ArticleAmerican journal of physiology. Cell physiology2023
A20 binding and inhibitor of nuclear factor kappa B (NF-κB)-1 (ABIN-1): a novel modulator of mitochondrial autophagy.
Article in American journal of physiology. Cell physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 10 citations in OpenAlex.
- Drp1 in M1 layer V GABAergic neurons orchestrates rTMS-mediated motor restoration and analgesia after spinal cord injury.Experimental & molecular medicine · 2026Article
- TNIP1 As A Potential Factor In Neuronal Survival, Growth and Differentiation in the Cerebellar Cortex.Cerebellum (London, England) · 2026Article
- Adjuvant therapies by anthocyanins potentially mitigating drug resistance and metastatic disease risks in stratified breast cancers: the 3PM-conceptual innovation targeted to NF-kappaB/EMT plasticity.The EPMA journal · 2026Article
- The Role of A20 in Cancer: Friend or Foe?Cells · 2025Review
- Review
- A TNIP1-driven systemic autoimmune disorder with elevated IgG4.Nature immunology · 2024Article
- REAP+: A single preparation for rapid isolation of nuclei, cytoplasm, and mitochondria.Analytical biochemistry · 2024Article
- NEMO reshapes the α-Synuclein aggregate interface and acts as an autophagy adapter by co-condensation with p62.Nature communications · 2023Article
- Mitophagy for cardioprotection.Basic research in cardiology · 2023Review
- Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling.International journal of molecular sciences · 2023Review
- TNIP1 inhibits selective autophagy via bipartite interaction with LC3/GABARAP and TAX1BP1.Molecular cell · 2023Article
- A novel regulator of selective autophagy: TNIP1/ABIN-1 modulates mitophagy.Autophagy reports · 2023Article
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Authors and funding
15 authors at 3 institutions in 2 countries.
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Abstract
A20 binding inhibitor of nuclear factor kappa B (NF-κB)-1 (ABIN-1), a polyubiquitin-binding protein, is a signal-induced autophagy receptor that attenuates NF-κB-mediated inflammation and cell death. The present study aimed to elucidate the potential role of ABIN-1 in mitophagy, a biological process whose outcome is decisive in diverse physiological and pathological settings. Microtubule-associated proteins 1A/1B light chain 3B-II (LC3B-II) was found to be in complex with ectopically expressed hemagglutinin (HA)-tagged-full length (FL)-ABIN-1. Bacterial expression of ABIN-1 and LC3A and LC3B showed direct binding of ABIN-1 to LC3 proteins, whereas mutations in the LC3-interacting region (LIR) 1 and 2 motifs of ABIN-1 abrogated ABIN-1/LC3B-II complex formation. Importantly, induction of autophagy in HeLa cells resulted in colocalization of ABIN-1 with LC3B-II in autophagosomes and with lysosomal-associated membrane protein 1 (LAMP-1) in autophagolysosomes, leading to degradation of ABIN-1 with p62. Interestingly, ABIN-1 was found to translocate to damaged mitochondria in HeLa-mCherry-Parkin transfected cells. In line with this observation, clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-mediated deletion of ABIN-1 significantly inhibited the degradation of the mitochondrial outer membrane proteins voltage-dependent anion-selective channel 1 (VDAC-1), mitofusin-2 (MFN2), and translocase of outer mitochondrial membrane (TOM)20. In addition, short interfering RNA (siRNA)-mediated knockdown of ABIN-1 significantly decreased lysosomal uptake of mitochondria in HeLa cells expressing mCherry-Parkin and the fluorescence reporter mt-mKEIMA. Collectively, our results identify ABIN-1 as a novel and selective mitochondrial autophagy regulator that promotes mitophagy, thereby adding a new player to the complex cellular machinery regulating mitochondrial homeostasis.
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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.