ArticleNeuroscience letters2012
Comparative distribution of protein components of the A20 ubiquitin-editing complex in normal human brain.
Article in Neuroscience letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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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
15 citing papers in PubMed, 23 citations in OpenAlex.
- Association of serum A20 levels with stroke-associated pneumonia, early neurological deterioration, and poor neurological prognosis following acute supratentorial intracerebral hemorrhage: a prospective cohort study.Frontiers in neurology · 2025Article
- A prospective cohort study on serum A20 as a prognostic biomarker of aneurysmal subarachnoid hemorrhage.World journal of emergency medicine · 2023Article
- Overexpression of the ubiquitin-editing enzyme A20 in the brain lesions of Multiple Sclerosis patients: moving from systemic to central nervous system inflammation.Brain pathology (Zurich, Switzerland) · 2021Article
- Ring Finger Protein 11 (RNF11) Modulates Dopamine Release in Drosophila.Neuroscience · 2021Article
- RNF11 at the Crossroads of Protein Ubiquitination.Biomolecules · 2020Review
- The ubiquitin-editing enzyme A20 regulates synapse remodeling and efficacy.Brain research · 2020Article
- A20-Binding Inhibitor of NF-Evidence-based complementary and alternative medicine : eCAM · 2020Article
- A20 Ameliorates Intracerebral Hemorrhage-Induced Inflammatory Injury by Regulating TRAF6 Polyubiquitination.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Upregulation of neuronal zinc finger protein A20 expression is required for electroacupuncture to attenuate the cerebral inflammatory injury mediated by the nuclear factor-kB signaling pathway in cerebral ischemia/reperfusion rats.Journal of neuroinflammation · 2016Article
- Article
- A20 deficiency causes spontaneous neuroinflammation in mice.Journal of neuroinflammation · 2014Article
- AAV2 production with optimized N/P ratio and PEI-mediated transfection results in low toxicity and high titer for in vitro and in vivo applications.Journal of virological methods · 2013Article
- NF-κB activity is inversely correlated to RNF11 expression in Parkinson's disease.Neuroscience letters · 2013Article
- RING finger protein 11 (RNF11) modulates susceptibility to 6-OHDA-induced nigral degeneration and behavioral deficits through NF-κB signaling in dopaminergic cells.Neurobiology of disease · 2013Article
- RNF11 modulates microglia activation through NF-κB signalling cascade.Neuroscience letters · 2012Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Activation of innate and adaptive immune responses is tightly regulated, as insufficient activation could result in defective clearance of pathogens, while excessive activation might lead to lethal systemic inflammation or autoimmunity. A20 functions as a negative regulator of innate and adaptive immunity by inhibiting NF-κB activation. A20 mediates its inhibitory function in a complex with other proteins including RNF11 and Itch, both E3 ubiquitin ligases and TAX1BP1, an adaptor protein. Since NF-κB has been strongly implicated in various neuronal functions, we predict that its inhibitor, the A20 complex, is also present in the nervous system. In efforts to better understand the role of A20 complex and NF-κB signaling pathway, we determined regional distribution of A20 mRNA as well as protein expression levels and distribution of RNF11, TAX1BP1 and Itch, in different brain regions. The distribution of TRAF6 was also investigated since TRAF6, also an E3 ligase, has an important role in NF-κB signaling pathway. Our investigations, for the first time, describe and demonstrate that the essential components of the A20 ubiquitin-editing complex are present and mainly expressed in neurons. The A20 complex components are also differentially expressed throughout the human brain. This study provides useful information about region specific expression of the A20 complex components that will be invaluable while determining the role of NF-κB signaling pathway in neuronal development and degeneration.
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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.