Relevant bibliographies by topics / AID/APOBEC family, APOBEC1, APOBEC3A, RNA editing

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'AID/APOBEC family, APOBEC1, APOBEC3A, RNA editing'

Author: Grafiati
Published: 14 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "AID/APOBEC family, APOBEC1, APOBEC3A, RNA editing"

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Mikl, Marie C., Ian N. Watt, Mason Lu, et al. "Mice Deficient in APOBEC2 and APOBEC3." Molecular and Cellular Biology 25, no. 16 (2005): 7270–77. http://dx.doi.org/10.1128/mcb.25.16.7270-7277.2005.

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ABSTRACT The activation-induced deaminase/apolipoprotein B-editing catalytic subunit 1 (AID/APOBEC) family comprises four groups of proteins. Both AID, a lymphoid-specific DNA deaminase that triggers antibody diversification, and APOBEC2 (function unknown) are found in all vertebrates examined. In contrast, APOBEC1, an RNA-editing enzyme in gastrointestinal cells, and APOBEC3 are restricted to mammals. The function of most APOBEC3s, of which there are seven in human but one in mouse, is unknown, although several human APOBEC3s act as host restriction factors that deaminate human immunodeficien
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Chu, Charles C., Xiao-Jie Yan, Arvind Dhayalan, et al. "The Correlation of APOBEC Gene Family Member Expression with Worse CLL Patient Outcome Suggests a Role in CLL Mutational Evolution." Blood 126, no. 23 (2015): 363. http://dx.doi.org/10.1182/blood.v126.23.363.363.

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Abstract A mutational signature consistent with APOBEC (apolipoprotein B mRNA editing enzyme, catalytic polypeptide) activity has been identified in somatic mutations found in large-scale surveys of ultra-deep sequencing data from many human cancers including chronic lymphocytic leukemia (CLL). APOBEC is a cytidine deaminase family made up of eleven genes, including AID (activation-induced cytidine deaminase) and APOBEC3B, both of which have been implicated in somatic mutation in various cancers, including CLL. These observations have led to the hypothesis that APOBEC cytidine deaminases may b
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Talluri, Srikanth, Mehmet Kemal Samur, Jialan Shi, et al. "Critical Role for Apobec and Its Interacting Partners in Mediating Mutations and Cell Growth in Multiple Myeloma (MM)." Blood 132, Supplement 1 (2018): 4462. http://dx.doi.org/10.1182/blood-2018-99-118441.

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Abstract The APOBEC family of cytidine deaminases include AID (activity induced deaminase) and 10 related APOBEC enzymes (A1,A2,A3A,A3B,A3C,A3D,A3F,A3G,A3H and A4). AID is well studied for its role in somatic hyper mutation and class switch recombination of immunoglobulin genes. APOBECs (apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like) have been shown to have roles in mRNA editing and in antiviral immunity. Recently, a causal role for the AID/APOBECs in inducing somatic mutations in myeloma has been proposed and we have previously published that APOBEC signature mutations as a
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Naumann, Jordan A., Prokopios P. Argyris, Michael A. Carpenter, et al. "DNA Deamination Is Required for Human APOBEC3A-Driven Hepatocellular Carcinoma In Vivo." International Journal of Molecular Sciences 24, no. 11 (2023): 9305. http://dx.doi.org/10.3390/ijms24119305.

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Although the APOBEC3 family of single-stranded DNA cytosine deaminases is well-known for its antiviral factors, these enzymes are rapidly gaining attention as prominent sources of mutation in cancer. APOBEC3′s signature single-base substitutions, C-to-T and C-to-G in TCA and TCT motifs, are evident in over 70% of human malignancies and dominate the mutational landscape of numerous individual tumors. Recent murine studies have established cause-and-effect relationships, with both human APOBEC3A and APOBEC3B proving capable of promoting tumor formation in vivo. Here, we investigate the molecular
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5

Malim, Michael H. "APOBEC proteins and intrinsic resistance to HIV-1 infection." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1517 (2008): 675–87. http://dx.doi.org/10.1098/rstb.2008.0185.

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Members of the APOBEC family of cellular polynucleotide cytidine deaminases, most notably APOBEC3G and APOBEC3F, are potent inhibitors of HIV-1 infection. Wild type HIV-1 infections are largely spared from APOBEC3G/F function through the action of the essential viral protein, Vif. In the absence of Vif, APOBEC3G/F are encapsidated by budding virus particles leading to excessive cytidine (C) to uridine (U) editing of negative sense reverse transcripts in newly infected cells. This registers as guanosine (G) to adenosine (A) hypermutations in plus-stranded cDNA. In addition to this profoundly de
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Talluri, Srikanth, Mehmet Kemal Samur, Leutz Buon, et al. "Dysregulated Aid/Apobec Family Proteins Promote Genomic Instability in Multiple Myeloma." Blood 128, no. 22 (2016): 803. http://dx.doi.org/10.1182/blood.v128.22.803.803.

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Abstract The AID/APOBEC family of cytidine deaminase proteins includes AID (activity induced deaminase), and 10 related APOBEC enzymes (A1, A2, A3A, A3B, A3C, A3D, A3F, A3G, A3H and A4). AID has been well-studied for its role in somatic hyper mutation and class switch recombination of immunoglobulin genes whereas APOBECs (apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like) have been shown to have roles in mRNA editing and in antiviral immunity. Dysregulated activity of APOBECs causes C >T transitions or C>G, C>A transversions in DNA. We have recently shown APOBEC signatu
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7

Vieira, Valdimara C., and Marcelo A. Soares. "The Role of Cytidine Deaminases on Innate Immune Responses against Human Viral Infections." BioMed Research International 2013 (2013): 1–18. http://dx.doi.org/10.1155/2013/683095.

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The APOBEC family of proteins comprises deaminase enzymes that edit DNA and/or RNA sequences. The APOBEC3 subgroup plays an important role on the innate immune system, acting on host defense against exogenous viruses and endogenous retroelements. The role of APOBEC3 proteins in the inhibition of viral infection was firstly described for HIV-1. However, in the past few years many studies have also shown evidence of APOBEC3 action on other viruses associated with human diseases, including HTLV, HCV, HBV, HPV, HSV-1, and EBV. APOBEC3 inhibits these viruses through a series of editing-dependent an
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8

Kazuma, Yasuhiro, Kotaro Shirakawa, Anamaria Daniela Sarca, et al. "Interactome Analysis of APOBEC3B in Multiple Myeloma." Blood 134, Supplement_1 (2019): 1259. http://dx.doi.org/10.1182/blood-2019-126856.

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Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) family proteins restrict retroviruses and retrotransposons by inducing hypermutation or degradation of the replication intermediates through their DNA cytidine deaminase activity. APOBECs can also act as endogenous sources of DNA damage that mutate many human cancers. Accumulation of APOBEC signature mutations is associated with disease progression and poor overall survival in multiple myeloma (Walker et al. Nat Commun, 2015). Among APOBEC3 enzymes, APOBEC3B (A3B) is the only family member that is predominantly located in
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Bulliard, Yannick, Priscilla Turelli, Ute F. Röhrig, et al. "Functional Analysis and Structural Modeling of Human APOBEC3G Reveal the Role of Evolutionarily Conserved Elements in the Inhibition of Human Immunodeficiency Virus Type 1 Infection and Alu Transposition." Journal of Virology 83, no. 23 (2009): 12611–21. http://dx.doi.org/10.1128/jvi.01491-09.

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ABSTRACT Retroelements are important evolutionary forces but can be deleterious if left uncontrolled. Members of the human APOBEC3 family of cytidine deaminases can inhibit a wide range of endogenous, as well as exogenous, retroelements. These enzymes are structurally organized in one or two domains comprising a zinc-coordinating motif. APOBEC3G contains two such domains, only the C terminal of which is endowed with editing activity, while its N-terminal counterpart binds RNA, promotes homo-oligomerization, and is necessary for packaging into human immunodeficiency virus type 1 (HIV-1) virions
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10

Lerner, Taga, F. Papavasiliou, and Riccardo Pecori. "RNA Editors, Cofactors, and mRNA Targets: An Overview of the C-to-U RNA Editing Machinery and Its Implication in Human Disease." Genes 10, no. 1 (2018): 13. http://dx.doi.org/10.3390/genes10010013.

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One of the most prevalent epitranscriptomic modifications is RNA editing. In higher eukaryotes, RNA editing is catalyzed by one of two classes of deaminases: ADAR family enzymes that catalyze A-to-I (read as G) editing, and AID/APOBEC family enzymes that catalyze C-to-U. ADAR-catalyzed deamination has been studied extensively. Here we focus on AID/APOBEC-catalyzed editing, and review the emergent knowledge regarding C-to-U editing consequences in the context of human disease.
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Dissertations / Theses on the topic "AID/APOBEC family, APOBEC1, APOBEC3A, RNA editing"

1

Torrini, Serena. "Physiological and pathological perspectives in the biology of APOBEC deaminases." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1194433.

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The thesis is focus on RNA editing mediated by two AID/APOBEC family members. The aim of my work was the investigation of possible novel factors that regulate hAPOBEC1 expression or cofactors which help the deaminase to exert its activity. First, I characterised cellular models for their proliferation and clonogenic activities as well as cell cycle distribution evaluating a combinatorial effect of hAPOBEC1 and RBM47 which lead to a decrease in cell growth. I investigated the role of RNA editing beyond the lipid transport by high-throughput sequencing which provided me information regarding n
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