The p27 catalytic subunit of the apolipoprotein B mRNA editing enzyme is a cytidine deaminase.

Navaratnam, Naveenan; Morrison, John R.; Bhattacharya, Shoumo; Patel, Dushyant V.; Funahashi, Toru; Giannoni, Federico; Teng, Babie; Davidson, Nicholas O.; Scott, James

doi:10.1016/s0021-9258(19)36836-x

Cited by 262 publications

(39 citation statements)

References 33 publications

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“…Apolipoprotein B (apoB) mRNA editing involves cytidine to uridine conversion at nucleotide 6666 and creates an in-frame translation stop codon (UAA) from a glutamine codon (CAA) (2,3). Site-specific editing of apoB mRNA is mediated by a cytidine deaminase, APOBEC-1 (4-6) whose activity on RNA is dependent upon its assembly with one or more auxiliary proteins (4,5,7) as an editosome (8).…”

Section: Introductionmentioning

confidence: 99%

The Neurofibromatosis Type I Messenger RNA Undergoes Base-Modification RNA Editing

Skuse

Cappione

Sowden

et al. 1996

Nucleic Acids Research

121

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A functional mooring sequence, known to be required for apolipoprotein B (apoB) mRNA editing, exists in the mRNA encoding the neurofibromatosis type I (NF1) tumor suppressor. Editing of NF1 mRNA modifies cytidine in an arginine codon (CGA) at nucleotide 2914 to a uridine (UGA), creating an in frame translation stop codon. NF1 editing occurs in normal tissue but was several-fold higher in tumors. In vitro editing and transfection assays demonstrated that apoB and NF1 RNA editing will take place in both neural tumor and hepatoma cells. Unlike apoB, NF1 editing did not demonstrate dependence on rate-limiting quantities of APOBEC-1 (the apoB editing catalytic subunit) suggesting that different trans-acting factors may be involved in the two editing processes.

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Section: Introductionmentioning

confidence: 99%

The Neurofibromatosis Type I Messenger RNA Undergoes Base-Modification RNA Editing

Skuse

Cappione

Sowden

et al. 1996

Nucleic Acids Research

121

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“…The first APOBEC to be described was APOBEC1 (A1) through its ability to edit the mRNA encoding APOB protein, thereby producing an isoform involved in lipid metabolism [12,75]. However, A1 has also shown to be involve in demethylation events, for example A1 promotes nestin demethylation.…”

Section: Genomic and Epigenomic Contributions Of Apobecs To Non-immune Physiologymentioning

confidence: 99%

“…AID (activation-induced cytosine deaminase) is arguably the evolutionary founding member and has been extensively studied in the context of somatic hypermutation (SHM) and class-switch recombination (CSR) during antibody diversification [10,11]. APOBECs are also involved in several physiological processes including lipid metabolism (APOBEC1) [12], musculogenesis (APOBEC2) [13], retroelement restriction (APOBEC3s) [14], DNA damage (AID, APOBEC3s) [15], and cell homeostasis [16]. Despite their beneficial roles, dysregulation of APOBECs is associated with several diseases [17,18].…”

mentioning

confidence: 99%

APOBECs orchestrate genomic and epigenomic editing across health and disease

et al. 2021

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APOBEC proteins can deaminate cytosine residues in DNA and RNA. This can lead to somatic mutations, DNA breaks, RNA modifications, or DNA demethylation in a selective manner. APOBECs function in various cellular compartments and recognize different nucleic acid motifs and structures. They orchestrate a wide array of genomic and epigenomic modifications, thereby affecting various cellular functions positively or negatively, including immune editing, viral and retroelement restriction, DNA damage responses, DNA demethylation, gene expression, and tissue homeostasis. Furthermore, the cumulative increase in genomic and epigenomic editing with aging could also, at least in part, be attributed to APOBEC function. We synthesize our cumulative understanding of APOBEC activity in a unifying overview and discuss their genomic and epigenomic impact in physiological, pathological, and technological contexts. HighlightsGenomic and epigenomic effects of apolipoprotein B mRNA editing cytosine deaminases (APOBECs) are tightly controlled and are essential for physiological immune and non-immune processes.Pathological APOBEC off-target effects are often observed because of altered catalytic activity or dysregulation, and/or synergies with other predisposing factors such as infections, inflammation, or DNA repair defects.APOBEC mutation signatures are documented in various cancers. They are also involved in autoimmune diseases, triple nucleotide repeat diseases, and diabetes, among others.Possible APOBEC signatures in aging tissues also highlight their potential contribution to this process at the genomic and epigenomic levels.Advances in gene-editing technologies combined with APOBEC mechanistic insights are ushering in the era of APOBECs as therapeutic targets, potentially closing the loop of negative versus positive gene-editing effects.

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“…We reasoned that a strategy which alters the sequence near methylation sites would enable m 6 A detection by standard RNA-seq and thus overcome the major limitations of current methods. APOBEC1 is a cytidine deaminase which targets DNA and RNA to induce cytidine to uridine (C to U) editing 7 . Although initially discovered for its ability to edit the ApoB mRNA, APOBEC1 has since been utilized in CRISPR/Cas9-based genome editing approaches to induce C to U conversion at targeted single-stranded DNA sites 8 .…”

Section: Introductionmentioning

confidence: 99%

Faculty Opinions recommendation of DART-seq: an antibody-free method for global m6A detection.

Smith

2020

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature

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m 6 A is a widespread RNA modification which influences nearly every aspect of the mRNA life cycle. Our understanding of m 6 A has been facilitated by the development of global m 6 A mapping methods, which use antibodies to immunoprecipitate methylated RNA. However, these methods have several limitations, including high input RNA requirements and cross-reactivity to other RNA modifications. Here, we present DART-Seq (deamination adjacent to RNA modification targets), an antibody-free method for detecting m 6 A sites. In DART-Seq, the cytidine deaminase APOBEC1 is fused to the m 6 A-binding YTH domain. APOBEC1-YTH expression in cells induces C to U deamination at sites adjacent to m 6 A residues, which are detected using standard RNA-Seq. DART-Seq identifies thousands of m 6 A sites in cells from as little as 10 nanograms of total RNA and can detect m 6 A accumulation in cells over time. Additionally, we use long-read DART-Seq to gain new insights into m 6 A distribution along the length of individual transcripts.

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The p27 catalytic subunit of the apolipoprotein B mRNA editing enzyme is a cytidine deaminase.

Cited by 262 publications

References 33 publications

The Neurofibromatosis Type I Messenger RNA Undergoes Base-Modification RNA Editing

The Neurofibromatosis Type I Messenger RNA Undergoes Base-Modification RNA Editing

APOBECs orchestrate genomic and epigenomic editing across health and disease

Faculty Opinions recommendation of DART-seq: an antibody-free method for global m6A detection.

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