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Journal articles

Academic literature on the topic 'APOBEC family'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "APOBEC family"

1

Dang, Ying, Xiaojun Wang, Walter J. Esselman, and Yong-Hui Zheng. "Identification of APOBEC3DE as Another Antiretroviral Factor from the Human APOBEC Family." Journal of Virology 80, no. 21 (2006): 10522–33. http://dx.doi.org/10.1128/jvi.01123-06.

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ABSTRACT A tandem arrayed gene cluster encoding seven cytidine deaminase genes is present on human chromosome 22. These are APOBEC3A, APOBEC3B, APOBEC3C, APOBEC3DE, APOBEC3F, APOBEC3G, and APOBEC3H. Three of them, APOBEC3G, APOBEC3F, and APOBEC3B, block replication of human immunodeficiency virus type 1 (HIV-1) and many other retroviruses. In addition, APOBEC3A and APOBEC3C block intracellular retrotransposons and simian immunodeficiency virus (SIV), respectively. In opposition to APOBEC genes, HIV-1 and SIV contain a virion infectivity factor (Vif) that targets APOBEC3F and APOBEC3G for polyu

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2

Chu, Charles C., Stefano Vergani, Xiao-Jie Yan, et al. "APOBEC gene family expression and hallmarks in chronic lymphocytic leukemia." Journal of Immunology 198, no. 1_Supplement (2017): 76.16. http://dx.doi.org/10.4049/jimmunol.198.supp.76.16.

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Abstract The hallmark activity of APOBEC (apolipoprotein B mRNA editing enzyme, catalytic polypeptide) family of cytidine deaminases, including activation-induced deaminase (AID) and APOBEC3 genes, has been detected in somatic mutation signatures by ultra-deep sequencing of the genomes of many cancers, including chronic lymphocytic leukemia (CLL). The acquisition of these mutations is hypothesized to lead to the progression towards aggressive disease in cancer. To examine this in CLL, we tested if increased APOBEC family member gene expression in CLL cells, as measured by microarray and quanti

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3

Caswell, Deborah, and Charles Swanton. "Distinct Mutagenic Activity of APOBEC3G Cytidine Deaminase Identified in Bladder Cancer." Cancer Research 83, no. 4 (2023): 487–88. http://dx.doi.org/10.1158/0008-5472.can-22-3598.

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Abstract The APOBEC cytidine deaminase enzyme family is linked to mutational signatures identified in cancer. While previous work has provided insights into the role of APOBEC3A and APOBEC3B in mutational processes in cancer, understanding of the mutational signatures induced by other APOBEC family members is limited. In this issue of Cancer Research, Liu and colleagues investigated the role of APOBEC3G (A3G) in bladder cancer. The authors revealed that transgenic expression of A3G in a murine bladder cancer model promotes tumorigenesis and induces a unique mutational signature distinct from p

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4

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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5

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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6

Harris, Reuben S., Matthew C. Jarvis, Michael A. Carpenter, et al. "Abstract P5-12-01: Apobec mutation signature in breast cancer explained by combinatorial action of apobec3a and apobec3b." Cancer Research 82, no. 4_Supplement (2022): P5–12–01—P5–12–01. http://dx.doi.org/10.1158/1538-7445.sabcs21-p5-12-01.

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Abstract Background: Mutations drive the initiation and progression of cancer. A leading druggable source of mutation in cancer is enzymatic deamination of single-stranded DNA cytosines by cellular APOBEC3 enzymes. Cytosine-to-uracil deamination can result in a variety of different mutational outcomes including DNA breakage and chromosomal aberrations as well as single base substitution mutations. The latter are comprised of C-to-T and C-to-G mutations in TCA or TCT trinucleotides and attributable to the intrinsic preference of several APOBEC3 family members for binding to these motifs. This m

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7

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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8

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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9

Köck, Josef, and Hubert E. Blum. "Hypermutation of hepatitis B virus genomes by APOBEC3G, APOBEC3C and APOBEC3H." Journal of General Virology 89, no. 5 (2008): 1184–91. http://dx.doi.org/10.1099/vir.0.83507-0.

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Hepatitis B virus (HBV) is a DNA virus that causes liver disease and replicates by reverse transcription of an RNA template. Previous studies have reported that HBV genomes bearing G→A hypermutation are present at low frequency in human serum. These mutations are most likely due to the activity of apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like (APOBEC) cytosine deaminases, cellular proteins known to confer innate immunity against retroviruses by generating lethal hypermutations in viral genomes. This study assessed APOBEC3G, APOBEC3C and APOBEC3H, three members of this protein

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10

Granadillo Rodríguez, Milaid, Ben Flath, and Linda Chelico. "The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead." Open Biology 10, no. 12 (2020): 200188. http://dx.doi.org/10.1098/rsob.200188.

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Cancer is considered a group of diseases characterized by uncontrolled growth and spread of abnormal cells and is propelled by somatic mutations. Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) family of enzymes are endogenous sources of somatic mutations found in multiple human cancers. While these enzymes normally act as an intrinsic immune defence against viruses, they can also catalyse ‘off-target’ cytidine deamination in genomic single-stranded DNA intermediates. The deamination of cytosine forms uracil, which is promutagenic in DNA. Key factors to trigger the

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