Human TNFRSF25 blocking peptide

Name: Human TNFRSF25 blocking peptide
SKU: DAG-P0378
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Nature

Synthetic

Tag/Conjugate

Unconjugated

SequenceSimilarities

16 amino amino terminus of human DR3.

Purity

> 95 % by SDS-PAGE.

Format

Lyophilized

Preservative

0.02% Sodium Azide

Storage

Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles. PBS with 0.1% BSA 0.02% sodium azide pH7.2

Reconstitution

TNFRSF25 peptide is supplied as 1mg of dried peptide. When the peptide is reconstituted in 1 mL strile water, the concentration will be 1 mg/mL.

Introduction

The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor is expressed preferentially in the tissues enriched in lymphocytes, and it may play a role in regulating lymphocyte homeostasis. This receptor has been shown to stimulate NF-kappa B activity and regulate cell apoptosis. The signal transduction of this receptor is mediated by various death domain containing adaptor proteins. Knockout studies in mice suggested the role of this gene in the removal of self-reactive T cells in the thymus. Multiple alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported, most of which are potentially secreted molecules. The alternative splicing of this gene in B and T cells encounters a programmed change upon T-cell activation, which predominantly produces full-length, membrane bound isoforms, and is thought to be involved in controlling lymphocyte proliferation induced by T-cell activation. [provided by RefSeq, Jul 2008]

Entrez Gene ID

8718

Synonyms

TNFRSF25; tumor necrosis factor receptor superfamily, member 25; DR3; TR3; DDR3; LARD; APO-3; TRAMP; WSL-1; WSL-LR; TNFRSF12; tumor necrosis factor receptor superfamily member 25; protein WSL-1; death receptor beta; apoptosis inducing receptor; apoptosis-inducing receptor AIR; apoptosis-mediating receptor DR3; apoptosis-mediating receptor TRAMP; death domain receptor 3 soluble form; lymphocyte-associated receptor of death; tumor necrosis factor receptor superfamily, member 12 (translocating chain-association membrane protein);

Citations

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Documents

pdf COA

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pdf Datasheet

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References

The Cancer Genome Atlas dataset-based analysis of aberrantly expressed genes by GeneAnalytics in thymoma associated myasthenia gravis: focusing on T cells

JOURNAL OF THORACIC DISEASE

Authors: Xi, Jianying; Wang, Liang; Yan, Chong; Song, Jie; Song, Yang; Chen, Ji; Zhu, Yongjun; Chen, Zhiming; Jin, Chun; Ding, Jianyong; Zhao, Chongbo

Abstract

Background: Myasthenia gravis (MG) is a group of autoimmune disease which could be accompanied by thymoma. Many differences have been observed between thymoma-associated MG (IAMG) and non-MG thymoma (NMG). However, the molecular difference between them remained unknown. This study aimed to explore the differentially expressed genes (DEGs) between the two categories and to elucidate the possible pathogenesis of TAMG further. Methods: DEGs were calculated using the RNA-Sequencing data from 11 TAMG and 10 NMG in The Cancer Genome Atlas (TCGA) database. GeneAnalytics was performed to characterize the associations between DEGs and tissues and cells, diseases, gene ontology (GO) terms, pathways, phenotypes, and drug/ compounds, respectively. Genes related to T cells were sorted out using LifeMapDiscovery Cells and Tissues Database. Genes directly related to the phenotype of autoimmune diseases that were identified by VarElect were validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Results: The expression level of 169 genes showed a significant difference between the two groups, with 94 up-regulated and 75 down-regulated. Overexpression of six genes (ATM, SFIPB, ANKRD55, 1177-4, CCR7, TNFRSF25), which are expressed in T cells and directly related to autoimmune disease through VarElect, was identified. The overexpression of soluble BTLA (sBTLA) (P=0.027), CCR7 (P=0.0018), TNFRSF25 (P=0.0013) and ANKRD55 (P=0.0026) was validated by RT-qPCR in thymoma tissues from our center. Conclusions: Overexpression of sBTLA, CCR7, TNFRSF25 and ANKRD55 was identified and validated by RT-qPCR, which could partly explain the underlying pathogenesis in TAMG.

TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

JOURNAL OF EXPERIMENTAL MEDICINE

Authors: Pappu, Bhanu P.; Borodovsky, Anna; Zheng, Timothy S.; Yang, Xuexian; Wu, Ping; Dong, Xingwen; Weng, Shawn; Browning, Beth; Scott, Martin L.; Ma, Li; Su, Lihe; Tian, Qiang; Schneider, Pascal; Flavell, Richard A.; Dong, Chen; Burkly, Linda C.

Abstract

T helper type 17 (Th17) cells play an important pathogenic function in autoimmune diseases; their regulation, however, is not well understood. We show that the expression of a tumor necrosis factor receptor family member, death receptor 3 (DR3; also known as TNFRSF25), is selectively elevated in Th17 cells, and that TL1A, its cognate ligand, can promote the proliferation of effector Th17 cells. To further investigate the role of the TL1A-DR3 pathway in Th17 regulation, we generated a TL1A-deficient mouse and found that TL1A(-/-) dendritic cells exhibited a reduced capacity in supporting Th17 differentiation and proliferation. Consistent with these data, TL1A(-/)-animals displayed decreased clinical severity in experimental autoimmune encephalomyelitis (EAE). Finally, we demonstrated that during EAE disease progression, TL1A was required for the optimal differentiation as well as effector function of Th17 cells. These observations thus establish an important role of the TL1A-DR3 pathway in promoting Th17 cell function and Th17-mediated autoimmune disease.