Results 51 to 60 of about 6,750 (198)

APOBEC2 Is a Monomer in Solution: Implications for APOBEC3G Models [PDF]

Biochemistry, 2012
Although the physiological role of APOBEC2 is still largely unknown, a crystal structure of a truncated variant of this protein was determined several years ago [Prochnow, C. (2007) Nature445, 447-451]. This APOBEC2 structure had considerable impact in the HIV field because it was considered a good model for the structure of APOBEC3G, an important HIV ...
Troy C, Krzysiak, Jinwon, Jung, James, Thompson, David, Baker, Angela M, Gronenborn   +4 more
openaire   +2 more sources

Structural and functional assessment of APOBEC3G macromolecular complexes [PDF]

Methods, 2016
There are eleven members in the human APOBEC family of proteins that are evolutionarily related through their zinc-dependent cytidine deaminase domains. The human APOBEC gene clusters arose on chromosome 6 and 22 through gene duplication and divergence to where current day APOBEC proteins are functionally diverse and broadly expressed in tissues ...
Bogdan, Polevoda, William M, McDougall, Ryan P, Bennett, Jason D, Salter, Harold C, Smith   +4 more
openaire   +2 more sources

Male predominant association with Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G variants (rs6001417, rs35228531, rs8177832) predict protection against HIV-1 infection

Advancements in Life Sciences, 2020
Background: Human immunodeficiency virus (HIV) infection, it is a global health concern mainly lead to acquired immune deficiency syndrome (AIDS). There are numerous limitations of this infection particularly in the form of host factors which may limit ...
Qaisar Ali, Arshad Jamal, Sajjad Ullah, Ahmed Bilal Waqar   +3 more
doaj  

Population level analysis of human immunodeficiency virus type 1 hypermutation and its relationship with APOBEC3G and vif genetic variation [PDF]

, 2006
APOBEC3G and APOBEC3F restrict human immunodeficiency virus type 1 (HIV-1) replication in vitro through the induction of G!92A hypermutation; however, the relevance of this host antiviral strategy to clinical HIV-1 is currently not known.
Nolan, D., Gaudieri, S., Keller, J., Moore, C., Pace, C., James, I., Mallal, S.   +6 more
core  

AID and Apobec3G haphazard deamination and mutational diversity [PDF]

Cellular and Molecular Life Sciences, 2012
Activation-induced deoxycytidine deaminase (AID) and Apobec 3G (Apo3G) cause mutational diversity by initiating mutations on regions of single-stranded (ss) DNA. Expressed in B cells, AID deaminates C → U in actively transcribed immunoglobulin (Ig) variable and switch regions to initiate the somatic hypermutation (SHM) and class switch recombination ...
Malgorzata, Jaszczur, Jeffrey G, Bertram, Phuong, Pham, Matthew D, Scharff, Myron F, Goodman   +4 more
openaire   +2 more sources

Uracil DNA glycosylase counteracts APOBEC3G-induced hypermutation of hepatitis B viral genomes: excision repair of covalently closed circular DNA. [PDF]

PLoS Pathogens, 2013
The covalently closed circular DNA (cccDNA) of the hepatitis B virus (HBV) plays an essential role in chronic hepatitis. The cellular repair system is proposed to convert cytoplasmic nucleocapsid (NC) DNA (partially double-stranded DNA) into cccDNA in ...
Kouichi Kitamura, Zhe Wang, Sajeda Chowdhury, Miyuki Simadu, Miki Koura, Masamichi Muramatsu   +5 more
doaj   +1 more source

Human APOBEC3G suppresses homologous recombination and LIG4‐independent end joining in DNA double‐strand break repair

The FEBS Journal, EarlyView.
Chromosomal DNA double‐strand breaks (DSBs) are repaired by homologous recombination and nonhomologous end joining (NHEJ). Recent work has additionally established theta‐mediated end‐joining (TMEJ) as a mechanism for DSB joining. Cells lacking NHEJ and TMEJ can repair DSBs in a homology‐dependent manner.
Shinta Saito, Miori Murayama, Usaki Arai, Sekifumi Akatsu, Ami Yamamoto, Misaki Kadoguchi, Noritaka Adachi   +6 more
wiley   +1 more source

Definition of the interacting interfaces of Apobec3G and HIV-1 Vif using MAPPIT mutagenesis analysis [PDF]

, 2009
The host restriction factor Apobec3G is a cytidine deaminase that incorporates into HIV-1 virions and interferes with viral replication. The HIV-1 accessory protein Vif subverts Apobec3G by targeting it for proteasomal degradation.
Uyttendaele, Isabel, Frank Peelman, Clayton, Reginald, Van Schouwbroeck Bertrand, Kurth Julia, Annick Verhee, Catteeuw Dominiek, Reginald Clayton, Hallenberger, S, Lavens Delphine, Clayton, R, Kurth, Julia, Verhee, Annick, Catteeuw, Dominiek, José Heyden, Uyttendaele Isabel, Hallenberger Sabine, Sabine Hallenberger, Bertrand Van Schoubroeck, Heyden José, Clayton Reginald, Julia Kurth, Van Der Heyden, José, Peelman, Frank, Van Schoubroeck, B, Van Schoubroeck, Bertrand Van Schouwbroeck, Hallenberger, Sabine, Dominiek Catteeuw, Jan Tavernier, Lavens, Delphine, Jose ́ Van Der Heyden, Van Schouwbroeck, Bertrand, Kurth, J, José Van der Heyden, Isabel Uyttendaele, Delphine Lavens, Peelman Frank, Tavernier, Jan, Tavernier Jan   +39 more
core   +1 more source

Natural variation in Vif: differential impact on APOBEC3G/3F and a potential role in HIV-1 diversification. [PDF]

PLoS Pathogens, 2005
The HIV-1 Vif protein counteracts the antiviral activity exhibited by the host cytidine deaminases APOBEC3G and APOBEC3F. Here, we show that defective vif alleles can readily be found in HIV-1 isolates and infected patients. Single residue changes in the
Viviana Simon, Veronique Zennou, Deya Murray, Yaoxing Huang, David D Ho, Paul D Bieniasz   +5 more
doaj   +2 more sources

APOBEC3G mRNA expression in exposed seronegative and early stage HIV infected individuals decreases with removal of exposure and with disease progression

Retrovirology, 2009
Background APOBEC3G is an antiretroviral factor that acts by inducing G to A mutations. In this study, we examined the expression of APOBEC3G in uninfected HIV-1 exposed individuals at the time of their partner's diagnosis and one year later.
Reyes-Terán Gustavo, Torres Klintsy J, Hernández-Juan Ramón, Ormsby Christopher E, Vázquez-Pérez Joel A   +4 more
doaj   +1 more source