ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2009
APOBEC3G: an intracellular centurion.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- HIV-1 Vif disrupts phosphatase feedback regulation at the kinetochore, leading to a pronounced pseudo-metaphase arrest.bioRxiv : the preprint server for biology · 2024Article
- The Evolution of Severe Acute Respiratory Syndrome Coronavirus-2 during Pandemic and Adaptation to the Host.Journal of molecular evolution · 2021Article
- HIV-1 Vif's Capacity To Manipulate the Cell Cycle Is Species Specific.Journal of virology · 2018Article
- Insights into DNA substrate selection by APOBEC3G from structural, biochemical, and functional studies.PloS one · 2018Article
- Cyclin F/FBXO1 Interacts with HIV-1 Viral Infectivity Factor (Vif) and Restricts Progeny Virion Infectivity by Ubiquitination and Proteasomal Degradation of Vif Protein through SCFThe Journal of biological chemistry · 2017Article
- A Novel Regulator of Activation-Induced Cytidine Deaminase/APOBECs in Immunity and Cancer: Schrödinger's CATalytic Pocket.Frontiers in immunology · 2017Review
- Crystal structure of DNA cytidine deaminase ABOBEC3G catalytic deamination domain suggests a binding mode of full-length enzyme to single-stranded DNA.The Journal of biological chemistry · 2015Article
- Ty3 Retrotransposon Hijacks Mating Yeast RNA Processing Bodies to Infect New Genomes.PLoS genetics · 2015Article
- Correlation of APOBEC3 in tumor tissues with clinico-pathological features and survival from hepatocellular carcinoma after curative hepatectomy.International journal of clinical and experimental medicine · 2015Article
- RNase L restricts the mobility of engineered retrotransposons in cultured human cells.Nucleic acids research · 2014Article
- Human protein Staufen-2 promotes HIV-1 proliferation by positively regulating RNA export activity of viral protein Rev.Retrovirology · 2014Article
- Positioning of APOBEC3G/F mutational hotspots in the human immunodeficiency virus genome favors reduced recognition by CD8+ T cells.PloS one · 2014Article
- Host Factors and HIV-1 Replication: Clinical Evidence and Potential Therapeutic Approaches.Frontiers in immunology · 2013Review
- Prototype foamy virus Bet impairs the dimerization and cytosolic solubility of human APOBEC3G.Journal of virology · 2013Article
- Lentivirus restriction by diverse primate APOBEC3A proteins.Virology · 2013Article
- Article
- Activation of innate anti-viral immune response genes in symptomatic benign prostatic hyperplasia.Genes and immunity · 2012Article
- Emerging complexities of APOBEC3G action on immunity and viral fitness during HIV infection and treatment.Retrovirology · 2012Review
- LINE-1 retroelements complexed and inhibited by activation induced cytidine deaminase.PloS one · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The intrinsic antiretroviral factor APOBEC3G (A3G) is highly active against HIV-1 and other retroviruses. In different cell types, A3G is expressed in high-molecular-mass (HMM) RNA- protein complexes or low-molecular-mass (LMM) forms displaying different biological activities. In resting CD4 T cells, a LMM form of A3G potently restricts HIV-1 infection soon after virion entry. However, when T cells are activated, LMM A3G is recruited into HMM complexes that include Staufen-containing RNA granules. These complexes are probably nucleated by the induced expression of Alu/hY retroelement RNAs that accompany T-cell activation. HMM A3G sequesters these retroelement RNAs away from the nuclear long interspersed nuclear element-derived enzymes required for Alu/hY retrotransposition. Human immunodeficiency virus (HIV) exploits this 'window of opportunity' provided by the loss of LMM A3G in activated CD4 T cells to productively infect these cells. During HIV virion formation, newly synthesized LMM A3G is preferentially encapsidated but only under conditions where Vif is absent and thus not able to target A3G for proteasome-mediated degradation. Together, these findings highlight the discrete functions of the different forms of A3G. LMM A3G opposes the external threat posed by exogenous retroviruses, while HMM A3G complexes oppose the internal threat posed by the retrotransposition of select types of retroelements.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.