspase-3 and of a particular cleaved form of this caspase during the early signals of heat shock plus TRAIL-induced apoptosis.
- Data suggest that osteoprotegerin inhibits osteoclast apoptosis, at least in part, by binding and thus inhibiting endogenously produced TRAIL in human osteoclast cultures.
- TTP plasma-mediated apoptosis appears to involve IFNG-induced acceleration of c-FLIP degradation, sensitizing cells to TRAIL-mediated caspase-8 activation and cell death.
- Novel therapeutic approaches using TRAIL or agonistic TRAIL receptor antibodies in combination with proteasome inhibitors may represent a promising approach to reactivate apoptosis in therapy-resistant high-grade gliomas
- In Down Syndrome placentas, an inverse relationship between the expression levels of keratin-8 and TRAIL was observed.
- The results indicated that the expression levels of TRAIL mRNA, and serum sTRAIL were significantly elevated in ankylosing spondylitis (AS) patients.
- rpS6, especially in its unphosphorylated form, is a selective mediator of TRAIL-induced apoptosis
- P73 and caspase-cleaved p73 fragments localize to mitochondria and augment TRAIL-induced apoptosis
- Involvement of protective autophagy in TRAIL resistance of apoptosis-defective tumor cells
- both mTRAIL and sTRAIL might be involved in the development and progression of primary biliary cirrhosis and chronic hepatitis B in humans, but the mechanisms might be different
- ABT-737 augments TRAIL-induced cell killing by unsequestering Bim and Bak and enhancing a Bax conformational change induced by TRAIL.
- proteasome inhibitor NPI-0052 inhibits the transcription repressor Yin Yang 1 (YY1) which regulates TRAIL resistance and negatively regulates DR5 transcription.
- DJ-1 is specifically expressed in thyroid carcinomas and not in the normal thyroid; the protein modulates the response to TRAIL-mediated apoptosis in human neoplastic thyroid cells, at least partially through its antioxidant property
- TRAIL may increase the anticancer efficacy of microtubule-targeting drugs.
- single amino acid substitution of Asp at residue position 218 of TRAIL to His or Tyr was predicted to have a favorable effect on DR4 binding specificity
- Human T-cell blasts are not sensitive to FasL or Apo2L/TRAIL-induced apoptosis unless they get reactivated, but either of those ligands inhibits their growth in the absence of cell death due to cell cycle arrest.
- TRAIL-induced activation of PKC-delta mediates regulation of the phospholipid scramblase3-induced changes in cardiolipin.
- role of TRAIL in osteoclastogenesis; study demonstrated that recombinant TRAIL inhibits osteoclast formation, but only at relatively high concentrations
- The altered ability of neutrophils to secrete sTRAIL may have different implications for the immune response of patients with oral cavity cancer cells at different stages of disease.
- analysis of the signaling dynamics during apoptosis initiation via the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor pathway
- inhibition of TRAIL signaling works through interaction of CD73 with death receptor 5, as CD73 and death receptor 5 could be coimmunoprecipitated and were shown to be colocalized in the plasma membrane by confocal microscopy
- Cellular resistance to TRAIL could be developed through phosphorylation (activation) of Akt and phosphorylation (inactivation) of PTEN in acute lymphoblastic leukemia cells.
- FADD protein, human; Humans; MCL1 protein, human; Mutagenesis; NF-kappa B
- early clinical trial data suggest that rhApo2L/TRAIL is generally safe and provide preliminary evidence for potential antitumor activity
- These results reveal a new AP-1 site within the TRAIL promoter functionally involved in TGF-beta-induced TRAIL expression and apoptosis in hepatomas.
- TRAIL expression is induced on primary human innate and adaptive immune cells in response to cytokines produced during influenza infection and that TRAIL sensitivity is increased in influenza virus-infected cells
- Androgenic protection from TRAIL-induced apoptosis is via enhanced transcription of FLIP in prostate cancer cells. Loss of androgen-sensitivity in androgen-depletion-independent prostate cancer cells. Potential target for therapy of prostate cancer.
- major role of soluble TRAIL in protecting cornea and conjunctiva from tumor formation and/or invasion
- Induction of apoptosis by TRAIL results in suppression of hepatitis C virus (HCV)protein expression by a mechanism that may contribute to elimination of HCV-infected hepatocytes.
- five genes (TNFSF10/TRAIL, IL1RN, IFI27, GZMB, and CCR5) were upregulated and three genes (CLK1, TNFAIP3 and BTG1) were downregulated in at least three out of four subpopulations during acute GVHD.
- These results suggest that TRAIL has alternative biological functions in addition to its role in inducing apoptosis in human malignant astrocytoma cells.
- Overexpression of FLIP reduced TRAIL and TNF-alpha-induced apoptosis in ML-1 cells. However, while FLIPL completely abrogated apoptosis, FLIPS allowed for BID cleavage and caspase-3 activation.
- Src and ADAM-17-mediated shedding of transforming growth factor-alpha is a mechanism of acute resistance to TRAIL.
- TRAIL is expressed in the intestine and influences fibroblast survival.
- TRAIL death receptors (DR4 and DR5) undergo constitutive endocytosis in some breast cancer cells