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https://www.readbyqxmd.com/read/28900073/-molecular-mechanisms-of-hiv-1-genetic-diversity
#1
D V Sosin, N A Tchurikov
High genetic diversity of HIV-1 is the main factor behind the fact that HIV infection is widespread and difficult to treat. Although a limited number (or only one) of virus particles enters the blood upon infection, the particles are replicated in infected cells and rapidly produce new genetic variants that are resistant to the host immune system and antiretroviral drugs. This circumstance hampers the development of anti-HIV-1 vaccines and requires new antiretroviral drugs to be designed. The cause of the high variation of HIV-1 is related to the properties of its reverse transcriptase, which is error prone and often makes mistakes when transcribing virus RNA...
July 2017: Molekuliarnaia Biologiia
https://www.readbyqxmd.com/read/28889380/detection-of-apobec3-proteins-and-catalytic-activity-in-urothelial-carcinoma
#2
Ananda Ayyappan Jaguva Vasudevan, Wolfgang Goering, Dieter Häussinger, Carsten Münk
Members of the APOBEC3 (A3) family of enzymes were shown to act in an oncogenic manner in several cancer types. Immunodetection of APOBEC3A (A3A), APOBEC3B (A3B), and APOBEC3G (A3G) proteins is particularly challenging due to the large sequence homology of these proteins and limited availability of antibodies. Here we combine independent immunoblotting with an in vitro activity assay technique, to detect and categorize specific A3s expressed in urothelial bladder cancer and other cancer cells.
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28883657/deamination-independent-restriction-of-line-1-retrotransposition-by-apobec3h
#3
Yuqing Feng, Mariam H Goubran, Tyson B Follack, Linda Chelico
The APOBEC3 family of cytosine deaminase enzymes are able to restrict replication of retroelements, such as LINE-1. However, each of the seven APOBEC3 enzymes have been reported to act differentially to prevent LINE-1 retrotransposition and the mechanisms of APOBEC3-mediated LINE-1 inhibition has not been well understood. The prevailing view for many years was that APOBEC3-mediated LINE-1 inhibition was deamination-independent and relied on APOBEC3s blocking the LINE-1 reverse transcriptase DNA polymerization or transport of the LINE-1 RNA into the nucleus...
September 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28878238/apobec3a-is-an-oral-cancer-prognostic-biomarker-in-taiwanese-carriers-of-an-apobec-deletion-polymorphism
#4
Ting-Wen Chen, Chi-Ching Lee, Hsuan Liu, Chi-Sheng Wu, Curtis R Pickering, Po-Jung Huang, Jing Wang, Ian Yi-Feng Chang, Yuan-Ming Yeh, Chih-De Chen, Hsin-Pai Li, Ji-Dung Luo, Bertrand Chin-Ming Tan, Timothy En Haw Chan, Chuen Hsueh, Lichieh Julie Chu, Yi-Ting Chen, Bing Zhang, Chia-Yu Yang, Chih-Ching Wu, Chia-Wei Hsu, Lai-Chu See, Petrus Tang, Jau-Song Yu, Wei-Chao Liao, Wei-Fan Chiang, Henry Rodriguez, Jeffrey N Myers, Kai-Ping Chang, Yu-Sun Chang
Oral squamous cell carcinoma is a prominent cancer worldwide, particularly in Taiwan. By integrating omics analyses in 50 matched samples, we uncover in Taiwanese patients a predominant mutation signature associated with cytidine deaminase APOBEC, which correlates with the upregulation of APOBEC3A expression in the APOBEC3 gene cluster at 22q13. APOBEC3A expression is significantly higher in tumors carrying APOBEC3B-deletion allele(s). High-level APOBEC3A expression is associated with better overall survival, especially among patients carrying APOBEC3B-deletion alleles, as examined in a second cohort (n = 188; p = 0...
September 6, 2017: Nature Communications
https://www.readbyqxmd.com/read/28841445/apobec3b-lysine-residues-are-dispensable-for-dna-cytosine-deamination-hiv-1-restriction-and-nuclear-localization
#5
Amy M Molan, Heather M Hanson, Cynthia M Chweya, Brett D Anderson, Gabriel J Starrett, Christopher M Richards, Reuben S Harris
The APOBEC3 DNA cytosine deaminase family comprises a fundamental arm of the innate immune response and is best known for retrovirus restriction. Several APOBEC3 enzymes restrict HIV-1 and related retroviruses by deaminating viral cDNA cytosines to uracils compromising viral genomes. Human APOBEC3B (A3B) shows strong virus restriction activities in a variety of experimental systems, and is subjected to tight post-translational regulation evidenced by cell-specific HIV-1 restriction activity and active nuclear import...
August 22, 2017: Virology
https://www.readbyqxmd.com/read/28825755/influence-of-the-dna-sequence-length-and-ph-on-deaminase-activity-as-well-as-the-roles-of-the-amino-acid-residues-around-the-catalytic-center-of-apobec3f
#6
Li Wan, Takashi Nagata, Masato Katahira
APOBEC3F (A3F), an apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) family protein, catalyzes cytosine-to-uracil conversion in single-stranded (ss) DNA. A3F acts as an inhibitor of retrovirus replication and exhibits antiviral activity against viral infectivity factor (Vif)-deficient human immunodeficiency virus 1 (HIV-1). Previous studies have mostly been focused on the interaction between A3F and Vif, and the studies on A3F's deamination properties are limited. Here, we report comprehensive characterization of the deaminase activity and ssDNA binding of the C-terminal domain (CTD) of A3F...
August 21, 2017: Physical Chemistry Chemical Physics: PCCP
https://www.readbyqxmd.com/read/28825669/roles-of-apobec3a-and-apobec3b-in-human-papillomavirus-infection-and-disease-progression
#7
REVIEW
Cody J Warren, Joseph A Westrich, Koenraad Van Doorslaer, Dohun Pyeon
The apolipoprotein B messenger RNA-editing, enzyme-catalytic, polypeptide-like 3 (APOBEC3) family of cytidine deaminases plays an important role in the innate immune response to viral infections by editing viral genomes. However, the cytidine deaminase activity of APOBEC3 enzymes also induces somatic mutations in host genomes, which may drive cancer progression. Recent studies of human papillomavirus (HPV) infection and disease outcome highlight this duality. HPV infection is potently inhibited by one family member, APOBEC3A...
August 21, 2017: Viruses
https://www.readbyqxmd.com/read/28809145/moderate-sensitivity-of-mouse-mammary-tumour-virus-to-inhibition-by-human-apobec3g
#8
Constantine James Konstantoulas, Benedikt Hagen, Stanislav Indik
Infectivity of the mouse mammary tumour virus (MMTV) is inhibited by mouse APOBEC3 (mA3) which is efficiently packaged into virions. As the inhibition is only partial, the virus can replicate in tissues expressing mA3 and complete its replication cycle. Here, we have examined the sensitivity of MMTV to inhibition by a human orthologue of mA3, A3G. We report that the virus containing A3G is only moderately susceptible to inhibition by the human factor. Whereas the vif-deficient HIV-1 vector produced in human epithelial cells expressing endogenous levels of A3G was efficiently inhibited, an MMTV vector remained fully infectious...
September 2017: Journal of General Virology
https://www.readbyqxmd.com/read/28794032/recombinant-origins-of-pathogenic-and-nonpathogenic-mouse-gammaretroviruses-of-polytropic-host-range
#9
Devinka Bamunusinghe, Qingping Liu, Ronald Plishka, Michael A Dolan, Matthew Skorski, Andrew J Oler, Venkat R K Yedavalli, Alicia Buckler-White, Janet W Hartley, Christine A Kozak
Ecotropic, xenotropic and polytropic mouse leukemia viruses (E-, X-, P-MLVs) exist in mice as infectious viruses and endogenous retroviruses (ERVs) inserted into mouse chromosomes. All 3 MLV subgroups are linked to leukemogenesis, which involves generation of recombinants with polytropic host range. Although P-MLVs are deemed to be the proximal agents of disease induction, few biologically characterized infectious P-MLVs have been sequenced for comparative analysis. We analyzed the complete genomes of 16 naturally occurring infectious P-MLVs, 12 of which were typed for pathogenic potential...
August 9, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28767398/the-30-kb-deletion-in-the-apobec3-cluster-decreases-apobec3a-and-apobec3b-expression-and-creates-a-transcriptionally-active-hybrid-gene-but-does-not-associate-with-breast-cancer-in-the-european-population
#10
Katarzyna Klonowska, Wojciech Kluzniak, Bogna Rusak, Anna Jakubowska, Magdalena Ratajska, Natalia Krawczynska, Danuta Vasilevska, Karol Czubak, Marzena Wojciechowska, Cezary Cybulski, Jan Lubinski, Piotr Kozlowski
APOBEC3B, in addition to other members of the APOBEC3 gene family, has recently been intensively studied due to its identification as a gene whose activation in cancer is responsible for a specific pattern of massively occurring somatic mutations. It was recently shown that a common large deletion in the APOBEC3 cluster (the APOBEC3B deletion) may increase the risk of breast cancer. However, conflicting evidence regarding this association was also reported. In the first step of our study, using different approaches, including an in-house designed multiplex ligation-dependent probe amplification assay, we analyzed the structure of the deletion and showed that although the breakpoints are located in highly homologous regions, which may generate recurrent occurrence of similar but not identical deletions, there is no sign of deletion heterogeneity...
July 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/28655787/cytosine-deaminase-apobec3a-sensitizes-leukemia-cells-to-inhibition-of-the-dna-replication-checkpoint
#11
Abby M Green, Konstantin Budagyan, Katharina E Hayer, Morgann A Reed, Milan R Savani, Gerald B Wertheim, Matthew D Weitzman
Mutational signatures in cancer genomes have implicated the APOBEC3 cytosine deaminases in oncogenesis, possibly offering a therapeutic vulnerability. Elevated APOBEC3B expression has been detected in solid tumors, but expression of APOBEC3A (A3A) in cancer has not been described to date. Here, we report that A3A is highly expressed in subsets of pediatric and adult acute myelogenous leukemia (AML). We modeled A3A expression in the THP1 AML cell line by introducing an inducible A3A gene. A3A expression caused ATR-dependent phosphorylation of Chk1 and cell-cycle arrest, consistent with replication checkpoint activation...
September 1, 2017: Cancer Research
https://www.readbyqxmd.com/read/28646470/apobec3b-and-il-6-form-a-positive-feedback-loop-in-hepatocellular-carcinoma-cells
#12
Shuran Li, Xueyang Bao, Duowei Wang, Linjun You, Xianjing Li, Hongbao Yang, Jinsong Bian, Yun Wang, Yong Yang
APOBEC3 protein families, a DNA cytidine deaminase, were up-regulated in multiple tumors. However, the relationship between Hepatocellular carcinoma (HCC) and APOBEC3B (A3B) remains unknown. It has been confirmed that interleukin-6 (IL-6) has significant impacts on oncogenesis of HCC. Here, we reported that the expression of IL-6 was substantially up-regulated by A3B in HepG2 cells. A3B induced IL-6 expression through relocating HuR to enhance the IL-6 mRNA stability. Further analysis indicated that IL-6 also increased the expression of A3B through JAK1/STAT3 signaling pathway, which formed a positive feedback to maintain the continuous expression of A3B and IL-6, and thereby promoted the prolonged non-resolving inflammation...
May 29, 2017: Science China. Life Sciences
https://www.readbyqxmd.com/read/28637869/heat-shock-proteins-stimulate-apobec-3-mediated-cytidine-deamination-in-the-hepatitis-b-virus
#13
COMPARATIVE STUDY
Zhigang Chen, Thomas L Eggerman, Alexander V Bocharov, Irina N Baranova, Tatyana G Vishnyakova, Roger Kurlander, Amy P Patterson
Apolipoprotein B mRNA-editing enzyme catalytic subunit 3 (APOBEC-3) enzymes are cytidine deaminases that are broadly and constitutively expressed. They are often up-regulated during carcinogenesis and candidate genes for causing the major single-base substitution in cancer-associated DNA mutations. Moreover, APOBEC-3s are involved in host innate immunity against many viruses. However, how APOBEC-3 mutational activity is regulated in normal and pathological conditions remains largely unknown. Heat shock protein levels are often elevated in both carcinogenesis and viral infection and are associated with DNA mutations...
August 11, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28620460/a-putative-antiviral-role-of-plant-cytidine-deaminases
#14
Susana Martín, José M Cuevas, Ana Grande-Pérez, Santiago F Elena
BACKGROUND: A mechanism of innate antiviral immunity operating against viruses infecting mammalian cells has been described during the last decade.  Host cytidine deaminases ( e.g., APOBEC3 proteins) edit viral genomes, giving rise to hypermutated nonfunctional viruses; consequently, viral fitness is reduced through lethal mutagenesis.  By contrast, sub-lethal hypermutagenesis may contribute to virus evolvability by increasing population diversity.  To prevent genome editing, some viruses have evolved proteins that mediate APOBEC3 degradation...
2017: F1000Research
https://www.readbyqxmd.com/read/28604942/micrornas-regulate-apobec-gene-expression
#15
REVIEW
Wei Cao, Wei Wu
Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) is a family of evolutionarily conserved cytidine deaminases, encoded by eleven genes located in the human genome. APOBECs play key roles in innate immunity through their ability to mutagenize viral DNA and restrict rival replication. Recent cancer genomics revealed APOBEC3 subtype-mediated APOBEC-signature mutations are common in a broad spectrum of human cancers. The pervasive APOBEC3 activation in the host genome which converts cytosine to uracile during RNA editing has been suggested to depend on ATR/chk1 pathways...
June 12, 2017: Histology and Histopathology
https://www.readbyqxmd.com/read/28516844/clues-for-two-step-virion-infectivity-factor-regulation-by-core-binding-factor-beta
#16
Youwei Ai, Jianzhang Ma, Xiaojun Wang
Lentiviruses threaten human and animal health. Virion infectivity factor (Vif) is essential for the infectivity of most lentiviruses, except for the equine infectious anaemia virus (EIAV). Vif promotes viral infectivity by recruiting a Cullin-based E3 ligase to induce the degradation of a class of host restriction factors, named APOBEC3. Core binding factor beta (CBF-β) is necessary for several primate lentiviral Vif functions, including HIV-1 Vif. Although much progress has been made in understanding the contribution of CBF-β to Vif function, the precise mechanism has not yet been fully elucidated...
May 2017: Journal of General Virology
https://www.readbyqxmd.com/read/28482907/a-conflict-of-interest-the-evolutionary-arms-race-between-mammalian-apobec3-and-lentiviral-vif
#17
REVIEW
Yusuke Nakano, Hirofumi Aso, Andrew Soper, Eri Yamada, Miyu Moriwaki, Guillermo Juarez-Fernandez, Yoshio Koyanagi, Kei Sato
Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3) proteins are mammalian-specific cellular deaminases and have a robust ability to restrain lentivirus replication. To antagonize APOBEC3-mediated antiviral action, lentiviruses have acquired viral infectivity factor (Vif) as an accessory gene. Mammalian APOBEC3 proteins inhibit lentiviral replication by enzymatically inserting G-to-A hypermutations in the viral genome, whereas lentiviral Vif proteins degrade host APOBEC3 via the ubiquitin/proteasome-dependent pathway...
May 8, 2017: Retrovirology
https://www.readbyqxmd.com/read/28475648/hiv-1-competition-experiments-in-humanized-mice-show-that-apobec3h-imposes-selective-pressure-and-promotes-virus-adaptation
#18
Yusuke Nakano, Naoko Misawa, Guillermo Juarez-Fernandez, Miyu Moriwaki, Shinji Nakaoka, Takaaki Funo, Eri Yamada, Andrew Soper, Rokusuke Yoshikawa, Diako Ebrahimi, Yuuya Tachiki, Shingo Iwami, Reuben S Harris, Yoshio Koyanagi, Kei Sato
APOBEC3 (A3) family proteins are DNA cytosine deaminases recognized for contributing to HIV-1 restriction and mutation. Prior studies have demonstrated that A3D, A3F, and A3G enzymes elicit a robust anti-HIV-1 effect in cell cultures and in humanized mouse models. Human A3H is polymorphic and can be categorized into three phenotypes: stable, intermediate, and unstable. However, the anti-viral effect of endogenous A3H in vivo has yet to be examined. Here we utilize a hematopoietic stem cell-transplanted humanized mouse model and demonstrate that stable A3H robustly affects HIV-1 fitness in vivo...
May 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28452355/crystal-structure-of-apobec3a-bound-to-single-stranded-dna-reveals-structural-basis-for-cytidine-deamination-and-specificity
#19
Takahide Kouno, Tania V Silvas, Brendan J Hilbert, Shivender M D Shandilya, Markus F Bohn, Brian A Kelch, William E Royer, Mohan Somasundaran, Nese Kurt Yilmaz, Hiroshi Matsuo, Celia A Schiffer
Nucleic acid editing enzymes are essential components of the immune system that lethally mutate viral pathogens and somatically mutate immunoglobulins, and contribute to the diversification and lethality of cancers. Among these enzymes are the seven human APOBEC3 deoxycytidine deaminases, each with unique target sequence specificity and subcellular localization. While the enzymology and biological consequences have been extensively studied, the mechanism by which APOBEC3s recognize and edit DNA remains elusive...
April 28, 2017: Nature Communications
https://www.readbyqxmd.com/read/28443724/genetic-diversity-of-hiv-1-gene-vif-among-treatment-naive-brazilians
#20
Fabiola Villanova, Marta Barreiros, Luiz Mário Janini, Ricardo Sobhie Diaz, Élcio Leal
HIV-1 has the Vif protein, which binds to human antiviral proteins APOBEC3 to form complexes to be degraded by cellular proteolysis. To further explore HIV-1 diversity at the population level, we analyzed blood samples from 317 treatment-naive patients in Brazil. In this study, we explored the correlations of Vif polymorphisms with clinical parameters of the patients and found that mutation K22H is associated with low CD4(+) cell counts and higher viral loads. Phylogenetic analysis of the vif gene indicated that subtype B was predominant in ∼77% (243/317) of the patients, followed by HIV-1 F ∼18% (56/317), and subtype C ∼4% (12/317); five samples were BF recombinants (∼1% of patients), and one was an AG recombinant...
September 2017: AIDS Research and Human Retroviruses
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