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our results demonstrated that nanovectorization of TRAIL with BNNTs enhanced its binding to both DR4 (zeige HLADRB4 Proteine) and DR5 receptors at 37 degrees C. Our novel nanovector could potentially be used for delivering TRAIL to cells for cancer treatment
Both S1P (zeige MBTPS1 Proteine) and caspase-8 (zeige CASP8 Proteine) are critical for TRAF2 (zeige TRAF2 Proteine) stabilization, polyubiquitination, subsequent activation of JNK (zeige MAPK8 Proteine)/AP1 (zeige FOSB Proteine) signaling and MMP1 (zeige MMP1 Proteine) 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 (zeige DDIT3 Proteine) 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 (zeige NFkBP65 Proteine)-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 (zeige RAB1A Proteine)-like extracellular miR (zeige MLXIP Proteine)-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 (zeige KDM4A Proteine) 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 (zeige EIF4EBP1 Proteine) dephosphorylation exerting positive influence on their anti-tumor activities.
Death receptor5 pathway and mitochondrial pathway, which are likely mediated by HIF-1alpha (zeige HIF1A Proteine), contribute to hypoxia-induced spermatocyte apoptosis.
Authors demonstrate, for the first time, expression of TNF-related apoptosis-inducing ligand (TRAIL (zeige TNFSF10 Proteine)) and its signaling death receptor 5 (DR5) in the murine inner ear.
Malignant transformation in the endometrium is related to reduction of membrane DR4 (zeige HLADRB4 Proteine) and DR5 expression.
TRAIL expression by osteoclast-like cells is increased in the presence of RANKL (zeige TNFSF11 Proteine) and after scraping; DcR2 (zeige TNFRSF10D Proteine) 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 (zeige CD34 Proteine)(+) 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