TNFRSF10C Antibodies

Tumor necrosis factor receptor superfamily member 10C (TNFRSF10C)

Receptor for the cytotoxic ligand TRAIL.

Lacks a cytoplasmic death domain and hence isn't capable of inducing apoptosis.

May protect cells from TRAIL mediated apoptosis by competing with TRAIL-R1 and R2 for binding to the ligand. .

Gene Information

Human
Gene Name:	TNFRSF10C
Uniprot:	O14798
Entrez:	8794

Family

Belongs to:
No superfamily

Alternative Names

Antagonist decoy receptor for TRAIL/Apo-2L; CD263 antigen; CD263; cytotoxic TRAIL receptor-3; DcR1; DCR1MGC149502; Decoy receptor 1; Decoy TRAIL receptor without death domain; LITMGC149501; Lymphocyte inhibitor of TRAIL; TNFRSF10C; TRAIL R3; TRAIL receptor 3; TRAIL receptor without an intracellular domain; TRAILR3; TRAIL-R3; TRAILR3TNF-related apoptosis-inducing ligand receptor 3; TRIDDCR1-TNFR; tumor necrosis factor receptor superfamily member 10C; tumor necrosis factor receptor superfamily, member 10c, decoy without anintracellular domain

Molecular Weight

Mass (kDA):
27.407 kDA

Genomic Context

Human
Location:	8p21.3
Sequence:	8; NC_000008.11 (23102921..23117445)

Tissue Specificity

Higher expression in normal tissues than in tumor cell lines. Highly expressed in peripheral blood lymphocytes, spleen, skeletal muscle, placenta, lung and heart.

Subcellular Localizations

Cell membrane; Lipid-anchor, GPI-anchor.

Diseases

• Malignant Neoplasms
• Neoplasms
• Carcinoma
• Adenocarcinoma
• Leukemia
• Malignant Paraganglionic Neoplasm
• Neuroblastoma
• Colonic Neoplasms
• Leukemia, Myelocytic, Acute
• Malignant Tumor Of Colon
• Autoimmune Reaction
• Melanoma
• Ovarian Neoplasm

• Myeloid Leukemia
• Mammary Neoplasms
• Autoimmune Diseases
• Inflammation
• Liver Neoplasms
• Malignant Squamous Cell Neoplasm
• Tumor Progression

Pathways

• Cell Death
• Methylation
• Induction Of Apoptosis
• Dna Methylation
• Sensitization
• Pathogenesis
• Drug Resistance
• Programmed Cell Death
• Gene Silencing
• Localization
• Rna Interference
• Demethylation
• Cell Growth

• Transport
• Heterochromatin Maintenance
• Hyperphosphorylation
• Dna Hypomethylation
• Cellular Senescence
• Vasculogenesis
• Regulation Of Programmed Cell Death

PTMs

• Methylation
• Cleavage

• Phosphorylation
• Demethylation

• Glycosylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TNFRSF10C

Boster Bio: Best Uses Of The TNFRSF10C Marker

Boster Bio: High-affinity Primary Antibodies provides more information on the TNFRSF10C marker. We also discuss its Clinical uses. The TNFRSF10C marker is a protein that has biological activity specific to the TNFRSF10 subunit. Boster has developed this marker in a way that allows scientists worldwide to submit their results. Scientists can use it to identify species and samples. These results are regarded as the best in their field.

Primary antibodies of high-affinity

The mouse anti-TRAIL R3/TNFRSF10C monoclonal antibody recognizes human TRAIL R3/TNFRSF10C in direct ELISAs, Western Blots, and flow cytometry assays. It is also useful for ELISA applications using the universal biotin-streptavidin platform. The antibody was found to detect pZap70 within T cells that were exposed to lipid bilayers with either short- or long-range high-affinity molecules.

Lin J and Weiss A first described the TNFRSF10C mark in 2001. They discovered that TCR signalling was mediated through a ligand that binds with the TCR. They also discovered the membrane-tethered OKT3MA can activate human T cells by binding to them. The authors concluded, however, that the anti-TNFRSF10C antibody may accumulate sufficient triggering forces on TCR to activate T Cells.

T cell-dependent immune responses result in the selection of high-affinity cells that differentiate into memory cells. It remains to be understood how this selection happens. Fas-deficient lpr mice show impaired selection for high-affinity B cell in germinal centers. Inefficient negative selectivity may be a factor. The memory compartment is established in control mice mainly by early GC precursors. In lpr-deficient mice, late GC precursors are recruited, resulting in accumulation of heavily mutated memory B cells.

In vitro, calcium mobilization from TCR microclusters is inducible by the anti-CD3 long-chain scFv. It co-localizes also with CD45. High-affinity anti CD3 scFvs inducing cytokine release Calcium mobilization is also induced by the antibodies in activated T cells.

The scFvs were conjugated to glass beads decorated with anti-CD3 scFv. The glass beads were then incubated for 2 x105 primary T cells from humans and the TNFRSF10C label. The cells were washed and counted at eight positions. The results of the experiment showed that high-affinity scFvs bind more than low-affinity scFvs.

TNFRSF10C encodes a member the tumor necrosis family which protects cells against TRAIL-induced apoptosis. It is controlled by p53, and inducible via DNA damage. It is expressed on neuronal as well as astrocyte cells. It participates in the KEGG pathways along with TNFRSF10C. This receptor also participates in apoptosis, cytokine-cytotoxicity, and TRAIL-mediated cell death.

TNFRSF10C Symbol

The TNFRSF10C marker belongs to the TRAIL group of tumor necrosis receptors. There are many names for this gene. The protein binds with several members of the TNF superfamily, including TNFRSF10A/TRAILR1, TNFRSF10B/TRAILR2, TNFRSF10B/TRAILR2, TNFRSF10C/TRAILR4 TNFRSF11B/OPG. The extracellular domain for human TRAIL is composed of amino acids 39-281. The numbering corresponds to SEQ ID NO: 96.

Clinical applications

The TNFRSF10C gene encodes a member in the tumor necrosis family. It protects cells against TRAIL-induced apoptosis. It is controlled via the p53 genes and inducible from DNA damage. Its receptors are located on neuronal cells and astrocytes. Both TNFRSF10C, and TNFRSF10D are involved with the same KEGG pathway. They are involved in apoptosis, epithelial-to-mesenchymal transition, and cancer pathways. They interact with the MST1-receptor, a protein that induces cell death.

In addition to detecting a tumorspecific mutation in patients with a high phenotype and TNFRSF10C methylation levels significantly increased in CRC cells, Therefore, TNFRSF10C hypermethylation may play a role in cancer risk assessment. Moreover, TNFRSF10C methylation levels were negatively correlated with tumor cell expression. Additionally, 5'AZA-5-deoxycytidine treatment influenced TNFRSF10C methylation.

This marker is a good candidate for COPD patients. Recent studies have demonstrated its potential. It may eventually lead to the identification COPD Biomarkers. Its identification will help physicians and researchers identify patients who may benefit from COPD treatments. To determine if it can be used to detect COPD, more research will be necessary. These studies will provide information to improve clinical practice.