Results 171 to 180 of about 6,750 (198)

Identification of an HIV-1 replication inhibitor which rescues host restriction factor APOBEC3G in Vif–APOBEC3G complex

Antiviral Research, 2015
HIV-1 Vif protein is one of the most crucial accessory proteins for viral replication. It efficiently counteracts the important host restriction factor APOBEC3G (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G, A3G) which is lethal to HIV-1 by causing G to A mutation of viral genome.
Hui Chen, Ting Pan
exaly   +3 more sources

Functional domains of APOBEC3G required for antiviral activity

Journal of Cellular Biochemistry, 2004
AbstractThe viral protein, Vif, is essential for the production of infectious progeny virions in natural target cells of human immunodeficiency virus type 1 (HIV‐1). Several recent reports indicate that Vif acts by antagonizing the activity of an endogenous human antiviral protein, APOBEC3G.
David J Volsky
exaly   +3 more sources

Expression of APOBEC3G in kidney cells

Tissue Antigens, 2006
AbstractThe apolipoprotein B mRNA‐editing enzyme, catalytic polypeptide‐like 3G (APOBEC3G), a member of the APOBEC family possessing DNA mutator activity through cytosine deamination, is reported to play an important role in host defense against infections such as those of hepatitis B virus and human immunodeficiency virus.
Y, Komohara, S, Suekane, M, Noguchi, K, Matsuoka, A, Yamada, K, Itoh   +5 more
openaire   +2 more sources

APOBEC3G and HIV-1: Strike and counterstrike

Current HIV/AIDS Reports, 2006
APOBEC3G (A3G), a deoxycytidine deaminase, is a powerful host antiretroviral factor that can restrict HIV-1 infection. This restriction is counteracted by the HIV-1 virion infectivity factor (Vif) protein, whose activity culminates in depletion of A3G from infected cells.
Vanessa B, Soros, Warner C, Greene
openaire   +3 more sources

Inhibition of Hepatitis B Virus Replication by APOBEC3G

Science, 2004
To replicate efficiently, viruses must overcome innate defense mechanisms. Human APOBEC3G is a cytidine deaminase that represents one such barrier, conferring broad intracellular antiretroviral protection.
Turelli, Priscilla, Mangeat, Bastien, Jost, Stephanie, Vianin, Sandrine, Trono, Didier   +4 more
openaire   +4 more sources

APOBEC3G governs to ensure cellular oncogenic transformation

Blood Cells, Molecules, and Diseases, 2015
The oncogenic potential of APOBEC3G gene was recently appreciated by the finding that revealed inhibitory influence of APOBEC3G upon micro-RNA mediated repression of the gene responsible for hepatic metastasis. Here we report for the first time that sustained APOBEC3G expression is the characteristic trait exhibited by various cancer cells of different
Anuradha, Garg, Deepak, Kaul, Nalini, Chauhan   +2 more
openaire   +2 more sources

Unedited inhibition of HBV replication by APOBEC3G

Journal of Hepatology, 2004
Inhibition of hepatitis B virus replication by APOBEC3G. Turelli P, Mangeat B, Jost S, Vianin S, Trono D. [Science 2004; 303: 1829]
openaire   +3 more sources

Apobec3G-Based Strategies to Defeat HIV Infection

Current HIV Research, 2016
To suppress HIV infection, host cells have evolved numerous defenses that generally belong to the innate and adaptive immune responses. Over the last decade, extensive efforts have been focused on understanding HIV restriction factors and mechanisms of evasion.
Xiaozhuo, Ran, Zhujun, Ao, Xiaojian, Yao
openaire   +2 more sources

Hypermutation by intersegmental transfer of APOBEC3G cytidine deaminase

Nature Structural & Molecular Biology, 2008
Deamination of cytidine residues in single-stranded DNA (ssDNA) is an important mechanism by which apolipoprotein B mRNA-editing, catalytic polypeptide-like (APOBEC) enzymes restrict endogenous and exogenous viruses. The dynamic process underlying APOBEC-induced hypermutation is not fully understood.
Roni, Nowarski, Elena, Britan-Rosich, Tamar, Shiloach, Moshe, Kotler   +3 more
openaire   +2 more sources

APOBEC3G and Emergence of Pathogenic SIV

2014
In nature, new diseases arise when existing viruses adapt to infect new host species. For example, pandemic human immunodeficiency virus type 1 (HIV-1) and AIDS are the result of such a cross-species transmission of a lentivirus from its reservoir (chimpanzees) to humans.
openaire   +1 more source