Human TNFSF10

Name: Human TNFSF10
SKU: DAG346
Rating: 5 (1 reviews)

Human TNFSF10, recombinant protein from E. coli

COA

SDS

Datasheet

Summary

Nature

Recombinant

Tag/Conjugate

Unconjugated

Format

Purified, Lyophilized. We recommend a quick spin followed byreconstitution in water to a concentration of 0.5-1.0 mg/ml. This solution canthen be diluted into other aqueou buffers and stored at 2-8°C (up to oneweek) or –20°C for future use.

Concentration

0.3 mg/ml(prior to lyophilization)

Buffer

Lyophilizedfrom 10mM Sodium phosphate, pH 7.0 containing 110mM Sodium Chloride

Preservative

None

Storage

2-8°C short term, -20°C long term

Introduction

The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein preferentially induces apoptosis in transformed and tumor cells, but does not appear to kill normal cells although it is expressed at a significant level in most normal tissues. This protein binds to several members of TNF receptor superfamily including TNFRSF10A/TRAILR1, TNFRSF10B/TRAILR2, TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4, and possibly also to TNFRSF11B/OPG. The activity of this protein may be modulated by binding to the decoy receptors TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4, and TNFRSF11B/OPG that cannot induce apoptosis. The binding of this protein to its receptors has been shown to trigger the activation of MAPK8/JNK, caspase 8, and caspase 3. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2010]

Antigen Description

In the field of cellbiology, TNF-related apoptosis-inducing ligand (TRAIL), is a proteinfunctioning as a ligand that induces the process of cell death calledapoptosis. TRAIL has also been designated CD253 (cluster of differentiation253).

Keywords

TNFSF10; tumor necrosis factor (ligand) superfamily, member 10; TL2; APO2L; CD253; TRAIL; Apo-2L; tumor necrosis factor ligand superfamily member 10; Apo-2 ligand; TNF-related apoptosis inducing ligand TRAIL; tumor necrosis factor (ligand) family, member

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Documents

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References

Transcriptomic analysis of reproductive damage in the epididymis of male Kunming mice induced by chronic infection of Toxoplasma gondii PRU strain

PARASITES & VECTORS

Authors: Zheng, Yu-Xiang; Zhang, Xiu-Xiang; Hernandez, Jorge A.; Mahmmod, Yasser S.; Huang, Wan-Yi; Li, Gui-Feng; Wang, Ya-Pei; Zhou, Xue; Li, Xiu-Ming; Yuan, Zi-Guo

Abstract

Background Some researchers have reported that Toxoplasma gondii can cause serious reproductive impairment in male animals. Specifically, T. gondii destroy the quality of sperm in the epididymis, which affects their sexual ability. However, among such studies, none have investigated the male reproductive transcriptome. Therefore, to investigate the relationship between T. gondii and sperm maturation, we infected mice with T. gondii prugniaud (PRU) strain and performed transcriptome sequencing of the epididymis. Results Compared with the control group, 431 upregulated and 229 downregulated differentially expressed genes (DEGs) were found (P-value < 0.05, false discovery rate (FDR) < 0.05 and |log2 (fold change)| >= 1). According to results of a bioinformatics analysis, Gene Ontology (GO) function is divided into three categories: cellular component, molecular function and biological process. Upon performing GO analysis, we found that some DEGs correlated with an integral part of membrane, protein complex, cell surface, ATP binding, immune system process, signal transduction and metabolic process which are responsible for the epididymal injury. DEGs were mapped to 101 unique KEGG pathways. Pathways such as cytokine-cytokine receptor interaction, glycolysis/gluconeogenesis and apoptosis are closely related to sperm quality. Moreover, Tnfsf10 and spata18 can damage the mitochondria in sperm, which decreases sperm motility and morphology. Conclusions We sequenced the reproductive system of male mice chronically infected with T. gondii, which provides a new direction for research into male sterility caused by Toxoplasma infection. This work provides valuable information and a comprehensive database for future studies of the interaction between T. gondii infection and the male reproductive system.

Risk of Ovarian Cancer and the NF-kappa B Pathway: Genetic Association with IL1A and TNFSF10

CANCER RESEARCH

Authors: Charbonneau, Bridget; Block, Matthew S.; Bamlet, William R.; Vierkant, Robert A.; Kalli, Kimberly R.; Fogarty, Zachary; Rider, David N.; Sellers, Thomas A.; Tworoger, Shelley S.; Poole, Elizabeth; Risch, Harvey A.; Salvesen, Helga B.; Kiemeney, Lambertus A.; Baglietto, Laura; Giles, Graham G.; Severi, Gianluca; Trabert, Britton; Wentzensen, Nicolas; Chenevix-Trench, Georgia; Whittemore, Alice S.; Sieh, Weiva; Chang-Claude, Jenny; Bandera, Elisa V.; Orlow, Irene; Terry, Kathryn; Goodman, Marc T.; Thompson, Pamela J.; Cook, Linda S.; Rossing, Mary Anne; Ness, Roberta B.; Narod, Steven A.; Kupryjanczyk, Jolanta; Lu, Karen; Butzow, Ralf; Doerk, Thilo; Pejovic, Tanja; Campbell, Ian; Le, Nhu D.; Bunker, Clareann H.; Bogdanova, Natalia; Runnebaum, Ingo B.; Eccles, Diana; Paul, James; Wu, Anna H.; Gayther, Simon A.; Hogdall, Estrid; Heitz, Florian; Kaye, Stanley B.; Karlan, Beth Y.; Anton-Culver, Hoda; Gronwald, Jacek; Hogdall, Claus K.; Lambrechts, Diether; Fasching, Peter A.; Menon, Usha; Schildkraut, Joellen; Pearce, Celeste Leigh; Levine, Douglas A.; Kjaer, Susanne Kruger; Cramer, Daniel; Flanagan, James M.; Phelan, Catherine M.; Brown, Robert; Massuger, Leon F. A. G.; Song, Honglin; Doherty, Jennifer A.; Krakstad, Camilla; Liang, Dong; Odunsi, Kunle; Berchuck, Andrew; Jensen, Allan; Lubinski, Jan; Nevanlinna, Heli; Bean, Yukie T.; Lurie, Galina; Ziogas, Argyrios; Walsh, Christine; Despierre, Evelyn; Brinton, Louise; Hein, Alexander; Rudolph, Anja; Dansonka-Mieszkowska, Agnieszka; Olson, Sara H.; Harter, Philipp; Tyrer, Jonathan; Vitonis, Allison F.; Brooks-Wilson, Angela; Aben, Katja K.; Pike, Malcolm C.; Ramus, Susan J.; Wik, Elisabeth; Cybulski, Cezary; Lin, Jie; Sucheston, Lara; Edwards, Robert; McGuire, Valerie; Lester, Jenny; du Bois, Andreas; Lundvall, Lene; Wang-Gohrke, Shan; Szafron, Lukasz M.; Lambrechts, Sandrina; Yang, Hannah; Beckmann, Matthias W.; Pelttari, Liisa M.; Van Altena, Anne M.; van den Berg, David; Halle, Mari K.; Gentry-Maharaj, Aleksandra; Schwaab, Ira; Chandran, Urmila; Menkiszak, Janusz; Ekici, Arif B.; Wilkens, Lynne R.; Leminen, Arto; Modugno, Francesmary; Friel, Grace; Rothstein, Joseph H.; Vergote, Ignace; Garcia-Closas, Montserrat; Hildebrandt, Michelle A. T.; Sobiczewski, Piotr; Kelemen, Linda E.; Pharoah, Paul D. P.; Moysich, Kirsten; Knutson, Keith L.; Cunningham, Julie M.; Fridley, Brooke L.; Goode, Ellen L.

Abstract

A missense single-nucleotide polymorphism (SNP) in the immune modulatory gene IL1A has been associated with ovarian cancer risk (rs17561). Although the exact mechanism through which this SNP alters risk of ovarian cancer is not clearly understood, rs17561 has also been associated with risk of endometriosis, an epidemiologic risk factor for ovarian cancer. Interleukin-1 alpha (IL1A) is both regulated by and able to activate NF-kappa B, a transcription factor family that induces transcription of many proinflammatory genes and may be an important mediator in carcinogenesis. We therefore tagged SNPs in more than 200 genes in the NF-kB pathway for a total of 2,282 SNPs (including rs17561) for genotype analysis of 15,604 cases of ovarian cancer in patients of European descent, including 6,179 of high-grade serous (HGS), 2,100 endometrioid, 1,591 mucinous, 1,034 clear cell, and 1,016 low-grade serous, including 23,235 control cases spanning 40 studies in the Ovarian Cancer Association Consortium. In this large population, we confirmed the association between rs17561 and clear cell ovarian cancer [OR, 0.84; 95% confidence interval (CI), 0.76-0.93; P = 0.00075], which remained intact even after excluding participants in the prior study (OR, 0.85; 95% CI, 0.75-0.95; P = 0.006). Considering a multiple-testing-corrected significance threshold of P < 2.5 x 10(-5), only one other variant, the TNFSF10 SNP rs6785617, was associated significantly with a risk of ovarian cancer (low malignant potential tumors OR, 0.85; 95% CI, 0.79-0.91; P = 0.00002). Our results extend the evidence that borderline tumors may have a distinct genetic etiology. Further investigation of how these SNPs might modify ovarian cancer associations with other inflammation-related risk factors is warranted.