Recombinant Human TNFRSF10B Protein

Name: Recombinant Human TNFRSF10B Protein
Brand: Beta LifeScience
SKU: BL-1717SG
Availability: InStock

Collections: All products, Buy cytokines, chemokines, and growth factors for research online, High-quality recombinant proteins, Tumor necrosis factors and receptors (tnfs)

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Product Overview

Tag	N/A
Host Species	Human
Accession	O14763
Background	TNFRSF10B is a member of the TNFR superfamily and is a cell surface receptor that is involved in apoptosis. It contains an intracellular death domain and can be activated by binding to either membrane-anchored or soluble TRAIL/Apo2L. Diseases associated with TNFRSF10B include squamous cell carcinoma, head and neck and oral cavity cancer. Among its related pathways are Akt Signaling and Akt Signaling. It is closely related to TRAIL R1/DR4, sharing 55% amino acid sequence identity.
Description	Recombinant Human TNFRSF10B was produced in E. coli. This protein is purified with our unique purification methods.
Source	E.coli
Molecular Weight	15.0 kDa
Purity	For specific purity information on a given lot, see related COA.
Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Formulation	Recombinant protein is supplied in 50mM Tris-HCl, pH 7.5, 50mM NaCl, 10mM Glutathione, 0.25mM DTT, 0.1mM EDTA, 0.1mM PMSF and 25% glycerol.
Stability	The recombinant protein is stable for up to 12 months at -70°C
Usage	For Research Use Only
Storage	Recombinant Human TNFRSF10B Protein should be stored should be stored at < -70°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Target Details

Target Function	Receptor for the cytotoxic ligand TNFSF10/TRAIL. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. Promotes the activation of NF-kappa-B. Essential for ER stress-induced apoptosis.
Subcellular Location	Membrane; Single-pass type I membrane protein.
Database References	HGNC: 11905 OMIM: 275355 KEGG: hsa:8795 STRING: 9606.ENSP00000276431 UniGene: PMID: 28181527 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. PMID: 28762762 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 PMID: 29278689 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 PMID: 28748573 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 PMID: 28981087 Knocking-down of TRAIL-DR5 gene in breast cancer cells MCF-7 markedly decreased the mRNA and protein levels of the autophagy-related factors. PMID: 29268854 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. PMID: 28702823 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 PMID: 27827395 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. PMID: 27222248 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. PMID: 27788485 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. PMID: 28482915 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 PMID: 28498480 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 PMID: 27506940 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 PMID: 28270124 PU.1 supports TRAIL-induced cell death by inhibiting RelA-mediated cell survival and inducing DR5 expression. PMID: 28362429 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. PMID: 28092099 The oncogene-like extracellular miR-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. PMID: 27129166 Data show that 4EGI-1 compound induced apoptosis in nasopharyngeal carcinoma cells through the death receptor 5 (DR5) on 4E-BP1 dephosphorylation exerting positive influence on their anti-tumor activities. PMID: 26942880 Results show that downregulation of DR4 and DR5 by SLC26A2 confers resistance to TRAIL. PMID: 28108622 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. PMID: 28746849 Oridonin analog CYD-6-28 induces apoptosis at least partially by inducing the expression of death receptor 5 in breast neoplasms. PMID: 27387452 The authors show that cholesterol is necessary for the covalent dimerization of DR5 transmembrane domains. PMID: 27720987 Mono treatment with lexatumumab was not sufficient to induce apoptosis in pancreatic cancer cells, whereas focal adhesion kinase inhibitor PF573228 significantly sensitized lexatumumab-induced apoptosis. Western blotting analysis revealed that lexatumumab and PF573228 combination treatment increased death receptor 5 but decreased Bcl-xL expression. PMID: 28459212 MG132 possesses anti-gallbladder cancer potential that correlate with regulation of DR5-dependent pathway. PMID: 27277541 CAPE/TRAIL stimulated apoptosis through the binding of TRAIL to DR5. Moreover, expression of transcription factor C/EBP homologous protein (CHOP) markedly increased in response to CAPE and transient knockdown of CHOP abolished CAPE/TRAIL-mediated apoptosis. PMID: 27260301 Decreased level of placental TRAIl-R2 and previous C-section were found to be significantly correlated to placenta accreta. PMID: 26992667 Results show that calmodulin (CaM) directly binds to death receptor-5 (DR5) in a calcium dependent manner in breast cancer cells. PMID: 27129269 Bee venom inhibits colon cancer cell growth, and these anti-proliferative effects may be related to the induction of apoptosis by activation of DR4 and DR5 and inhibition of NF-kappaB activity. PMID: 26561202 study involving a relatively large sample size showed that TNFRSF10 eQTL SNPs within lncRNAs might influence both hepatocellular carcinoma development and HBV infection PMID: 26297860 Data show that when death receptor 5 (DR5) is suppressed, caspase-8 may recruit and stabilize TNF receptor-associated factor 2 (TRAF2) to form a metastasis and invasion signaling complex, resulting in activation of ERK signaling. PMID: 26510914 Synthetic lipid bilayers displaying the membrane protein ligand Apo2L/TRAIL were used to stimulate death receptor-expressing cells in a modular, scalable format PMID: 26458551 Methionine Deprivation Induces a Targetable Vulnerability in Triple-Negative Breast Cancer Cells by Enhancing TRAIL Receptor-2 Expression PMID: 25724522 Studied an array of TRAIL-R1 and TRAIL-R2 specific variants on pancreatic cancer cells. PMID: 26138346 The expression of two proapoptotic genes, FAS and DR5, was significantly lower in tumor samples than in adjacent normal tissues PMID: 25795228 In an osteotropic variant of MDA-MB-231 breast cancer cells, TRAIL-R2 knockdown leads to downregulation of HMGA2, p-Src, p-Akt and CXCR4 and increased E-cadherin expression. These changes diminished occurrence of skeletal metastases in vivo. PMID: 25909161 mutant genotype (CT+TT) of DR5 (rs1047266) may exert a negative synergistic effect on crohn disease. PMID: 26418999 Studied the apoptosis of hepatic stellate cells induced by SEA; found it could be reduced in hepatic stellate cells that were treated with p53-specific siRNA and in hepatic stellate cells that were treated with DR5-specific shRNA. PMID: 25144704 Taken together, our results strongly suggest that FLLL12 induces apoptosis of lung cancer cell lines by posttranscriptional regulation of DR5 through activation of protein tyrosine phosphatase(s). PMID: 25917567 findings highlight novel mechanisms underlying endoplasmic reticulum stress-induced TNFRSF10A and TNFRSF10B expressions and apoptosis. PMID: 25770212 DR5 expression is dramatically reduced as a function of higher prostate tumor grade. PMID: 25174820 was statistically significant association between DR5 expression and tumor site of asal cell and squamous cell carcinoma skin cancers PMID: 24212133 Data suggest that H-Ras inhibits TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through downregulation of surface death receptors DR4/DR5. PMID: 25026275 Over-expression of TRAIL-R2 is associated with breast cancer. PMID: 25230899 The results show that both TRAIL-R1 and TRAIL-R2 are highly expressed on human oligodendrocyte progenitors. PMID: 25845236 Further analysis demonstrated that PARP inhibitor treatment results in activation of the FAS and TNFRSF10B (death receptor 5 (DR5)) promoters, increased Fas and DR5 mRNA, and elevated cell surface expression of these receptors in sensitized cells PMID: 24895135 This study demonstrated lower apoptosis correlated with a deficiency of DR5 cell surface expression by CD4 T cells upon HIV-1 stimulation. PMID: 25110157 Report RR5 up-regulation in alveolar epithelial cells from idiopathic pulmonary fibrosis patients. PMID: 24551275 Primary EOC is associated with lower TRAIL-R2 and BCL2 expression levels, while metastatic EOC is associated with higher expression of these genes. PMID: 24190693 Parthenolide triggers extrinsic apoptosis by up-regulating TNFRSF10B and intrinsic apoptosis through increasing the expression of PMAIP1. PMID: 24387758 Cotreatment with MESC and an ERK inhibitor (PD98059) significantly increased the expression of DR5 to induce apoptosis...MESC may induce apoptosis via the ERK pathway and may be a potential anticancer drug candidate against human oral MEC. PMID: 24270523

FAQs

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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

To learn more about how to properly dissolve the lyophilized recombinant protein, please visit Lyophilization FAQs.

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Recombinant Human TNFRSF10B Protein

Recombinant Human TNFRSF10B Protein

Product Overview

Target Details

FAQs