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Human TNFSF10 Protein expressed in Wheat germ - ABIN1323209
Borbone, De Rosa, Siciliano, Altucci, Croce, Fusco: Up-regulation of miR-146b and down-regulation of miR-200b contribute to the cytotoxic effect of histone deacetylase inhibitors on ras-transformed thyroid cells. in The Journal of clinical endocrinology and metabolism 2013
TRAIL protects against insulin resistance, NAFLD and vascular inflammation. Increasing TRAIL levels may be an attractive therapeutic strategy, to reduce features of diabetes, as well as liver and vascular injury, so commonly observed in individuals with NAFLD.
data strongly suggest that XIAP-mediated inhibition of final caspase-3 processing is the last and major hurdle in TRAIL-induced apoptosis in NCI-H460 cells, which can be overcome by Smac in a Bcl-2 level dependent manner.
Patients harboring the homozygous AA genotype of TRAIL SNPs rs1131568 and rs1131579 and the TT genotype of the TRAIL SNP rs1131580 had lower overall survival and higher rates of extrahepatic recurrence (EHR) than patients harboring the wild type or heterozygous genotypes.
TRAIL synergistically sensitized irradiation-induced apoptosis in glioblastoma stem-like cells by increasing DR5 expression and decreasing cFLIP expression.
Serum TRAIL concentrations are significantly reduced in patients with early preeclampsia.
The combination treatment with ILz:rhTRAIL and bortezomib was able to induce cell death in both TRAIL-susceptible and TRAIL-resistant cancer cells through the intracellular TRAIL signaling pathway. The efficiency of cell death was dependent on the properties of TRAIL under the environment provided by bortezomib. The combination treatment-induced cell death was not regulated by bortezomib-induced ER stress response or by a
A significant relationship was found between TRAIL polymorphisms and the susceptibility and severity of intervertebral disc degeneration in Han Chinese.
The authors demonstrate that BAP1 deubiquitinase activity and its association with ASXL1 to form the Polycomb repressive deubiquitinase complex (PR-DUB) impacts TRAIL sensitivity implicating transcriptional modulation as an underlying mechanism.
High expression level of Galectin-3 and low expression level of TRAIL were found to be positively correlated with the shorter median survival time and overall survival time.
Genes related to the extrinsic pathway of apoptosis including a receptor for TRAIL.
Nelfinavir induces ER stress in renal cancer cells and sensitizes them to TRAIL.
DR5-Cbl-b/c-Cbl-TRAF2 complex inhibited TRAIL-induced apoptosis by promoting TRAF2-mediated polyubiquitination of caspase-8 in gastric cancer cells.
We found that the combination of alpha-mangostin with TRAIL induced apoptosis of SAS cells through the mitochondrial pathway via activation of caspase-9 and -3/7, following release of cytochrome c. This apoptosis was induced by S/G2/M-phase arrest. Immunopositivity for c-Myc was observed in the cytoplasm of tumor cells in 16 (40%) of the 40 cases of human oral squamous cell carcinoma (HOSCC).
this study characterized in juvenile systemic lupus erythematosus a distinct profile from adult SLE that comprises increased sFas, sTRAIL, and reduced sFasL, notably in patients with active disease and with nephritis.
Notch1 activation also suppressed A549 cell apoptosis by inhibiting the PI3K/pAkt pathway and activating the caspase-3 pathway in cooperation with TRAIL. Combining Notch1 signal with TRAIL inhibited PI3K, phosphorylated Akt and phosphorylated STAT3 expressions.
we show that executioner caspase activation of the apoptotic nuclease CAD/DFF40 is essential for TRAIL-induced mutations in surviving cells. As exposure to chemotherapy drugs also activates apoptotic caspases and presumably CAD, we hypothesized that these pathways may also contribute to the mutagenesis induced by conventional chemotherapy drugs, perhaps augmenting the mutations that arise from direct DNA damage
Cultured HCN-2 neurons were incubated at different times with GITRL and/or TRAIL, and thereafter nucleic acid and protein expression were measured. HCN-2 cells do not express GITRL mRNA, but the latter is induced after treatment with TRAIL. Cells did not express the GITRL receptor GITR mRNA, neither in control cultures, nor after treatment with TRAIL. TRAIL, when associated to GITRL, exerted additive toxic effects.
OPG and OPG/TRAIL ratio expression were significantly increased in rheumatoid arthritis patients compared to controls (fold change = 1.79, p = 0.013 and 2.07, p = 0.030, respectively), RANKL/OPG ratio was significantly decreased (fold change = 0.50, p = 0.020). No significant differences were found between patients and controls in RANKL and TRAIL expression.
DR5 has a dual role in death and survival signaling, which results in TRAIL resistance in cancer cells.
Dynamin isoforms differentially regulate the endocytosis and apoptotic signaling downstream of TRAIL-death receptor (TRAIL-DR) complexes in cancer cells. TRAIL stimulation activates ryanodine receptor-mediated calcium release from endoplasmic reticulum stores, leading to calcineurin-mediated dephosphorylation and activation of Dyn1, TRAIL-DR endocytosis, and increased resistance to TRAIL-induced apoptosis.
Data suggest forkhead box protein O1 (FoxO1) involvement in the regulation of TNF-related apoptosis-inducing ligand TRAIL and Fas ligand FasL expression during follicular atresia.
The chromosomal location of the porcine TNFSF10 gene was determined by FISH of a specific BAC clone to metaphase chromosomes The chromosomal location of the porcine TNFSF10 gene was determined by FISH of a specific BAC clone to metaphase chromosomes.
xTRAIL1 can cause apoptosis, probably mediated through xDR-Ms, in larval red blood cells, but may not kill adult RBCs, presumably owing to PKC activation, as part of the mechanism for RBC switching
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. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, TNF-related apoptosis inducing ligand TRAIL
, chemokine tumor necrosis factor ligand superfamily member 10
, tumor necrosis factor (ligand) family, member 10
, tumor necrosis factor apoptosis-inducing ligand splice variant delta
, tumor necrosis factor ligand superfamily member 10
, TNF-related apoptosis inducing ligand
, TNF-related apoptosis-inducing ligand
, tumor necrosis factor-related apoptosis-inducing ligand
, TNF-related apoptosis-inducing ligand 1
, tumor necrosis factor related apoptosis inducing ligand 1
, tumor necrosis factor (ligand) superfamily, member 10 like 2
, tumor necrosis factor (ligand) superfamily, member 10
, tumor necrosis factor ligand 6A
, tumor necrosis factor superfamily member 10