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1

McDonnell, Mollie M., Suzanne C. Karvonen, Amit Gaba, Ben Flath, Linda Chelico, and Michael Emerman. "Highly-potent, synthetic APOBEC3s restrict HIV-1 through deamination-independent mechanisms." PLOS Pathogens 17, no. 6 (2021): e1009523. http://dx.doi.org/10.1371/journal.ppat.1009523.

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The APOBEC3 (A3) genes encode cytidine deaminase proteins with potent antiviral and anti-retroelement activity. This locus is characterized by duplication, recombination, and deletion events that gave rise to the seven A3s found in primates. These include three single deaminase domain A3s (A3A, A3C, and A3H) and four double deaminase domain A3s (A3B, A3D, A3F, and A3G). The most potent of the A3 proteins against HIV-1 is A3G. However, it is not clear if double deaminase domain A3s have a generalized functional advantage to restrict HIV-1. In order to test whether superior restriction factors c
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2

Chen, Xiaohong, Hongwei Zhou, Yufei Zou, et al. "Effects of LMW-GS Allelic Variations at the Glu-A3 Locus on Fresh Wet Noodle and Frozen Cooked Noodle Quality." Foods 14, no. 9 (2025): 1546. https://doi.org/10.3390/foods14091546.

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Low molecular weight glutenin subunits (LMW-GSs) in wheat are critical functional proteins that regulate the processing quality of flour-based products. This study utilized two sets of near-isogenic lines (NILs) derived from the wheat cultivars Zhoumai 22 and Zhoumai 23 to investigate the effects of allelic variations at the Glu-A3 locus—specifically Glu-A3a, Glu-A3b, Glu-A3c, Glu-A3d, Glu-A3e, Glu-A3f, and Glu-A3g—on protein content, gluten properties, dough farinograph properties, cooking properties of fresh wet noodles (FWNs), and textural properties of FWNs and frozen cooked noodles (FZNs)
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3

Takei, Hisashi, Masanori Fujii, Sohei Nakayama, et al. "Alternative Splicing of APOBEC3D Generates Functional Diversity and Its Role As a DNA Mutator." Blood 128, no. 22 (2016): 5107. http://dx.doi.org/10.1182/blood.v128.22.5107.5107.

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Abstract Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) protein family consists of 11 members: APOBEC1, APOBEC2, seven APOBEC3s (A3s) (A/B/C/D/F/G/H), APOBEC4, and the activation-induced deaminase (AID). APOBEC1, A3s, and AID have cytidine deaminase activity and induce a cytidine (C) to thymidine (T) transition. The main function of A3s is to trigger an innate immune response to viral infection such as human immunodeficiency virus-1. Recently, it was reported that several APOBEC family proteins can induce somatic mutations into genomic DNA and thus promote cancer deve
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4

Zhou, Hongwei, Yingquan Zhang, Yanning Yang, et al. "Effects of Low-Molecular-Weight Glutenin Subunit Encoded by Glu-A3 on Gluten and Chinese Fresh Noodle Quality." Foods 12, no. 16 (2023): 3124. http://dx.doi.org/10.3390/foods12163124.

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Low-molecular-weight glutenin subunits (LMW-GS) account for 40% of the total wheat grain gluten protein fraction, which plays a significant role in the formation of noodle processing quality. The goal of this study was to clarify the effects of the major LMW-GS encoded by Glu-A3 on gluten and Chinese fresh noodle (CFN) quality. Four near-isogenic lines (NILs) were used as materials in this study, respectively carrying alleles Glu-A3a, Glu-A3b, Glu-A3c, and Glu-A3e, against the background of wheat variety Xiaoyan 22. The grain protein and its component contents and the gluten content, gluten in
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5

Marin, Mariana, Sheetal Golem, Kristine M. Rose, Susan L. Kozak, and David Kabat. "Human Immunodeficiency Virus Type 1 Vif Functionally Interacts with Diverse APOBEC3 Cytidine Deaminases and Moves with Them between Cytoplasmic Sites of mRNA Metabolism." Journal of Virology 82, no. 2 (2007): 987–98. http://dx.doi.org/10.1128/jvi.01078-07.

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ABSTRACT VifIIIB, which has been a standard model for the viral infectivity factor of human immunodeficiency virus type 1 (HIV-1), binds the cytidine deaminase APOBEC3G (A3G) and induces its degradation, thereby precluding its lethal incorporation into assembling virions. Additionally, VifIIIB less efficiently degrades A3F, another potent anti-HIV-1 cytidine deaminase. Although the APOBEC3 paralogs A3A, A3B, and A3C have weaker anti-HIV-1 activities and are only partially degraded by VifIIIB, we found that VifIIIB induces their emigration from the nucleus to the cytosol and thereby causes net
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6

Vasudevan, Ananda Ayyappan Jaguva, Sander H. J. Smits, Astrid Höppner, Dieter Häussinger, Bernd W. Koenig, and Carsten Münk. "Structural features of antiviral DNA cytidine deaminases." Biological Chemistry 394, no. 11 (2013): 1357–70. http://dx.doi.org/10.1515/hsz-2013-0165.

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Abstract The APOBEC3 (A3) family of cytidine deaminases plays a vital role for innate defense against retroviruses. Lentiviruses such as HIV-1 evolved the Vif protein that triggers A3 protein degradation. There are seven A3 proteins, A3A-A3H, found in humans. All A3 proteins can deaminate cytidines to uridines in single-stranded DNA (ssDNA), generated during viral reverse transcription. A3 proteins have either one or two cytidine deaminase domains (CD). The CDs coordinate a zinc ion, and their amino acid specificity classifies the A3s into A3Z1, A3Z2, and A3Z3. A3 proteins occur as monomers, d
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7

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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8

Pery, Erez, Kottampatty S. Rajendran, Andrew Jay Brazier, and Dana Gabuzda. "Regulation of APOBEC3 Proteins by a Novel YXXL Motif in Human Immunodeficiency Virus Type 1 Vif and Simian Immunodeficiency Virus SIVagm Vif." Journal of Virology 83, no. 5 (2008): 2374–81. http://dx.doi.org/10.1128/jvi.01898-08.

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ABSTRACT The APOBEC3 cytidine deaminases are potent antiviral factors that restrict the replication of human immunodeficiency virus type 1 (HIV-1). In HIV-1-infected CD4+ T cells, the viral accessory protein Vif binds to APOBEC3G (A3G), APOBEC3F (A3F), and APOBEC3C (A3C) and targets these proteins for polyubiquitination by forming an E3 ubiquitin ligase with cullin 5. Previous studies identified regions of HIV-1 Vif, 40YRHHY44 and 12QVDRMR17, which are important for interaction with A3G and A3F, respectively, and showed that Vif residues 54 to 71 are sufficient for A3G binding. Here, we identi
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9

Libre, Camille, Tanja Seissler, Santiago Guerrero, et al. "A Conserved uORF Regulates APOBEC3G Translation and Is Targeted by HIV-1 Vif Protein to Repress the Antiviral Factor." Biomedicines 10, no. 1 (2021): 13. http://dx.doi.org/10.3390/biomedicines10010013.

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The HIV-1 Vif protein is essential for viral fitness and pathogenicity. Vif decreases expression of cellular restriction factors APOBEC3G (A3G), A3F, A3D and A3H, which inhibit HIV-1 replication by inducing hypermutation during reverse transcription. Vif counteracts A3G at several levels (transcription, translation, and protein degradation) that altogether reduce the levels of A3G in cells and prevent its incorporation into viral particles. How Vif affects A3G translation remains unclear. Here, we uncovered the importance of a short conserved uORF (upstream ORF) located within two critical ste
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10

Nakashima, Masaaki, Shingo Kitamura, Teppei Kurosawa, et al. "Crystal structure of the Vif-interaction domain of the anti-viral APOBE3F." Acta Crystallographica Section A Foundations and Advances 70, a1 (2014): C123. http://dx.doi.org/10.1107/s2053273314098763.

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Human cells express a family of cytidine deaminases, called APOBEC3 (A3) (A3A, B, C, D, F, G, and H). The family enzymes, especially A3G and A3F potentially inhibit replication of retroviruses including HIV-1. However, HIV-1 overcomes the A3-mediated antiviral system by expressing a virus-encoded antagonist, viral infectivity factor (Vif) protein. In HIV-1-infected cells, Vif specifically binds with A3 followed by proteasomal degradation of A3. Hence, inhibition of the interaction between A3 and Vif is an attractive strategy for developing novel anti-HIV-1 drugs. To date, we have determined th
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11

Wang, Feng-xiang, Jialing Huang, Hangxiang Zhang, Xinliang Ma, and Hui Zhang. "APOBEC3G upregulation by alpha interferon restricts human immunodeficiency virus type 1 infection in human peripheral plasmacytoid dendritic cells." Journal of General Virology 89, no. 3 (2008): 722–30. http://dx.doi.org/10.1099/vir.0.83530-0.

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APOBEC3G (A3G), a member of cytidine deaminase family, has potent anti-human immunodeficiency virus type 1 (HIV-1) activity. It has been demonstrated that alpha interferon (IFN-α) can significantly enhance the expression of A3G in human primary resting CD4+ T-cells, macrophages and primary hepatocytes, subsequently decreasing their viral susceptibility. Plasmacytoid dendritic cells (pDCs) are key effectors in innate host immunity, mediating adaptive immune responses and stimulating IFN-α production in reaction to various stimuli. In this report, we demonstrate that IFN-α, either exogenously ad
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12

Krisko, John F., Nurjahan Begum, Caroline E. Baker, John L. Foster, and J. Victor Garcia. "APOBEC3G and APOBEC3F Act in Concert To Extinguish HIV-1 Replication." Journal of Virology 90, no. 9 (2016): 4681–95. http://dx.doi.org/10.1128/jvi.03275-15.

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ABSTRACTThe multifunctional HIV-1 accessory protein Vif counters the antiviral activities of APOBEC3G (A3G) and APOBEC3F (A3F), and some Vifs counter stable alleles of APOBEC3H (A3H). Studies in humanized mice have shown that HIV-1 lacking Vif expression is not viable. Here, we look at the relative contributions of the three APOBEC3s to viral extinction. Inoculation of bone marrow/liver/thymus (BLT) mice with CCR5-tropic HIV-1JRCSF(JRCSF) expressing avifgene inactive for A3G but not A3F degradation activity (JRCSFvifH42/43D) displayed either no or delayed replication. JRCSF expressing avifgene
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13

Koning, Fransje A., Edmund N. C. Newman, Eun-Young Kim, Kevin J. Kunstman, Steven M. Wolinsky, and Michael H. Malim. "Defining APOBEC3 Expression Patterns in Human Tissues and Hematopoietic Cell Subsets." Journal of Virology 83, no. 18 (2009): 9474–85. http://dx.doi.org/10.1128/jvi.01089-09.

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ABSTRACT Human APOBEC3 enzymes are cellular DNA cytidine deaminases that inhibit and/or mutate a variety of retroviruses, retrotransposons, and DNA viruses. Here, we report a detailed examination of human APOBEC3 gene expression, focusing on APOBEC3G (A3G) and APOBEC3F (A3F), which are potent inhibitors of human immunodeficiency virus type 1 (HIV-1) infection but are suppressed by HIV-1 Vif. A3G and A3F are expressed widely in hematopoietic cell populations, including T cells, B cells, and myeloid cells, as well as in tissues where mRNA levels broadly correlate with the lymphoid cell content (
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14

Perdiguero, Beatriz, María M. Lorenzo, and Rafael Blasco. "Vaccinia Virus A34 Glycoprotein Determines the Protein Composition of the Extracellular Virus Envelope." Journal of Virology 82, no. 5 (2007): 2150–60. http://dx.doi.org/10.1128/jvi.01969-07.

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ABSTRACT The outer envelope of the extracellular form of vaccinia virus contains five virus-encoded proteins, F13, A33, A34, A56, and B5, that, with the exception of A56, are implicated in virus egress or infectivity. A34, a type II transmembrane glycoprotein, is involved in the induction of actin tails, the release of enveloped virus from the surfaces of infected cells, and the disruption of the virus envelope after ligand binding prior to virus entry. To investigate interactions between A34 and other envelope proteins, a recombinant vaccinia virus (vA34RHA) expressing an epitope-tagged versi
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15

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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16

Stupfler, Benjamin, Cédric Verriez, Sarah Gallois-Montbrun, Roland Marquet, and Jean-Christophe Paillart. "Degradation-Independent Inhibition of APOBEC3G by the HIV-1 Vif Protein." Viruses 13, no. 4 (2021): 617. http://dx.doi.org/10.3390/v13040617.

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The ubiquitin–proteasome system plays an important role in the cell under normal physiological conditions but also during viral infections. Indeed, many auxiliary proteins from the (HIV-1) divert this system to its own advantage, notably to induce the degradation of cellular restriction factors. For instance, the HIV-1 viral infectivity factor (Vif) has been shown to specifically counteract several cellular deaminases belonging to the apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC3 or A3) family (A3A to A3H) by recruiting an E3-ubiquitin ligase complex and inducing the
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17

Atchekzaï, Jean, Bernard Bonnetot, Jean-Claude Duplan, Bernard Fenet, Bernard Ferage, and Henri Mongeot. "Unprecedented example of a3J(13C,11B) through a CCNB linkage." Magnetic Resonance in Chemistry 27, no. 7 (1989): 699–701. http://dx.doi.org/10.1002/mrc.1260270719.

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18

Kato, K., J. A. Trapani, J. Allopenna, B. Dupont, and S. Y. Yang. "Molecular analysis of the serologically defined HLA-Aw19 antigens. A genetically distinct family of HLA-A antigens comprising A29, A31, A32, and Aw33, but probably not A30." Journal of Immunology 143, no. 10 (1989): 3371–78. http://dx.doi.org/10.4049/jimmunol.143.10.3371.

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Abstract The HLA-Aw19 complex consists of a number of serologically cross-reactive Ag (i.e., A29, A30, A31, A32, and Aw33) which exhibit an epitope shared by HLA-B and -C proteins. To investigate the structural basis for these serologic cross-reactivities, we have cloned and determined the nucleotide sequences for A30, A31, and Aw33, and compared the predicted amino acid sequences with those already available for A29, A32, and other class I allelic products. All alleles of the Aw19 group contained A-locus-specific sequences, exhibiting "A-ness." The structural similarities between Aw19 polypep
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19

Perdiguero, Beatriz, and Rafael Blasco. "Interaction between Vaccinia Virus Extracellular Virus Envelope A33 and B5 Glycoproteins." Journal of Virology 80, no. 17 (2006): 8763–77. http://dx.doi.org/10.1128/jvi.00598-06.

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ABSTRACT The extracellular form of vaccinia virus acquires its outer envelope by wrapping with cytoplasmic membranes that contain at least seven virus-encoded proteins, of which four are glycoproteins. We searched for interactions between the vaccinia virus A33 glycoprotein and proteins A34, A36, B5, F12, and F13. First, when myc epitope-tagged A33 was expressed in combination with other envelope proteins, A33 colocalized with B5 and A36, suggesting that direct A33-B5 and A33-A36 interactions occur in the absence of infection. A recombinant vaccinia virus (vA33Rmyc) was constructed by introduc
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Barzak, Fareeda M., Timothy M. Ryan, Maksim V. Kvach, et al. "Small-Angle X-ray Scattering Models of APOBEC3B Catalytic Domain in a Complex with a Single-Stranded DNA Inhibitor." Viruses 13, no. 2 (2021): 290. http://dx.doi.org/10.3390/v13020290.

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In normal cells APOBEC3 (A3A-A3H) enzymes as part of the innate immune system deaminate cytosine to uracil on single-stranded DNA (ssDNA) to scramble DNA in order to give protection against a range of exogenous retroviruses, DNA-based parasites, and endogenous retroelements. However, some viruses and cancer cells use these enzymes, especially A3A and A3B, to escape the adaptive immune response and thereby lead to the evolution of drug resistance. We have synthesized first-in-class inhibitors featuring modified ssDNA. We present models based on small-angle X-ray scattering (SAXS) data that (1)
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21

Jost, Stéphanie, Priscilla Turelli, Bastien Mangeat, Ulrike Protzer, and Didier Trono. "Induction of Antiviral Cytidine Deaminases Does Not Explain the Inhibition of Hepatitis B Virus Replication by Interferons." Journal of Virology 81, no. 19 (2007): 10588–96. http://dx.doi.org/10.1128/jvi.02489-06.

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ABSTRACT Interferons (IFNs) play a major role in the control of hepatitis B virus (HBV), whether as endogenous cytokines limiting the spread of the virus during the acute phase of the infection or as drugs for the treatment of its chronic phase. However, the mechanism by which IFNs inhibit HBV replication has so far remained elusive. Here, we show that type I and II IFN treatment of human hepatocytes induces the production of APOBEC3G (A3G) and, to a lesser extent, that of APOBEC3F (A3F) and APOBEC3B (A3B) but not that of two other cytidine deaminases also endowed with anti-HBV activity, activ
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Qisthani, Nabila Noor, and Syarif Hidayatuloh. "Analisis Risiko Dampak Wabah Pandemi Covid-19 Terhadap Rantai Pasok IKM Batik Keraton." JURNAL TEKNIK INDUSTRI 11, no. 1 (2021): 37–42. http://dx.doi.org/10.25105/jti.v11i1.9664.

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Intisari— Indonesia merupakan salah satu negara yang terdampak covid-19 diberbagai sektor perekonomian, salah satunya adalah Usaha Mikro Kecil Menegah (UMKM). Ketidakstabilan rantai pasok mengakibatkan banyak UMKM tidak dapat menjalankan aktivitas bisnis seperti biasa. Terjadinya wabah pandemi covid-19 pada rantai pasok merupakan contoh dari distruption risk yaitu risiko yang tidak sering terjadi namun memiliki dampak yang besar terhadap rantai pasok. Salah satu UMKM yang terdampak covid-19 adalah IKM Batik Keraton yang merupakan salah satu industri penghasil batik yang terletak di Kota Pekalo
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Zhen, Anjie, Tao Wang, Ke Zhao, Yong Xiong, and Xiao-Fang Yu. "A Single Amino Acid Difference in Human APOBEC3H Variants Determines HIV-1 Vif Sensitivity." Journal of Virology 84, no. 4 (2009): 1902–11. http://dx.doi.org/10.1128/jvi.01509-09.

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ABSTRACT Several variants of APOBEC3H (A3H) have been identified in different human populations. Certain variants of this protein are particularly potent inhibitors of retrotransposons and retroviruses, including HIV-1. However, it is not clear whether HIV-1 Vif can recognize and suppress the antiviral activity of A3H variants, as it does with other APOBEC3 proteins. We now report that A3H_Haplotype II (HapII), a potent inhibitor of HIV-1 in the absence of Vif, can indeed be degraded by HIV-1 Vif. Vif-induced degradation of A3H_HapII was blocked by the proteasome inhibitor MG132 and a Cullin5
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Luo, Kun, Tao Wang, Bindong Liu, et al. "Cytidine Deaminases APOBEC3G and APOBEC3F Interact with Human Immunodeficiency Virus Type 1 Integrase and Inhibit Proviral DNA Formation." Journal of Virology 81, no. 13 (2007): 7238–48. http://dx.doi.org/10.1128/jvi.02584-06.

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ABSTRACT APOBEC3G (A3G) is a single-stranded DNA cytidine deaminase that targets retroviral minus-strand DNA and has potent antiviral activity against diverse retroviruses. However, the mechanisms of A3G antiviral functions are incompletely understood. Here we demonstrate that A3G, A3F, and, to a lesser extent, the noncatalytic A3GC291S block human immunodeficiency virus type 1 (HIV-1) replication by interfering with proviral DNA formation. In HIV-1 virions, A3G interacted with HIV-1 integrase and nucleocapsid, key viral factors for reverse transcription and integration. Unlike A3G, the weak a
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Delviks-Frankenberry, Krista A., Belete A. Desimmie, and Vinay K. Pathak. "Structural Insights into APOBEC3-Mediated Lentiviral Restriction." Viruses 12, no. 6 (2020): 587. http://dx.doi.org/10.3390/v12060587.

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Mammals have developed clever adaptive and innate immune defense mechanisms to protect against invading bacterial and viral pathogens. Human innate immunity is continuously evolving to expand the repertoire of restriction factors and one such family of intrinsic restriction factors is the APOBEC3 (A3) family of cytidine deaminases. The coordinated expression of seven members of the A3 family of cytidine deaminases provides intrinsic immunity against numerous foreign infectious agents and protects the host from exogenous retroviruses and endogenous retroelements. Four members of the A3 proteins
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Chen, Gongying, Zhiwen He, Tao Wang, Rongzhen Xu, and Xiao-Fang Yu. "A Patch of Positively Charged Amino Acids Surrounding the Human Immunodeficiency Virus Type 1 Vif SLVx4Yx9Y Motif Influences Its Interaction with APOBEC3G." Journal of Virology 83, no. 17 (2009): 8674–82. http://dx.doi.org/10.1128/jvi.00653-09.

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ABSTRACT The amino-terminal region of the Vif molecule in human immunodeficiency virus type 1 (HIV-1), HIV-2, and simian immunodeficiency virus (SIV) contains a conserved SLV/Ix4Yx9Y motif that was first described in 1992, but the importance of this motif for Vif function has not yet been examined. Our characterization of the amino acids surrounding this motif in HIV-1 Vif indicated that the region is critical for APOBEC3 suppression. In particular, amino acids K22, K26, Y30, and Y40 were found to be important for the Vif-induced degradation and suppression of cellular APOBEC3G (A3G). However,
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Dang, Ying, Xiaojun Wang, Tao Zhou, Ian A. York, and Yong-Hui Zheng. "Identification of a Novel WxSLVK Motif in the N Terminus of Human Immunodeficiency Virus and Simian Immunodeficiency Virus Vif That Is Critical for APOBEC3G and APOBEC3F Neutralization." Journal of Virology 83, no. 17 (2009): 8544–52. http://dx.doi.org/10.1128/jvi.00651-09.

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ABSTRACT The function of lentiviral Vif proteins is to neutralize the host antiviral cytidine deaminases APOBEC3G (A3G) and APOBEC3F (A3F). Vif bridges a cullin 5-based E3 ubiquitin ligase with A3G and A3F and mediates their degradation by proteasomes. Recent studies have found that Vif uses different domains to bind to A3G and A3F. A 14DRMR17 domain binds to A3F, 40YRHHY44 binds to A3G, and 69YxxL72 binds to both A3G and A3F. Here, we report another functional domain of Vif. Previously, we demonstrated that human immunodeficiency virus type 1 (HIV-1) Vif failed to mediate A3G proteasomal degr
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Breiman, Adrien, David C. J. Carpentier, Helen A. Ewles, and Geoffrey L. Smith. "Transport and stability of the vaccinia virus A34 protein is affected by the A33 protein." Journal of General Virology 94, no. 4 (2013): 720–25. http://dx.doi.org/10.1099/vir.0.049486-0.

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Vaccinia virus (VACV) has two infectious forms called intracellular mature virus and extracellular enveloped virus (EEV). Two of the seven viral proteins in the EEV outer envelope, A33 and A34, are type II membrane glycoproteins that each interact with another EEV protein called B5; however, evidence for direct A33–A34 interaction is lacking. The localization and stability of A34 is affected by B5 and here data are presented showing that A34 is also affected by A33. In the absence of A33, just as without B5, the level, localization and glycosylation profile of A34 was altered. However, the gly
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29

Russell, Rebecca A., and Vinay K. Pathak. "Identification of Two Distinct Human Immunodeficiency Virus Type 1 Vif Determinants Critical for Interactions with Human APOBEC3G and APOBEC3F." Journal of Virology 81, no. 15 (2007): 8201–10. http://dx.doi.org/10.1128/jvi.00395-07.

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ABSTRACT Human cytidine deaminases APOBEC3G (A3G) and APOBEC3F (A3F) inhibit replication of Vif-deficient human immunodeficiency virus type 1 (HIV-1). HIV-1 Vif overcomes these host restriction factors by binding to them and inducing their proteasomal degradation. The Vif-A3G and Vif-A3F interactions are attractive targets for antiviral drug development because inhibiting the interactions could allow the host defense mechanism to control HIV-1 replication. It was recently reported that the Vif amino acids D14RMR17 are important for functional interaction and degradation of the previously ident
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30

Miyagi, Eri, Charles R. Brown, Sandrine Opi, et al. "Stably Expressed APOBEC3F Has Negligible Antiviral Activity." Journal of Virology 84, no. 21 (2010): 11067–75. http://dx.doi.org/10.1128/jvi.01249-10.

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ABSTRACT APOBEC3F (A3F) is a member of the family of cytidine deaminases that is often coexpressed with APOBEC3G (A3G) in cells susceptible to HIV infection. A3F has been shown to have strong antiviral activity in transient-expression studies, and together with A3G, it is considered the most potent cytidine deaminase targeting HIV. Previous analyses suggested that the antiviral properties of A3F can be dissociated from its catalytic deaminase activity. We were able to confirm the deaminase-independent antiviral activity of exogenously expressed A3F; however, we also noted that exogenous expres
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Li, Zusheng, Anthony J. Clarke, and Terry J. Beveridge. "Gram-Negative Bacteria Produce Membrane Vesicles Which Are Capable of Killing Other Bacteria." Journal of Bacteriology 180, no. 20 (1998): 5478–83. http://dx.doi.org/10.1128/jb.180.20.5478-5483.1998.

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ABSTRACT Naturally produced membrane vesicles (MVs), isolated from 15 strains of gram-negative bacteria (Citrobacter,Enterobacter, Escherichia,Klebsiella, Morganella, Proteus,Salmonella, and Shigella strains), lysed many gram-positive (including Mycobacterium) and gram-negative cultures. Peptidoglycan zymograms suggested that MVs contained peptidoglycan hydrolases, and electron microscopy revealed that the murein sacculi were digested, confirming a previous modus operandi (J. L. Kadurugamuwa and T. J. Beveridge, J. Bacteriol. 174:2767–2774, 1996). MV-sensitive bacteria possessed A1α, A4α, A1γ,
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Russell, Rebecca A., Jessica Smith, Rebekah Barr, Darshana Bhattacharyya, and Vinay K. Pathak. "Distinct Domains within APOBEC3G and APOBEC3F Interact with Separate Regions of Human Immunodeficiency Virus Type 1 Vif." Journal of Virology 83, no. 4 (2008): 1992–2003. http://dx.doi.org/10.1128/jvi.01621-08.

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ABSTRACT Human APOBEC3G (A3G) and APOBEC3F (A3F) inhibit the replication of Vif-deficient human immunodeficiency virus type 1 (HIV-1). HIV-1 Vif overcomes these host restriction factors by binding to them and inducing their degradation. Thus, the Vif-A3G and Vif-A3F interactions are attractive targets for antiviral drug development, as inhibiting these interactions could allow the host defense mechanism to control HIV-1 replication. Recently, it has been reported that amino acids 105 to 156 of A3G are involved in the interaction with Vif; however, to date, the region of A3F involved in Vif bin
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Mbisa, Jean L., Wei Bu, and Vinay K. Pathak. "APOBEC3F and APOBEC3G Inhibit HIV-1 DNA Integration by Different Mechanisms." Journal of Virology 84, no. 10 (2010): 5250–59. http://dx.doi.org/10.1128/jvi.02358-09.

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ABSTRACT APOBEC3F (A3F) and APBOBEC3G (A3G) both are host restriction factors that can potently inhibit human immunodeficiency virus type 1 (HIV-1) replication. Their antiviral activities are at least partially mediated by cytidine deamination, which causes lethal mutations of the viral genome. We recently showed that A3G blocks viral plus-strand DNA transfer and inhibits provirus establishment in the host genome (J. L. Mbisa, R. Barr, J. A. Thomas, N. Vandegraaff, I. J. Dorweiler, E. S. Svarovskaia, W. L. Brown, L. M. Mansky, R. J. Gorelick, R. S. Harris, A. Engelman, and V. K. Pathak, J. Vir
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Gallois-Montbrun, Sarah, Rebecca K. Holmes, Chad M. Swanson, et al. "Comparison of Cellular Ribonucleoprotein Complexes Associated with the APOBEC3F and APOBEC3G Antiviral Proteins." Journal of Virology 82, no. 11 (2008): 5636–42. http://dx.doi.org/10.1128/jvi.00287-08.

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ABSTRACT The human apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3F (APOBEC3F [A3F]) and A3G proteins are effective inhibitors of infection by various retroelements and share ∼50% amino acid sequence identity. We therefore undertook comparative analyses of the protein and RNA compositions of A3F- and A3G-associated ribonucleoprotein complexes (RNPs). Like A3G, A3F is found associated with a complex array of cytoplasmic RNPs and can accumulate in RNA-rich cytoplasmic microdomains known as mRNA processing bodies or stress granules. While A3F RNPs display greater resistance to d
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Albin, John S., Guylaine Haché, Judd F. Hultquist, William L. Brown, and Reuben S. Harris. "Long-Term Restriction by APOBEC3F Selects Human Immunodeficiency Virus Type 1 Variants with Restored Vif Function." Journal of Virology 84, no. 19 (2010): 10209–19. http://dx.doi.org/10.1128/jvi.00632-10.

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ABSTRACT Tandem stop mutations K26X and H27X in human immunodeficiency virus type 1 (HIV-1) vif compromise virus replication in human T-cell lines that stably express APOBEC3F (A3F) or APOBEC3G (A3G). We previously reported that partial resistance to A3G could develop in these Vif-deficient viruses through a nucleotide A200-to-T/C transversion and a vpr null mutation, but these isolates were still susceptible to restriction by A3F. Here, long-term selection experiments were done to determine how these A3G-selected isolates might evolve to spread in the presence of A3F. We found that A3F, like
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Paprotka, Tobias, Narasimhan J. Venkatachari, Chawaree Chaipan, et al. "Inhibition of Xenotropic Murine Leukemia Virus-Related Virus by APOBEC3 Proteins and Antiviral Drugs." Journal of Virology 84, no. 11 (2010): 5719–29. http://dx.doi.org/10.1128/jvi.00134-10.

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ABSTRACT Xenotropic murine leukemia virus-related virus (XMRV), a gammaretrovirus, has been isolated from human prostate cancer tissue and from activated CD4+ T cells and B cells of patients with chronic fatigue syndrome, suggesting an association between XMRV infection and these two diseases. Since APOBEC3G (A3G) and APOBEC3F (A3F), which are potent inhibitors of murine leukemia virus and Vif-deficient human immunodeficiency virus type 1 (HIV-1), are expressed in human CD4+ T cells and B cells, we sought to determine how XMRV evades suppression of replication by APOBEC3 proteins. We found tha
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Dang, Ying, Roderick W. Davis, Ian A. York, and Yong-Hui Zheng. "Identification of 81LGxGxxIxW89 and 171EDRW174 Domains from Human Immunodeficiency Virus Type 1 Vif That Regulate APOBEC3G and APOBEC3F Neutralizing Activity." Journal of Virology 84, no. 11 (2010): 5741–50. http://dx.doi.org/10.1128/jvi.00079-10.

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ABSTRACT The human cytidine deaminases APOBEC3G (A3G) and APOBEC3F (A3F) potently restrict human immunodeficiency virus type 1 (HIV-1) replication, but they are neutralized by the viral protein Vif. Vif bridges A3G and A3F with a Cullin 5 (Cul5)-based E3 ubiquitin ligase and mediates their proteasomal degradation. This mechanism has been extensively studied, and several Vif domains have been identified that are critical for A3G and A3F neutralization. Here, we identified two additional domains. Via sequence analysis of more than 2,000 different HIV-1 Vif proteins, we identified two highly cons
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Tian, Chunjuan, Xianghui Yu, Wei Zhang, Tao Wang, Rongzhen Xu, and Xiao-Fang Yu. "Differential Requirement for Conserved Tryptophans in Human Immunodeficiency Virus Type 1 Vif for the Selective Suppression of APOBEC3G and APOBEC3F." Journal of Virology 80, no. 6 (2006): 3112–15. http://dx.doi.org/10.1128/jvi.80.6.3112-3115.2006.

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ABSTRACT APOBEC3G (A3G) and related cytidine deaminases, such as APOBEC3F (A3F), are potent inhibitors of retroviruses. Formation of infectious human immunodeficiency virus type 1 (HIV-1) requires suppression of multiple cytidine deaminases by Vif. Whether HIV-1 Vif recognizes various APOBEC3 proteins through a common mechanism is unclear. The domains in Vif that mediate APOBEC3 recognitions are also poorly defined. The N-terminal region of HIV-1 Vif is unusually rich in Trp residues, which are highly conserved. In the present study, we examined the role of these Trp residues in the suppressio
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Liu, Bindong, Phuong Thi Nguyen Sarkis, Kun Luo, Yunkai Yu, and Xiao-Fang Yu. "Regulation of Apobec3F and Human Immunodeficiency Virus Type 1 Vif by Vif-Cul5-ElonB/C E3 Ubiquitin Ligase." Journal of Virology 79, no. 15 (2005): 9579–87. http://dx.doi.org/10.1128/jvi.79.15.9579-9587.2005.

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ABSTRACT The human cytidine deaminase Apobec3F (h-A3F), a protein related to the previously recognized antiviral factor Apobec3G (h-A3G), has antiviral activity against human immunodeficiency virus type 1 (HIV-1) that is suppressed by the viral protein Vif. The mechanism of HIV-1 Vif-mediated suppression of h-A3F is not fully understood. Here, we demonstrate that while h-A3F, like h-A3G, was able to suppress primate lentiviruses other than HIV-1 (simian immunodeficiency virus from African green monkeys [SIVagm] and Rhesus macaques [SIVmac]), the interaction between Vif proteins and h-A3F appea
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40

Sturdivant, Michael S., Andrew S. Truong, Mi Zhou, Jeffrey S. Damrauer, and William Y. Kim. "Abstract 5156: The mutagenic effects of APOBEC3A and APOBEC3B in urothelial carcinoma." Cancer Research 83, no. 7_Supplement (2023): 5156. http://dx.doi.org/10.1158/1538-7445.am2023-5156.

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Abstract APOBEC3A (A3A) and APOBEC3B (A3B) are members of a family of cytidine deaminase enzymes that catalyze the removal of an amino group from cytosine nucleotides generating an uracil in its place that serve as a source of mutations. The resulting C→U transition has been linked to various oncogenic mutations, most predominately in bladder cancer. While both A3A and A3B activity can account for widespread changes to the genomic landscape, prior studies have shown tumor specific effects. In hepatocellular carcinoma, A3A has been shown to be the only APOBEC3 family member capable of driving t
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41

Wang, Rong-Fu, Samuel L. Johnston, Scott Southwood, Alessandro Sette, and Steven A. Rosenberg. "Recognition of an Antigenic Peptide Derived from Tyrosinase-Related Protein-2 by CTL in the Context of HLA-A31 and -A33." Journal of Immunology 160, no. 2 (1998): 890–97. http://dx.doi.org/10.4049/jimmunol.160.2.890.

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Abstract Tumor-infiltrating lymphocytes (TILs) derived from tumor-bearing patients recognize tumor-associated Ags presented by MHC class I molecules. The infusion of TIL586 along with IL-2 into the autologous patient with metastatic melanoma resulted in the objective regression of tumor. Two T cell epitopes derived from tumor Ags, tyrosinase-related protein (TRP)-1 and TRP-2, were shown to be recognized by HLA-A31 restricted TIL586 and its T cell clones. In this study we tested the hypothesis that these two peptides can be recognized by CTL from non-HLA-A31 patients with melanoma. It was found
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Болаев, В. К., Л. Г. Моисейкина, А. В. Убушаева, and К. В. Болаева. "DETERMINATION OF GENE POOL OF HORSES OF INTRA- BREED TYPE “TSELINNYJ” OF KALMYK BREED." Horse breeding and equestrian sports, no. 1 (February 13, 2020): 17–19. http://dx.doi.org/10.25727/hs.2020.1.54435.

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Проблема использования лошадей калмыцкой породы, как наиболее приспособленных к условиям аридных территорий и являющихся экологическими, придается большое значение. Главным условием экономической целесообразности является улучшение мясной продуктивности калмыцкой лошади, что было достигнуто выведением нового внутрипородного мясного типа «Целинный». Целью нашей работы было выявление генотипического статуса лошадей внутрипородного мясного типа «Целинный» калмыцкой породы по ДНК с использованием ISSR анализа. ПЦР проводили на амплификаторе «Терцик» с использованием набора GenePakTM PCR Core (IsoG
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Nakashima, Masaaki, Hirotaka Ode, Takashi Kawamura, et al. "Structural Insights into HIV-1 Vif-APOBEC3F Interaction." Journal of Virology 90, no. 2 (2015): 1034–47. http://dx.doi.org/10.1128/jvi.02369-15.

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ABSTRACTThe HIV-1 Vif protein inactivates the cellular antiviral cytidine deaminase APOBEC3F (A3F) in virus-infected cells by specifically targeting it for proteasomal degradation. Several studies identified Vif sequence motifs involved in A3F interaction, whereas a Vif-binding A3F interface was proposed based on our analysis of highly similar APOBEC3C (A3C). However, the structural mechanism of specific Vif-A3F recognition is still poorly understood. Here we report structural features of interaction interfaces for both HIV-1 Vif and A3F molecules. Alanine-scanning analysis of Vif revealed tha
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44

Mulder, Lubbertus C. F., Marcel Ooms, Susan Majdak, et al. "Moderate Influence of Human APOBEC3F on HIV-1 Replication in Primary Lymphocytes." Journal of Virology 84, no. 18 (2010): 9613–17. http://dx.doi.org/10.1128/jvi.02630-09.

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ABSTRACT Multiple APOBEC3 proteins are expressed in HIV-1 target cells, but their individual contributions to viral suppression when expressed at endogenous levels remain largely unknown. We used an HIV NL4-3 mutant that selectively counteracts APOBEC3G (A3G) but not APOBEC3F (A3F) to dissect the relative contribution of A3F to the inhibition of HIV-1 replication in primary human lymphocytes (peripheral blood mononuclear cells [PBMCs]). This HIV Vif mutant replicated similarly to wild-type virus in PBMCs, suggesting that the effect of A3F on HIV restriction in these cells is limited. The diffe
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45

Gladwell, Wesley, Oriana Yost, Heather Li, et al. "APOBEC3G Is a p53-Dependent Restriction Factor in Respiratory Syncytial Virus Infection of Human Cells Included in the p53/Immune Axis." International Journal of Molecular Sciences 24, no. 23 (2023): 16793. http://dx.doi.org/10.3390/ijms242316793.

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Identifying and understanding genetic factors that influence the propagation of the human respiratory syncytial virus (RSV) can lead to health benefits and possibly augment recent vaccine approaches. We previously identified a p53/immune axis in which the tumor suppressor p53 directly regulates the expression of immune system genes, including the seven members of the APOBEC3 family of DNA cytidine deaminases (A3), which are innate immune sentinels against viral infections. Here, we examined the potential p53 and A3 influence in RSV infection, as well as the overall p53-dependent cellular and p
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46

Doceul, Virginie, Michael Hollinshead, Adrien Breiman, Kathlyn Laval, and Geoffrey L. Smith. "Protein B5 is required on extracellular enveloped vaccinia virus for repulsion of superinfecting virions." Journal of General Virology 93, no. 9 (2012): 1876–86. http://dx.doi.org/10.1099/vir.0.043943-0.

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Vaccinia virus (VACV) spreads across cell monolayers fourfold faster than predicted from its replication kinetics. Early after infection, infected cells repulse some superinfecting extracellular enveloped virus (EEV) particles by the formation of actin tails from the cell surface, thereby causing accelerated spread to uninfected cells. This strategy requires the expression of two viral proteins, A33 and A36, on the surface of infected cells and upon contact with EEV this complex induces actin polymerization. Here we have studied this phenomenon further and investigated whether A33 and A36 expr
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Sawyer, Aubrey M., Cristina C. Vaca, Neha Malik, et al. "Design and Characterization of Inhibitors of Cell-Mediated Degradation of APOBEC3G That Decrease HIV-1 Infectivity." Viruses 17, no. 4 (2025): 514. https://doi.org/10.3390/v17040514.

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The cytoplasmic human Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3 or A3) cytidine deaminases G and F (A3G and A3F) can block the spread of human immunodeficiency virus (HIV). HIV counteracts this cell-intrinsic defense through a viral protein called viral infectivity factor (Vif). Vif causes proteasomal degradation of A3G and A3F proteins (A3G/F) in HIV-producing cells to ensure infectivity of virions subsequently released from these cells. Here, we optimized a lead compound reported previously to boost cellular levels of A3G. The modified analogs designed, synth
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48

M. Abdnoor, Zahraa, Nasreen R.Jber, and Aliaa Saadoon Abdul-Razaq. "The Effect of 1,3,4-Oxadiazol and 1,2,4-Triazole Compounds on Urease and Pepsin Enzymes." Al-Nahrain Journal of Science 27, no. 1 (2024): 42–64. http://dx.doi.org/10.22401/anjs.27.1.06.

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The helicobacter pylori affected urease and pepsin enzymes in the stomach, so the object of this study is to screen the effect of bis 1,3,4-oxadiazole and bis 1,2,4, triazole derivatives compounds on h-pylori urease enzyme in vitro. The results show that urease was inhibited by all produced compounds when the concentration increased. The most effective urease inhibitor is determined to be the compounds (A3e, A3c, A3d and B3c). The clinical study involved studying the pepsin enzyme activity level in H-pyloripatients and control, the results found that the activity of pepsin elevated in h-pylori
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Castilha, Eliza Pizarro, Rosalba Biondo, Kleber Paiva Trugilo, Giulia Mariane Fortunato, Timothy Robert Fenton, and Karen Brajão de Oliveira. "APOBEC3 Proteins: From Antiviral Immunity to Oncogenic Drivers in HPV-Positive Cancers." Viruses 17, no. 3 (2025): 436. https://doi.org/10.3390/v17030436.

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The human APOBEC superfamily consists of eleven cytidine deaminase enzymes. Among them, APOBEC3 enzymes play a dual role in antiviral immunity and cancer development. APOBEC3 enzymes, including APOBEC3A (A3A) and APOBEC3B (A3B), induce mutations in viral DNA, effectively inhibiting viral replication but also promoting somatic mutations in the host genome, contributing to cancer development. A3A and A3B are linked to mutational signatures in over 50% of human cancers, with A3A being a potent mutagen. A3B, one of the first APOBEC3 enzymes linked to carcinogenesis, plays a significant role in HPV
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Prasetyo, Didik Eko. "Optimization of Two-Dimensional Ad Design with Persuasion Aspects Using Value Engineering and Analysis Hierarchy Process (Project : XYZ Singosari Car Salon)." Jurnal Indonesia Sosial Teknologi 5, no. 4 (2024): 1430–53. http://dx.doi.org/10.59141/jist.v5i4.926.

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XYZ Car Salon optimizes advertising to increase the company's turnover. In making advertisements requires expertise and understanding of graphic design and interesting content. Attractive design and content become the initial concern that affects customer psychology in making purchase decisions. The more attractive it is, the more effective the ad will be. This research includes a type of qualitative research, sampling using non-probability sampling methods with sampling techniques using purpose sampling, from a population of 45 experts obtained a sample of 31 respondents. The combination of d
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