ABINs: A20 binding inhibitors of NF-κB and apoptosis signaling
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ABINs have been described as three different proteins (ABIN-1, ABIN-2, ABIN-3) that bind the ubiquitin-editing nuclear factor-kappaB (NF-kappaB) inhibitor protein A20 and which show limited sequence homology. Overexpression of ABINs inhibits NF-kappaB activation by tumor necrosis factor (TNF) and several other stimuli. Similar to A20, ABIN-1 and ABIN-3 expression is NF-kappaB dependent, implicating a potential role for the A20/ABIN complex in the negative feedback regulation of NF-kappaB activation. Adenoviral gene transfer of ABIN-1 has been shown to reduce NF-kappaB activation in mouse liver and lungs. However, ABIN-1 as well as ABIN-2 deficient mice exhibit only slightly increased or normal NF-kappaB activation, respectively, possibly reflecting redundant NF-kappaB inhibitory activities of multiple ABINs. Other functions of ABINs might be non-redundant. For example, ABIN-1 shares with A20 the ability to inhibit TNF-induced apoptosis and as a result ABIN-1 deficient mice die during embryogenesis due to TNF-dependent fetal liver apoptosis. On the other hand, ABIN-2 is required for optimal TPL-2 dependent extracellularly regulated kinase activation in macrophages treated with TNF or Toll-like receptor ligands. ABINs have recently been shown to contain an ubiquitin-binding domain that is essential for their NF-kappaB inhibitory and anti-apoptotic activities. In this context, ABINs were proposed to function as adaptors between ubiquitinated proteins and other regulatory proteins. Alternatively, ABINs might disrupt signaling complexes by competing with other ubiquitin-binding proteins for the binding to specific ubiquitinated targets. Altogether, these findings implicate an important role for ABINs in the regulation of immunity and tissue homeostasis.
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The TNIP1 gene product is involved in the inhibition of the TNF-α signaling pathway and nuclear factor κB activation/translocation.
“For TNIP1, its gene product (TNF-α-induced protein 3-interacting protein 1) is involved in the inhibition of the TNF-α signaling pathway and nuclear factor κB activation/translocation33.”
From New insights into the genetic etiology of Alzheimer’s disease and related dementias (2022) · cites this paper as [33]
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- Authors
- Verstrepen, L., Carpentier, I., Verhelst, K., & Beyaert, R.
- Affiliations
- Vlaams Instituut voor Biotechnologie (BE)
- Corresponding author
- Beyaert, Rudi
- ORCID
- Beyaert, Rudi
- Venue
- Biochemical Pharmacology
- Publisher
- Elsevier BV
- Published
- 2009-07
- Volume
- 78
- Issue
- 2
- Pages
- 105-114
- ISSN
- 0006-2952 (ISSN-L)
- OpenAlex
- W2010220327
- Cited by
- 180
- References
- 76
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 7 · 2023: 1 · 2022: 5 · 2021: 6 · 2020: 10 · 2019: 5 · 2018: 16 · 2017: 16 · 2016: 18 · 2015: 11 · 2014: 12 · 2013: 15 · 2012: 12
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochemical Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- Funders
- Agentschap voor Innovatie door Wetenschap en Technologie
- Universiteit Gent
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- Abin, A20, NF-κB, ubiquitin-binding domain, TNF-induced apoptosis, negative feedback regulation, ERK activation, macrophages, embryonic lethality, immunity, tissue homeostasis, ubiquitinated proteins
- MeSH terms
- Tumor Necrosis Factor alpha-Induced Protein 3, Amino Acid Sequence, Animals, DNA-Binding Proteins, Humans, Molecular Sequence Data, Nuclear Proteins, Protein Binding, Proteins, Signal Transduction, NF-kappa B, Apoptosis, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, Apoptosis Regulatory Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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