Browse our TNFRSF10B Proteins (TNFRSF10B)

Human Tumor Necrosis Factor Receptor Superfamily, Member 10b (TNFRSF10B) interaction partners

1. the findings of this study indicated that luteolin effectively enhanced TRAILinitiated apoptosis, and that these effects were likely to be mediated by autophagy and JNKmediated DR5 expression.

2. analysis revealed that DR5 expression in CRC tended to be inversely associated with LCN2 expression. Downregulation of LCN2 enhances DR5 expression and promotes the TRAIL-induced apoptosis of TRAIL-resistant human colorectal cancer cells.

3. TRAIL synergistically sensitized irradiation-induced apoptosis in glioblastoma stem-like cells by increasing DR5 expression and decreasing cFLIP expression.

4. in vivo data confirmed that anti-tumor activity of bigelovin in Colorectal cancer (CRC)was through induction of apoptosis by up-regulating DR5 and increasing ROS. In conclusion, these results strongly suggested that bigelovin has potential to be developed as therapeutic agent for CRC patients

5. GDF-15 and TRAIL-R2 were the most powerful Proximity Extension Assay chip biomarkers in predicting long-term all-cause mortality in patients with acute myocardial infarction.

6. In contrast to apoptosis, necroptotic signaling was activated similarly by both DR4- or DR5-specific ligands..Our study provides the first systematic insight into DR4-/DR5-specific signaling in colorectal and pancreatic cancer cells

7. 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

8. We found that pharmacological application of Golgi stress leads to induction of death receptors (DRs) 4 and 5. DR4 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

9. Knocking-down of TRAIL-DR5 gene in breast cancer cells MCF-7 markedly decreased the mRNA and protein levels of the autophagy-related factors.

10. 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) and ET.

11. DR5, BIRC5/Survivin, XIAP, c-IAP1 and c-IAP2 mRNA expression are significantly deregulated in CRC and could provide a panel of markers with significant discriminatory value between CRC and normal colorectal tissue

12. DR5 has a dual role in death and survival signaling, which results in TRAIL resistance in cancer cells.

13. The B-Raf inhibitor PLX4032 induces DR5 upregulation exclusively in Ras-mutant cancer cells; this effect is dependent on Ras/c-Raf/MEK/ERK signaling activation.

14. 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

15. EPHB6 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.

16. our results demonstrated that nanovectorization of TRAIL with BNNTs enhanced its binding to both DR4 and DR5 receptors at 37 degrees C. Our novel nanovector could potentially be used for delivering TRAIL to cells for cancer treatment

17. Both S1P and caspase-8 are critical for TRAF2 stabilization, polyubiquitination, subsequent activation of JNK/AP1 signaling and MMP1 expression and final promotion of cell invasion.

18. 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

19. 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

20. siRNA silencing of CHOP 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

Mouse (Murine) Tumor Necrosis Factor Receptor Superfamily, Member 10b (TNFRSF10B) interaction partners

1. Targeting upregulated DR5 in alpha-SMA-expressing dermal myofibroblasts is a viable therapy for fibrosis in scleroderma.

2. TRAIL/TRAIL-R interaction regulates CD4(+) T cell activation in autoimmune inflammation and directly suppresses T cell activation via inhibiting TCR signaling, suggesting that TRAIL-R serves as a novel immune checkpoint in T cell responses.

3. Death receptor5 pathway and mitochondrial pathway, which are likely mediated by HIF-1alpha, contribute to hypoxia-induced spermatocyte apoptosis.

4. downregulation of cIAPs in PSC cholangiocytes may contribute to the development of the disease. Our results also indicate that inhibition of TRAIL signaling pathways may be beneficial in the treatment of PSC

5. Authors demonstrate, for the first time, expression of TNF-related apoptosis-inducing ligand (TRAIL) and its signaling death receptor 5 (DR5) in the murine inner ear.

6. Malignant transformation in the endometrium is related to reduction of membrane DR4 and DR5 expression.

7. TRAIL expression by osteoclast-like cells is increased in the presence of RANKL and after scraping; DcR2 expression peaks at 24 hours, and and decreases at 5 days; DR5 expression peaks at 5 days

8. Induction of death receptor 5 expression in tumor vasculature by perifosine restores the vascular disruption activity of TRAIL-expressing CD34(+) cells.

9. TRAIL-DR5 interaction promoted malignant behaviors of B16F10 cells.

10. 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

11. DR5 is selectively expressed by neuroprogenitor cells and newborn neurons.

12. 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.

13. NK cells inhibit dendritic cell cross-priming, but not direct priming, in a TRAIL/DR5-dependent manner.

14. Antibody-based therapy targeting DR5 is an efficient strategy not only to eliminate TRAIL-sensitive tumor cells.

15. presence and function of TRAIL and MK, a death-inducing ligand and its receptor, in mammalian preimplantation embryos.

16. binding of Fas-associated death domain (FADD) to the tumor necrosis factor-related apoptosis-inducing ligand receptor DR5 is regulated by the death effector domain of FADD

17. Inactivation of the TRAIL-R gene did not affect tumorigenesis in the thymus and intestines of p53 knock-out mice and mice mutated in the Adenomatous Polyposis Coli gene, respectively.

18. DR5 has a limited role during embryogenesis and early stages of development but plays an organ-specific role in the response to DNA-damaging stimuli.

19. ceramide acts as a common mediator of caspase-independent programmed cell death caused by death receptors such as mTRAIL-R2 and TNF-R55

20. These data demonstrate an important role for the TRAIL/DR5/FADD/caspase 8 pathway in the apoptosis associated with skeletal myoblast differentiation.