Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
In contrast to apoptosis, necroptotic signaling was activated similarly by both DR4 (show HLADRB4 Proteins)- or DR5-specific ligands..Our study provides the first systematic insight into DR4 (show HLADRB4 Proteins)-/DR5-specific signaling in colorectal and pancreatic cancer cells
These data suggest that the humanized anti-TRAIL-R2 monoclonal antibody or the second generation of the antibody may have an important clinical usage for cancer immunotherapy
We found that pharmacological application of Golgi stress leads to induction of death receptors (DRs (show PNN Proteins)) 4 and 5. DR4 (show HLADRB4 Proteins) appears to be primarily responsible for the initiation of cell death downstream of Golgi stress, whereas DR5 seems to be more important for cell death triggered by endoplasmic reticulum (ER) stress in specific cancer cell lines
Knocking-down of TRAIL-DR5 gene in breast cancer cells MCF-7 markedly decreased the mRNA and protein levels of the autophagy-related factors.
Antineoplasic agents etoposide (ET) and doxorubicin enhance the expression of Death receptor 5 (DR5) in triple-negative breast cancer (TNBC) cells. DR5 residue SerB68 is important in mediating the receptor-drug interaction. Apoptosis and DR5 expression are induced in xenograft mice and in TNBC patient-derived metastatic cells after treatment with TNF-Related Apoptosis-Inducing Ligand (TRAIL (show TNFSF10 Proteins)) and ET.
DR5, BIRC5/Survivin (show BIRC5 Proteins), XIAP (show XIAP Proteins), c-IAP1 (show BIRC2 Proteins) and c-IAP2 (show BIRC3 Proteins) mRNA expression are significantly deregulated in CRC (show CALR Proteins) and could provide a panel of markers with significant discriminatory value between CRC (show CALR Proteins) and normal colorectal tissue
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.
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