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Aid/apobec

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https://www.readbyqxmd.com/read/28479091/family-wide-comparative-analysis-of-cytidine-and-methylcytidine-deamination-by-eleven-human-apobec-proteins
#1
Fumiaki Ito, Yang Fu, Shen-Chi A Kao, Hanjing Yang, Xiaojiang S Chen
Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) proteins are a family of cytidine deaminases involved in various important biological processes such as antibody diversification/maturation, restriction of viral infection, and generation of somatic mutations. Catalytically active APOBEC proteins execute their biological functions mostly through deaminating cytosine (C) to uracil on single-stranded DNA/RNA. Activation-induced cytidine deaminase, one of the APOBEC members, was reported to deaminate methylated cytosine (mC) on DNA, and this mC deamination was proposed to be involved in the demethylation of mC for epigenetic regulation...
May 4, 2017: Journal of Molecular Biology
https://www.readbyqxmd.com/read/28472485/apobec3a-efficiently-deaminates-methylated-but-not-tet-oxidized-cytosine-bases-in-dna
#2
Emily K Schutsky, Christopher S Nabel, Amy K F Davis, Jamie E DeNizio, Rahul M Kohli
AID/APOBEC family enzymes are best known for deaminating cytosine bases to uracil in single-stranded DNA, with characteristic sequence preferences that can produce mutational signatures in targets such as retroviral and cancer cell genomes. These deaminases have also been proposed to function in DNA demethylation via deamination of either 5-methylcytosine (mC) or TET-oxidized mC bases (ox-mCs), which include 5-hydroxymethylcytosine, 5-formylcytosine and 5-carboxylcytosine. One specific family member, APOBEC3A (A3A), has been shown to readily deaminate mC, raising the prospect of broader activity on ox-mCs...
May 2, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28439266/a-novel-regulator-of-activation-induced-cytidine-deaminase-apobecs-in-immunity-and-cancer-schr%C3%A3-dinger-s-catalytic-pocket
#3
REVIEW
Justin J King, Mani Larijani
Activation-induced cytidine deaminase (AID) and its relative APOBEC3 cytidine deaminases boost immune response by mutating immune or viral genes. Because of their genome-mutating activities, AID/APOBECs are also drivers of tumorigenesis. Due to highly charged surfaces, extensive non-specific protein-protein/nucleic acid interactions, formation of polydisperse oligomers, and general insolubility, structure elucidation of these proteins by X-ray crystallography and NMR has been challenging. Hence, almost all available AID/APOBEC structures are of mutated and/or truncated versions...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28405512/high-expression-of-pd-1-ligands-is-associated-with-kataegis-mutational-signature-and-apobec3-alterations
#4
Amélie Boichard, Igor F Tsigelny, Razelle Kurzrock
Immunotherapy with checkpoint inhibitors, such as antibodies blocking the programmed cell-death receptor-1 (PD-1), has resulted in remarkable responses in patients having traditionally refractory cancers. Although response to PD-1 inhibitors correlates with PD-1 ligand (PD-L1 or PD-L2) expression, PD-1 ligand positivity represents only a part of the predictive model necessary for selecting patients predisposed to respond to immunotherapy. We used all genomic, transcriptomic, proteomic and phenotypic data related to 8,475 pan-cancer samples available in The Cancer Genome Atlas (TCGA) and conducted a logistic regression analysis based on a large set of variables, such as microsatellite instability (MSI-H), mismatch repair (MMR) alterations, polymerase δ (POLD1) and polymerase ε (POLE) mutations, activation-induced/apolipoprotein-B editing cytidine deaminases (AID/APOBEC) alterations, lymphocyte markers and mutation burden estimates to determine independent factors that associate with PD-1 ligand overexpression...
2017: Oncoimmunology
https://www.readbyqxmd.com/read/28381554/dna-mutagenic-activity-and-capacity-for-hiv-1-restriction-of-the-cytidine-deaminase-apobec3g-depend-on-whether-dna-or-rna-binds-to-tyrosine-315
#5
Bogdan Polevoda, Rebecca Joseph, Alan E Friedman, Ryan P Bennett, Rebecca Greiner, Thareendra De Zoysa, Ryan A Stewart, Harold C Smith
APOBEC3G (A3G) belongs to the AID/APOBEC protein family of cytidine deaminases (CDA) that bind to nucleic acids. A3G mutates the HIV genome by deamination of dC to dU, leading to accumulation of virus-inactivating mutations. Binding to cellular RNAs inhibits A3G binding to substrate single-stranded (ss) DNA and CDA activity. Bulk RNA and substrate ssDNA bind to the same three A3G tryptic peptides (amino acids 181-194, 314-320, and 345-374) that form parts of a continuously exposed protein surface extending from the catalytic domain in the C terminus of A3G to its N terminus...
May 26, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28362825/the-preferred-nucleotide-contexts-of-the-aid-apobec-cytidine-deaminases-have-differential-effects-when-mutating-retrotransposon-and-virus-sequences-compared-to-host-genes
#6
Jeffrey Chen, Thomas MacCarthy
The AID / APOBEC genes are a family of cytidine deaminases that have evolved in vertebrates, and particularly mammals, to mutate RNA and DNA at distinct preferred nucleotide contexts (or "hotspots") on foreign genomes such as viruses and retrotransposons. These enzymes play a pivotal role in intrinsic immunity defense mechanisms, often deleteriously mutating invading retroviruses or retrotransposons and, in the case of AID, changing antibody sequences to drive affinity maturation. We investigate the strength of various hotspots on their known biological targets by evaluating the potential impact of mutations on the DNA coding sequences of these targets, and compare these results to hypothetical hotspots that did not evolve...
March 2017: PLoS Computational Biology
https://www.readbyqxmd.com/read/27815903/analysis-of-nuclear-uracil-dna-glycosylase-nudg-turnover-during-the-cell-cycle
#7
Jennifer A Fischer, Salvatore J Caradonna
Uracil-DNA glycosylases (UDG/UNG) are enzymes that remove uracil from DNA and initiate base-excision repair. These enzymes play a key role in maintaining genomic integrity by reducing the mutagenic events caused by G:C to A:T transition mutations. The recent finding that a family of RNA editing enzymes (AID/APOBECs) can deaminate cytosine in DNA has raised the interest in these base-excision repair enzymes. The methodology presented here focuses on determining the regulation of the nuclear isoform of uracil-DNA glycosylase (nUDG), a 36,000 Da protein...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27716525/activation-induced-cytidine-deaminase-mutant-aid-his130pro-from-hyper-igm-2-patient-retained-mutagenic-activity-on-shm-artificial-substrate
#8
Hanen Ouadani, Imen Ben-Mustapha, Meriem Ben-Ali, Beya Larguèche, Tihana Jovanic, Sylvie Garcia, Benoit Arcangioli, Houda Elloumi-Zghal, Dahmani Fathallah, Mongia Hachicha, Hatem Masmoudi, François Rougeon, Mohamed-Ridha Barbouche
Activation induced cytidine deaminase (AID) is an essential enzyme for class switch recombination (CSR) and somatic hypermutation (SHM) during secondary immune response. Mutations in the AICDA gene are responsible for Hyper IgM 2 syndrome where both CSR and SHM or only CSR are affected. Indeed, triggering either of the two mechanisms requires the DNA deamination activity of AID. Besides, different domains of AID may be differentially involved in CSR and SHM through their interaction with specific cofactors...
November 2016: Molecular Immunology
https://www.readbyqxmd.com/read/27585283/functions-and-malfunctions-of-mammalian-dna-cytosine-deaminases
#9
REVIEW
Sachini U Siriwardena, Kang Chen, Ashok S Bhagwat
The AID/APOBEC family enzymes convert cytosines in single-stranded DNA to uracils, causing base substitutions and strand breaks. They are induced by cytokines produced during the body's inflammatory response to infections, and they help combat infections through diverse mechanisms. AID is essential for the maturation of antibodies and causes mutations and deletions in antibody genes through somatic hypermutation (SHM) and class-switch recombination (CSR) processes. One member of the APOBEC family, APOBEC1, edits mRNA for a protein involved in lipid transport...
October 26, 2016: Chemical Reviews
https://www.readbyqxmd.com/read/27527602/aid-apobec-network-reconstruction-identifies-pathways-associated-with-survival-in-ovarian-cancer
#10
Martin Svoboda, Anastasia Meshcheryakova, Georg Heinze, Markus Jaritz, Dietmar Pils, Dan Cacsire Castillo-Tong, Gudrun Hager, Theresia Thalhammer, Erika Jensen-Jarolim, Peter Birner, Ioana Braicu, Jalid Sehouli, Sandrina Lambrechts, Ignace Vergote, Sven Mahner, Philip Zimmermann, Robert Zeillinger, Diana Mechtcheriakova
BACKGROUND: Building up of pathway-/disease-relevant signatures provides a persuasive tool for understanding the functional relevance of gene alterations and gene network associations in multifactorial human diseases. Ovarian cancer is a highly complex heterogeneous malignancy in respect of tumor anatomy, tumor microenvironment including pro-/antitumor immunity and inflammation; still, it is generally treated as single disease. Thus, further approaches to investigate novel aspects of ovarian cancer pathogenesis aiming to provide a personalized strategy to clinical decision making are of high priority...
August 16, 2016: BMC Genomics
https://www.readbyqxmd.com/read/27485054/association-between-targeted-somatic-mutation-tsm-signatures-and-hgs-ovca-progression
#11
Robyn A Lindley, Patrick Humbert, Cliff Larner, Eric H Akmeemana, Christopher R R Pendlebury
Evidence already exists that the activation-induced cytidine deaminase (AID/APOBEC) and the adenosine deaminase (ADAR) families of enzymes are implicated as powerful mutagens in oncogenic processes in many somatic tissues. Each deaminase is identified by the DNA or RNA nucleotide sequence ("motif") surrounding the nucleotide targeted for deamination. The primary objective of this study is to develop an in silico approach to identify nucleotide sequence changes of the target motifs of key deaminases during oncogenesis...
September 2016: Cancer Medicine
https://www.readbyqxmd.com/read/27258794/structural-analysis-of-the-activation-induced-deoxycytidine-deaminase-required-in-immunoglobulin-diversification
#12
Phuong Pham, Samir A Afif, Mayuko Shimoda, Kazuhiko Maeda, Nobuo Sakaguchi, Lars C Pedersen, Myron F Goodman
Activation-induced deoxycytidine deaminase (AID) initiates somatic hypermutation (SHM) and class-switch recombination (CSR) by deaminating C→U during transcription of Ig-variable (V) and Ig-switch (S) region DNA, which is essential to produce high-affinity antibodies. Here we report the crystal structure of a soluble human AID variant at 2.8Å resolution that favors targeting WRC motifs (W=A/T, R=A/G) in vitro, and executes Ig V SHM in Ramos B-cells. A specificity loop extending away from the active site to accommodate two purine bases next to C, differs significantly in sequence, length, and conformation from APOBEC proteins Apo3A and Apo3G, which strongly favor pyrimidines at -1 and -2 positions...
July 2016: DNA Repair
https://www.readbyqxmd.com/read/27249646/apobec4-enhances-the-replication-of-hiv-1
#13
Daniela Marino, Mario Perković, Anika Hain, Ananda A Jaguva Vasudevan, Henning Hofmann, Kay-Martin Hanschmann, Michael D Mühlebach, Gerald G Schumann, Renate König, Klaus Cichutek, Dieter Häussinger, Carsten Münk
APOBEC4 (A4) is a member of the AID/APOBEC family of cytidine deaminases. In this study we found a high mRNA expression of A4 in human testis. In contrast, there were only low levels of A4 mRNA detectable in 293T, HeLa, Jurkat or A3.01 cells. Ectopic expression of A4 in HeLa cells resulted in mostly cytoplasmic localization of the protein. To test whether A4 has antiviral activity similar to that of proteins of the APOBEC3 (A3) subfamily, A4 was co-expressed in 293T cells with wild type HIV-1 and HIV-1 luciferase reporter viruses...
2016: PloS One
https://www.readbyqxmd.com/read/27235683/germinal-center-b-cell-associated-nuclear-protein-ganp-involved-in-rna-metabolism-for-b-cell-maturation
#14
N Sakaguchi, K Maeda
Germinal center B-cell-associated nuclear protein (GANP) is upregulated in germinal center B cells against T-cell-dependent antigens in mice and humans. In mice, GANP depletion in B cells impairs antibody affinity maturation. Conversely, its transgenic overexpression augments the generation of high-affinity antigen-specific B cells. GANP associates with AID in the cytoplasm, shepherds AID into the nucleus, and augments its access to the rearranged immunoglobulin (Ig) variable (V) region of the genome in B cells, thereby precipitating the somatic hypermutation of V region genes...
2016: Advances in Immunology
https://www.readbyqxmd.com/read/27056836/clustered-mutations-in-hominid-genome-evolution-are-consistent-with-apobec3g-enzymatic-activity
#15
Yishay Pinto, Orshay Gabay, Leonardo Arbiza, Aaron J Sams, Alon Keinan, Erez Y Levanon
The gradual accumulation of mutations by any of a number of mutational processes is a major driving force of divergence and evolution. Here, we investigate a potentially novel mutational process that is based on the activity of members of the AID/APOBEC family of deaminases. This gene family has been recently shown to introduce-in multiple types of cancer-enzyme-induced clusters of co-occurring somatic mutations caused by cytosine deamination. Going beyond somatic mutations, we hypothesized that APOBEC3-following its rapid expansion in primates-can introduce unique germline mutation clusters that can play a role in primate evolution...
May 2016: Genome Research
https://www.readbyqxmd.com/read/26926109/primpol-prevents-apobec-aid-family-mediated-dna-mutagenesis
#16
Bas Pilzecker, Olimpia Alessandra Buoninfante, Colin Pritchard, Olga S Blomberg, Ivo J Huijbers, Paul C M van den Berk, Heinz Jacobs
PrimPol is a DNA damage tolerant polymerase displaying both translesion synthesis (TLS) and (re)-priming properties. This led us to study the consequences of a PrimPol deficiency in tolerating mutagenic lesions induced by members of the APOBEC/AID family of cytosine deaminases. Interestingly, during somatic hypermutation, PrimPol counteracts the generation of C>G transversions on the leading strand. Independently, mutation analyses in human invasive breast cancer confirmed a pro-mutagenic activity of APOBEC3B and revealed a genome-wide anti-mutagenic activity of PRIMPOL as well as most Y-family TLS polymerases...
June 2, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/26843430/an-interplay-of-the-base-excision-repair-and-mismatch-repair-pathways-in-active-dna-demethylation
#17
Inga Grin, Alexander A Ishchenko
Active DNA demethylation (ADDM) in mammals occurs via hydroxylation of 5-methylcytosine (5mC) by TET and/or deamination by AID/APOBEC family enzymes. The resulting 5mC derivatives are removed through the base excision repair (BER) pathway. At present, it is unclear how the cell manages to eliminate closely spaced 5mC residues whilst avoiding generation of toxic BER intermediates and whether alternative DNA repair pathways participate in ADDM. It has been shown that non-canonical DNA mismatch repair (ncMMR) can remove both alkylated and oxidized nucleotides from DNA...
May 5, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/26608778/dna-editing-by-apobecs-a-genomic-preserver-and-transformer
#18
REVIEW
Binyamin A Knisbacher, Doron Gerber, Erez Y Levanon
Information warfare is not limited to the cyber world because it is waged within our cells as well. The unique AID (activation-induced cytidine deaminase)/APOBEC (apolipoprotein B mRNA editing enzyme, catalytic polypeptide) family comprises proteins that alter DNA sequences by converting deoxycytidines to deoxyuridines through deamination. This C-to-U DNA editing enables them to inhibit parasitic viruses and retrotransposons by disrupting their genomic content. In addition to attacking genomic invaders, APOBECs can target their host genome, which can be beneficial by initiating processes that create antibody diversity needed for the immune system or by accelerating the rate of evolution...
January 2016: Trends in Genetics: TIG
https://www.readbyqxmd.com/read/26476745/apobec3b-high-expression-status-is-associated-with-aggressive-phenotype-in-japanese-breast-cancers
#19
Miki Tsuboi, Arito Yamane, Jun Horiguchi, Takehiko Yokobori, Reika Kawabata-Iwakawa, Shinji Yoshiyama, Susumu Rokudai, Hiroki Odawara, Hideaki Tokiniwa, Tetsunari Oyama, Izumi Takeyoshi, Masahiko Nishiyama
BACKGROUND: The members of AID/APOBEC protein family possess cytidine deaminase activity that converts cytidine residue to uridine on DNA and RNA. Recent studies have shown the possible influence of APOBEC3B (A3B) as DNA mutators of breast cancer genome. However, the clinical significance of A3B expression in Japanese breast cancer has not been studied in detail. METHODS: Ninety-three primary breast cancer tissues (74 estrogen-receptor (ER) positive, 3 ER and HER2 positive, 6 HER2 positive, and 10 triple negative) including 37 tumor-normal pairs were assessed for A3B mRNA expression using quantitative real-time RT-PCR...
September 2016: Breast Cancer: the Journal of the Japanese Breast Cancer Society
https://www.readbyqxmd.com/read/26281709/characterization-of-the-catalytic-domain-of-human-apobec3b-and-the-critical-structural-role-for-a-conserved-methionine
#20
Sachini U Siriwardena, Thisari A Guruge, Ashok S Bhagwat
Human APOBEC3B deaminates cytosines in DNA and belongs to the AID/APOBEC family of enzymes. These proteins are involved in innate and adaptive immunity and may cause mutations in a variety of cancers. To characterize its ability to convert cytosines into uracils, we tested several derivatives of APOBEC3B gene for their ability to cause mutations in Escherichia coli. Through this analysis, a methionine residue at the junction of the amino-terminal domain (NTD) and the carboxy-terminal domain (CTD) was found to be essential for high mutagenicity...
September 25, 2015: Journal of Molecular Biology
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