ArticleCell death & disease2012
CLIPR-59 regulates TNF-α-induced apoptosis by controlling ubiquitination of RIP1.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 26 citations in OpenAlex.
- Exploring necroptosis: mechanistic analysis and antitumor potential of nanomaterials.Cell death discovery · 2025Review
- Golgi Complex: A Signaling Hub in Cancer.Cells · 2022Review
- Bcl-3 promotes TNF-induced hepatocyte apoptosis by regulating the deubiquitination of RIP1.Cell death and differentiation · 2022Article
- Spermidine activates RIP1 deubiquitination to inhibit TNF-α-induced NF-κB/p65 signaling pathway in osteoarthritis.Cell death & disease · 2020Article
- The roles of apoptosis, autophagy and unfolded protein response in arbovirus, influenza virus, and HIV infections.Virulence · 2019Review
- Transcriptomic Analysis of Stem Cells Treated with Moringin or Cannabidiol: Analogies and Differences in Inflammation Pathways.International journal of molecular sciences · 2019Article
- Death receptor 6 contributes to autoimmunity in lupus-prone mice.Nature communications · 2017Article
- ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells.The Journal of veterinary medical science · 2016Article
- Apoptosis, autophagy and unfolded protein response pathways in Arbovirus replication and pathogenesis.Expert reviews in molecular medicine · 2016Review
- Double-Stranded RNA Is Detected by Immunofluorescence Analysis in RNA and DNA Virus Infections, Including Those by Negative-Stranded RNA Viruses.Journal of virology · 2015Article
- ClipR-59 interacts with Elmo2 and modulates myoblast fusion.The Journal of biological chemistry · 2015Article
- Spy1 induces de-ubiquitinating of RIP1 arrest and confers glioblastoma's resistance to tumor necrosis factor (TNF-α)-induced apoptosis through suppressing the association of CLIPR-59 and CYLD.Cell cycle (Georgetown, Tex.) · 2015Article
- The two faces of receptor interacting protein kinase-1.Molecular cell · 2014Review
- Necrosis-dependent and independent signaling of the RIP kinases in inflammation.Cytokine & growth factor reviews · 2014Review
- DHHC17 palmitoylates ClipR-59 and modulates ClipR-59 association with the plasma membrane.Molecular and cellular biology · 2013Article
- CYLD deubiquitinates RIP1 in the TNFα-induced necrosome to facilitate kinase activation and programmed necrosis.PloS one · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Tumor necrosis factor-α (TNF-α) has important roles in several immunological events by regulating apoptosis and transcriptional activation of cytokine genes. Intracellular signaling mediated by TNF-receptor-type 1 (TNFR1) is constituted by two sequential protein complexes: Complex-I containing the receptor and Complex-II-containing Caspase-8. Protein modifications, particularly ubiquitination, are associated with the regulation of the formation of these complexes. However, the underlying mechanisms remain poorly defined. Here, we identified CLIP-170-related 59 kDa protein (CLIPR-59) as a novel adaptor protein for TNFR1. Experimental reduction of CLIPR-59 levels prevented induction of apoptosis and activation of caspases in the context of TNF-α signaling. CLIPR-59 binds TNFR1 but dissociates in response to TNF-α stimulation. However, CLIPR-59 is also involved in and needed for the formation of Complex-II. Moreover, CLIPR-59 regulates TNF-α-induced ubiquitination of receptor-interacting protein 1 (RIP1) by its association with CYLD, a de-ubiquitinating enzyme. These findings suggest that CLIPR-59 modulates ubiquitination of RIP1, resulting in the formation of Complex-II and thus promoting Caspase-8 activation to induce apoptosis by TNF-α.
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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.