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DR5 has a dual role in death and survival signaling, which results in TRAIL resistance in cancer cells.
The B-Raf (show SNRPE Proteins) inhibitor PLX4032 induces DR5 upregulation exclusively in Ras-mutant cancer cells; this effect is dependent on Ras/c-Raf (show RAF1 Proteins)/MEK (show MAP2K1 Proteins)/ERK (show EPHB2 Proteins) signaling activation.
ONC201 has potent antiproliferative and proapoptotic effects in a broad range of breast cancer subtypes, through TRAIL-dependent and TRAIL-independent mechanisms.The small-molecule ONC201 induces expression of TRAIL and its receptor DR5. ONC201 has entered clinical trials in advanced cancers. Here, we show that ONC201 is efficacious against both triple-negative breast cancers (TNBC) and non-TNBC cells
EPHB6 (show EPHB6 Proteins) induces marked fragmentation of the mitochondrial network in breast cancer cells of triple-negative origin. This response renders cancer cells more susceptible to DR5-mediated apoptosis.
our results demonstrated that nanovectorization of TRAIL with BNNTs enhanced its binding to both DR4 (show HLADRB4 Proteins) and DR5 receptors at 37 degrees C. Our novel nanovector could potentially be used for delivering TRAIL to cells for cancer treatment
Both S1P (show MBTPS1 Proteins) and caspase-8 (show CASP8 Proteins) are critical for TRAF2 (show TRAF2 Proteins) stabilization, polyubiquitination, subsequent activation of JNK (show MAPK8 Proteins)/AP1 (show FOSB Proteins) signaling and MMP1 (show MMP1 Proteins) expression and final promotion of cell invasion.
DNA fragmentation, mitochondrial membrane potential and western blot analyses showed that MIC inhibited the growth of these cells by both mitochondrialmediated and death receptor (DR5)mediated apoptosis pathways
targeting of lysosomes by chloroquine deregulates DR5 trafficking and abrogates 5-FU- but not TRAIL-stimulated cell elimination, hence suggesting a novel mechanism for receptor activation
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.
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