ArticleThe Journal of biological chemistry2014
Zinc-binding domain-dependent, deaminase-independent actions of apolipoprotein B mRNA-editing enzyme, catalytic polypeptide 2 (Apobec2), mediate its effect on zebrafish retina regeneration.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- APOBEC2 deficiency disrupts hematopoietic lineage commitment, resulting in emergence of dual identity lymphocytes in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- APOBEC2 safeguards skeletal muscle cell fate through binding chromatin and regulating transcription of non-muscle genes during myoblast differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Epigenetic mechanisms of Müller glial reprogramming mediating retinal regeneration.Frontiers in cell and developmental biology · 2023Review
- Vegf signaling between Müller glia and vascular endothelial cells is regulated by immune cells and stimulates retina regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Functions and consequences of AID/APOBEC-mediated DNA and RNA deamination.Nature reviews. Genetics · 2022Review
- Müller Glia-Mediated Retinal Regeneration.Molecular neurobiology · 2021Review
- Review
- Novel eye genes systematically discovered through an integrated analysis of mouse transcriptomes and phenome.Computational and structural biotechnology journal · 2020Article
- Epigenetics in neuronal regeneration.Seminars in cell & developmental biology · 2020Review
- Computational approaches for predicting key transcription factors in targeted cell reprogramming (Review).Molecular medicine reports · 2018Review
- Apobec2 deficiency causes mitochondrial defects and mitophagy in skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Genomic locus modulating corneal thickness in the mouse identifies POU6F2 as a potential risk of developing glaucoma.PLoS genetics · 2018Article
- The Role of RNA Editing in Cancer Development and Metabolic Disorders.Frontiers in endocrinology · 2018Review
- The preferred nucleotide contexts of the AID/APOBEC cytidine deaminases have differential effects when mutating retrotransposon and virus sequences compared to host genes.PLoS computational biology · 2017Article
- TOPORS, a Dual E3 Ubiquitin and Sumo1 Ligase, Interacts with 26 S Protease Regulatory Subunit 4, Encoded by the PSMC1 Gene.PloS one · 2016Article
- Modulating APOBEC expression enhances DNA vaccine immunogenicity.Immunology and cell biology · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Apobec/AID family of cytosine deaminases can deaminate cytosine and thereby contribute to adaptive and innate immunity, DNA demethylation, and the modification of cellular mRNAs. Unique among this family is Apobec2, whose enzymatic activity has been questioned and whose function remains poorly explored. We recently reported that zebrafish Apobec2a and Apobec2b (Apobec2a,2b) regulate retina regeneration; however, their mechanism of action remained unknown. Here we show that although Apobec2a,2b lack cytosine deaminase activity, they require a conserved zinc-binding domain to stimulate retina regeneration. Interestingly, we found that human APOBEC2 is able to functionally substitute for Apobec2a,2b during retina regeneration. By identifying Apobec2-interacting proteins, including ubiquitin-conjugating enzyme 9 (Ubc9); topoisomerase I-binding, arginine/serine-rich, E3 ubiquitin protein ligase (Toporsa); and POU class 6 homeobox 2 (Pou6f2), we uncovered that sumoylation regulates Apobec2 subcellular localization and that nuclear Apobec2 controls Pou6f2 binding to DNA. Importantly, mutations in the zinc-binding domain of Apobec2 diminished its ability to stimulate Pou6f2 binding to DNA, and knockdown of Ubc9 or Pou6f2 suppressed retina regeneration.
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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.