ArticleThe Journal of biological chemistry2010
Full-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-kappaB pathway.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
- Antibody deficiency associated with an inherited autosomal dominant mutation in TWEAK.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Urinary TWEAK reflects disease activity in ANCA-associated vasculitis.Clinical kidney journal · 2025Article
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
- Extracellular Vesicle-Associated TWEAK Contributes to Vascular Inflammation and Remodeling During Acute Cellular Rejection.JACC. Basic to translational science · 2023Article
- Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling.Frontiers in cell and developmental biology · 2023Review
- The TWEAK/Fn14/CD163 axis-implications for metabolic disease.Reviews in endocrine & metabolic disorders · 2022Review
- Impaired bidirectional communication between interneurons and oligodendrocyte precursor cells affects social cognitive behavior.Nature communications · 2022Article
- B- and T-Cell Subset Abnormalities in Monogenic Common Variable Immunodeficiency.Frontiers in immunology · 2022Review
- Lower Expression of TWEAK is Associated with Poor Survival and Dysregulate TIICs in Lung Adenocarcinoma.Disease markers · 2022Article
- Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- TRAF3 Modulation: Novel Mechanism for the Anti-inflammatory Effects of the Vitamin D Receptor Agonist Paricalcitol in Renal Disease.Journal of the American Society of Nephrology : JASN · 2020Article
- Review
- Clinical significance of serum interleukin-8 and soluble tumor necrosis factor-like weak inducer of apoptosis levels in patients with diabetic nephropathy.Journal of diabetes investigation · 2018Article
- Fn14 hepatic progenitor cells are associated with liver fibrosis in biliary atresia.Pediatric surgery international · 2017Article
- Identification of aurintricarboxylic acid as a selective inhibitor of the TWEAK-Fn14 signaling pathway in glioblastoma cells.Oncotarget · 2017Article
- TWEAK activation of the non-canonical NF-κB signaling pathway differentially regulates melanoma and prostate cancer cell invasion.Oncotarget · 2016Article
- Article
- The TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeutics.Oncogene · 2016Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Tumor necrosis factor (TNF) family members are initially synthesized as type II transmembrane proteins, but some of these proteins are substrates for proteolytic enzymes that generate soluble cytokines with biological activity. TWEAK (TNF-like weak inducer of apoptosis), a member of the TNF family, is a multifunctional cytokine that acts via binding to a cell surface receptor named Fn14 (fibroblast growth factor-inducible 14). Studies conducted to date indicate that TWEAK-producing cells can co-express both membrane-anchored and soluble TWEAK isoforms, but there is little information on TWEAK proteolytic processing. Also, it is presently unclear whether membrane-anchored TWEAK, like soluble TWEAK, is biologically active. Here we show that full-length human TWEAK is processed intracellularly by the serine protease furin and identify TWEAK amino acid residues 90-93 as the predominant furin recognition site. In addition, we report that full-length, membrane-anchored TWEAK can bind the Fn14 receptor on neighboring cells and activate the NF-kappaB signaling pathway. Thus, TWEAK can act in a juxtacrine manner to initiate cellular responses, and this property may be important for TWEAK function during physiological wound repair and disease pathogenesis.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.