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https://www.readbyqxmd.com/read/29100527/hpv11-e6-mutation-by-overexpression-of-apobec3a-and-effects-of-interferon-%C3%AF-on-apobec3s-and-hpv11-e6-expression-in-hpv11-hacat-cells
#1
Yongfang Wang, Xinyu Li, Shasha Song, Yang Sun, Jiafen Zhang, Changming Yu, Wei Chen
BACKGROUND: Condyloma acuminatum, infected by low-risk human papillomaviruses (e.g., HPV6 and HPV11), is one of the most widespread sexually transmitted diseases. Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 proteins (APOBEC3s, A3s) are cellular cytidine deaminases acting as antiviral factors through hypermutation of viral genome. However, it remains unknown whether A3s results in HPV11 gene mutations and interferon-ω (IFN-ω) exhibits antiviral activities through the A3s system...
November 3, 2017: Virology Journal
https://www.readbyqxmd.com/read/29100317/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
#2
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...
September 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/29064351/mechanisms-and-factors-that-drive-extensive-human-immunodeficiency-virus-type-1-hypervariability-an-overview
#3
Mahmoud Mohammad Yaseen, Nizar Mohammad Abuharfeil, Mohammad Ali Alqudah, Mohammad Mahmoud Yaseen
The extensive hypervariability of human immunodeficiency virus type-1 (HIV-1) populations represents a major barrier against the success of currently available antiretroviral therapy. Moreover, it is still the most important obstacle that faces the development of an effective preventive vaccine against this infectious virus. Indeed, several factors can drive such hypervariability within and between HIV-1 patients. These factors include: first, the very low fidelity nature of HIV-1 reverse transcriptase; second, the extremely high HIV-1 replication rate; and third, the high genomic recombination rate that the virus has...
October 24, 2017: Viral Immunology
https://www.readbyqxmd.com/read/29057505/ductal-cells-of-minor-salivary-glands-in-sj%C3%A3-gren-s-syndrome-patients-express-line-1-orf2p-and-apobec3b
#4
Eleni-Marina Kalogirou, Evangelia P Piperi, Konstantinos I Tosios, Evangelos Tsiambas, Galinos Fanourakis, Alexandra Sklavounou
BACKGROUND: Type I interferon activation is a hallmark event in Sjögren's syndrome. L1 retroelements stimulate plasmacytoid dendritic cells, activating the type I interferons, and are regulated by various mechanisms, including the APOBEC3 deaminases. As L1s are potential trigger factors in autoimmunity, we aimed to investigate the immunohistochemical localization of L1 ORF2 and its inhibitor APOBEC3B protein in minor salivary glands of Sjögren's syndrome patients. METHODS: Twenty minor salivary gland-tissue samples from 20 Sjögren's syndrome patients, classified according to Tarpley's histological criteria, and 10 controls were evaluated for L1 ORF2p and APOBEC3B expression via immunohistochemistry...
October 23, 2017: Journal of Oral Pathology & Medicine
https://www.readbyqxmd.com/read/29044109/apobec3h-structure-reveals-an-unusual-mechanism-of-interaction-with-duplex-rna
#5
Jennifer A Bohn, Keyur Thummar, Ashley York, Alice Raymond, W Clay Brown, Paul D Bieniasz, Theodora Hatziioannou, Janet L Smith
The APOBEC3 family of cytidine deaminases cause lethal hypermutation of retroviruses via deamination of newly reverse-transcribed viral DNA. Their ability to bind RNA is essential for virion infiltration and antiviral activity, yet the mechanisms of viral RNA recognition are unknown. By screening naturally occurring, polymorphic, non-human primate APOBEC3H variants for biological and crystallization properties, we obtained a 2.24-Å crystal structure of pig-tailed macaque APOBEC3H with bound RNA. Here, we report that APOBEC3H forms a dimer around a short RNA duplex and, despite the bound RNA, has potent cytidine deaminase activity...
October 18, 2017: Nature Communications
https://www.readbyqxmd.com/read/28983111/ifn-%C3%AE-mediated-base-excision-repair-pathway-correlates-with-antiviral-response-against-hepatitis-b-virus-infection
#6
Yong Li, Yuchen Xia, Meifang Han, Guang Chen, Dake Zhang, Wolfgang E Thasler, Ulrike Protzer, Qin Ning
Previous studies identified APOBEC deaminases as enzymes targeting hepatitis B virus (HBV) DNA in the nucleus thus affecting its persistence. Interferon (IFN)-α treated chimpanzees and hepatitis C patients showed elevated APOBEC expression. We thus hypothesized that the responses to IFN-α treatment of chronic hepatitis B (CHB) patients is influenced by IFN-induced base excision repair (BER). CHB-treatment naïve patients, patients treated with PEGylated IFN-α, and patients with sequential treatment of Entecavior and PEGylated IFN-α were recruited...
October 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28981865/enzyme-cycling-contributes-to-efficient-induction-of-genome-mutagenesis-by-the-cytidine-deaminase-apobec3b
#7
Madison B Adolph, Robin P Love, Yuqing Feng, Linda Chelico
The single-stranded DNA cytidine deaminases APOBEC3B, APOBEC3H haplotype I, and APOBEC3A can contribute to cancer through deamination of cytosine to form promutagenic uracil in genomic DNA. The enzymes must access single-stranded DNA during the dynamic processes of DNA replication or transcription, but the enzymatic mechanisms enabling this activity are not known. To study this, we developed a method to purify full length APOBEC3B and characterized it in comparison to APOBEC3A and APOBEC3H on substrates relevant to cancer mutagenesis...
September 18, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28963223/complete-genome-sequences-of-human-immunodeficiency-type-1-viruses-genetically-engineered-to-be-tropic-for-rhesus-macaques
#8
Masako Nomaguchi, Naoya Doi, Takaaki Koma, Akio Adachi
We have constructed two human immunodeficiency type 1 (HIV-1) derivatives, CXCR4 tropic and CCR5 tropic, that replicate in rhesus macaques. They are genetically engineered to be resistant to macaque restriction factors against HIV-1, including TRIM5α, APOBEC3, and tetherin proteins. The two HIV-1 variants described here are fundamental clones aiming for rhesus infection studies of HIV-1.
September 28, 2017: Genome Announcements
https://www.readbyqxmd.com/read/28958921/ifna2-p-ala120thr-impairs-the-inhibitory-activity-of-interferon-%C3%AE-2-against-the-hepatitis-b-virus-through-altering-its-binding-to-the-receptor
#9
Chuming Chen, Xiang Zhu, Wenxiong Xu, Fangji Yang, Genglin Zhang, Lina Wu, Yongyuan Zheng, Zhiliang Gao, Chan Xie, Liang Peng
BACKGROUND: Our previous study found that a rare genetic mutation IFNA2p.Ala120Thr affects the structure of IFN-α2 and contributes to increased host susceptibility to CHB. However, the way in which the single amino acid residue mutation affects IFN-α2 activity is unclear. The purpose of this research was to investigate the effects and mechanisms of IFNA2p.Ala120Thr on IFN-α2 activity. METHODS: Plasmid transfection of BL-21 was used to construct both wild type IFNA2 (wt) and p...
September 25, 2017: Antiviral Research
https://www.readbyqxmd.com/read/28900073/-molecular-mechanisms-of-hiv-1-genetic-diversity
#10
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
#11
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
#12
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
#13
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
#14
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...
November 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
#15
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
#16
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
#17
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-with-polytropic-host-range
#18
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-, and P-MLVs) exist in mice as infectious viruses and endogenous retroviruses (ERVs) inserted into mouse chromosomes. All three 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...
November 1, 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
#19
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
#20
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
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