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siRNA silencing of CHOP (show DDIT3 Proteins) significantly reduced cyproterone acetate-induced DR5 up-regulation and TRAIL sensitivity in prostate cancer cells. Our study shows a novel effect of cyproterone acetate on apoptosis pathways in prostate cancer cells and raises the possibility that a combination of TRAIL with cyproterone acetate could be a promising strategy for treating castration-resistant prostate cancer
PU.1 supports TRAIL-induced cell death by inhibiting RelA (show NFkBP65 Proteins)-mediated cell survival and inducing DR5 expression.
The results demonstrated CaM binding to DR5-mediated DISC in a calcium dependent manner and may identify CaM as a key regulator of DR5-mediated DISC formation for apoptosis in breast cancer.
The oncogene (show RAB1A Proteins)-like extracellular miR (show MLXIP Proteins)-1246 could act as a signaling messenger between irradiated and non-irradiated lung cancer cells, more importantly, it contributes to cell radioresistance by directly suppressing the DR5 gene.
These results reveal KDM4A (show KDM4A Proteins) as a key epigenetic silencer of TRAIL and DR5 in tumors.
Data show that 4EGI-1 compound induced apoptosis in nasopharyngeal carcinoma cells through the death receptor 5 (DR5) on 4E-BP1 (show EIF4EBP1 Proteins) dephosphorylation exerting positive influence on their anti-tumor activities.
hepatitis B virus (HBV) X protein (HBx) restricts TNFSF10 (show TNFSF10 Proteins) receptor signaling via macroautophagy/autophagy-mediated degradation of TNFRSF10B/DR5, a TNFSF10 (show TNFSF10 Proteins) death receptor.
Results show that downregulation of DR4 (show HLADRB4 Proteins) and DR5 by SLC26A2 (show SLC26A2 Proteins) confers resistance to TRAIL.
Study provides direct biophysical evidence that Death Receptor 5 disulfide-linked transmembrane (TM)-dimers open in response to ligand binding. Then, to probe the importance of the closed-to-open TM domain transition in the overall energetics of receptor activation, point-mutants (alanine to phenylalanine) in the predicted, tightly packed TM domain dimer interface were designed and tested.
High-order TRAIL oligomer formation in TRAIL-coated lipid nanoparticles enhances DR5 cross-linking and increases antitumour effect against colon cancer cells and xenograft tumors.
Death receptor5 pathway and mitochondrial pathway, which are likely mediated by HIF-1alpha (show HIF1A Proteins), contribute to hypoxia-induced spermatocyte apoptosis.
Authors demonstrate, for the first time, expression of TNF-related apoptosis-inducing ligand (TRAIL (show TNFSF10 Proteins)) and its signaling death receptor 5 (DR5) in the murine inner ear.
Malignant transformation in the endometrium is related to reduction of membrane DR4 (show HLADRB4 Proteins) and DR5 expression.
TRAIL expression by osteoclast-like cells is increased in the presence of RANKL (show TNFSF11 Proteins) and after scraping; DcR2 (show TNFRSF10D Proteins) expression peaks at 24 hours, and and decreases at 5 days; DR5 expression peaks at 5 days
Induction of death receptor 5 expression in tumor vasculature by perifosine restores the vascular disruption activity of TRAIL-expressing CD34 (show CD34 Proteins)(+) cells.
TRAIL-DR5 interaction promoted malignant behaviors of B16F10 cells.
results suggest that the transmembrane domains together with their adjacent stalk regions can play a major role in control of death receptor activation thereby contributing to cell type specific differences in TRAILR1 and TRAILR2 signaling
DR5 is selectively expressed by neuroprogenitor cells and newborn neurons.
Results suggest that excessive iodine could induce TRAIL and DR5 abnormal expression in thyroid. TRAIL band with DR5 to promote follicular cells apoptosis thus mediate thyroid destruction in EAT.
NK cells inhibit dendritic cell cross-priming, but not direct priming, in a TRAIL/DR5-dependent manner.
The protein encoded by this gene is a member of the TNF-receptor superfamily, and contains an intracellular death domain. This receptor can be activated by tumor necrosis factor-related apoptosis inducing ligand (TNFSF10/TRAIL/APO-2L), and transduces an apoptosis signal. Studies with FADD-deficient mice suggested that FADD, a death domain containing adaptor protein, is required for the apoptosis mediated by this protein. Two transcript variants encoding different isoforms and one non-coding transcript have been found for this gene.
tumor necrosis factor receptor superfamily, member 10b
, death receptor-M2
, death receptor-M1
, Fas-like protein
, TNF-related apoptosis-inducing ligand receptor 2
, apoptosis inducing protein TRICK2A/2B
, apoptosis inducing receptor TRAIL-R2
, cytotoxic TRAIL receptor-2
, death domain containing receptor for TRAIL/Apo-2L
, death receptor 5
, p53-regulated DNA damage-inducible cell death receptor(killer)
, tumor necrosis factor receptor superfamily member 10B
, tumor necrosis factor receptor-like protein ZTNFR9
, KILLER/DR5 TRAIL death-inducing receptor