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Gene Symbol |
TNFRSF25 |
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Aliases |
APO-3, DDR3, DR3, GEF720, LARD, PLEKHG5, TNFRSF12, TR3, TRAMP, WSL-1, WSL-LR |
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Entrez Gene ID |
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Gene Name |
TNF receptor superfamily member 25 |
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Chromosomal Location |
1p36.31 |
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HGNC ID |
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Summary |
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]
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RefSeq DNA |
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RefSeq mRNA |
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e!Ensembl
Gene |
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Transcript |
ENST00000647810, ENST00000485036, ENST00000480393, ENST00000377782, ENST00000356876, ENST00000351959, ENST00000414040, ENST00000351748, ENST00000348333, ENST00000502588, ENST00000502730, ENST00000510563, ENST00000481401 |
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Protein |
ENSP00000497258, ENSP00000431554, ENSP00000434129, ENSP00000367013, ENSP00000349341, ENSP00000337713, ENSP00000404274, ENSP00000326762, ENSP00000314451, ENSP00000423121, ENSP00000421976, ENSP00000424071, ENSP00000465381
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Protein Information |
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Protein Name |
Tumor necrosis factor receptor superfamily member 25, Guanine nucleotide exchange factor 720, PH domain-containing family G member 5, Pleckstrin homology domain-containing family G member 5, apoptosis inducing receptor, apoptosis-inducing receptor AIR, apoptosis-mediating receptor DR3, apoptosis-mediating receptor TRAMP, death domain receptor 3 soluble form, death receptor beta, lymphocyte-associated receptor of death, protein WSL-1, tumor necrosis factor receptor superfamily, member 12 (translocating chain-association membrane protein) |
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Function |
Receptor for TNFSF12/APO3L/TWEAK. Interacts directly with the adapter TRADD. Mediates activation of NF-kappa-B and induces apoptosis. May play a role in regulating lymphocyte homeostasis |
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UniProt |
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PDB |
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Interactions |
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STRING |
MINT |
IntAct |
ENSP00000371054 |
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Q9Y581 |
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View interactions
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Associated Diseases
Disease group | Disease Name | References |
Digestive System Diseases |
Inflammatory Bowel Diseases |
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Endocrine System Diseases |
PCOS |
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Immune System Diseases |
Autoimmune Diseases |
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Musculoskeletal Diseases |
Necrosis |
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Neoplasms |
Genitourinary Cancer |
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References |
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Jansen Erik, Laven Joop S E, Dommerholt Henri B R, Polman Jan, van Rijt Cindy, van den Hurk Caroline, Westland Jolanda, Mosselman Sietse, Fauser Bart C J M |
Global Business Inteligence Center, NV Organon, PO Box 20, 5340 BH Oss, The Netherlands. erik.jansen@organon.com |
Mol Endocrinol. 2004 Dec;18(12):3050-63. doi: 10.1210/me.2004-0074. Epub 2004 Aug |
Abstract
Polycystic ovary syndrome (PCOS) represents the most common cause of anovulatory infertility and affects 5-10% of women of reproductive age. The etiology of PCOS is still unknown. The current study is the first to describe consistent differences in gene expression profiles in human ovaries comparing PCOS patients vs. healthy normoovulatory individuals. The microarray analysis of PCOS vs. normal ovaries identifies dysregulated expression of genes encoding components of several biological pathways or systems such as Wnt signaling, extracellular matrix components, and immunological factors. Resulting data may provide novel clues for ovarian dysfunction in PCOS. Intriguingly, the gene expression profiles of ovaries from (long-term) androgen-treated female-to-male transsexuals (TSX) show considerable overlap with PCOS. This observation provides supportive evidence that androgens play a key role in the pathogenesis of PCOS. Presented data may contribute to a better understanding of dysregulated pathways in PCOS, which might ultimately reveal novel leads for therapeutic intervention. |
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