ArticleRetrovirology2011
The cellular source for APOBEC3G's incorporation into HIV-1.
Article in Retrovirology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers, 1 of them a synthesis that pooled it.
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
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Gene expression profiling of host lipid metabolism in SARS-CoV-2 infected patients: a systematic review and integrated bioinformatics analysis.BMC infectious diseases · 2024Pooled it
- Mutations of Glu560 within HIV-1 Envelope Glycoprotein N-terminal heptad repeat region contribute to resistance to peptide inhibitors of virus entry.Retrovirology · 2019Article
- Enterovirus 71 antagonizes the inhibition of the host intrinsic antiviral factor A3G.Nucleic acids research · 2018Article
- The role of cytidine deaminases on innate immune responses against human viral infections.BioMed research international · 2013Review
- Intrinsic immunity against retrotransposons by APOBEC cytidine deaminases.Frontiers in microbiology · 2013Article
- Emerging complexities of APOBEC3G action on immunity and viral fitness during HIV infection and treatment.Retrovirology · 2012Review
- Retraction: The cellular source for APOBEC3G's incorporation into HIV-1.Retrovirology · 2011Article
- Function of membrane rafts in viral lifecycles and host cellular response.Biochemistry research international · 2011Article
Corrections and comments
- Retraction · 2011-11-05Duplication of/in Image · Objections by Third Party ·
- Retracted
Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundHuman APOBEC3G (hA3G) has been identified as a cellular inhibitor of HIV-1 infectivity. Viral incorporation of hA3G is an essential step for its antiviral activity. Although the mechanism underlying hA3G virion encapsidation has been investigated extensively, the cellular source of viral hA3G remains unclear.
resultsPrevious studies have shown that hA3G forms low-molecular-mass (LMM) and high-molecular-mass (HMM) complexes. Our work herein provides evidence that the majority of newly-synthesized hA3G interacts with membrane lipid raft domains to form Lipid raft-associated hA3G (RA hA3G), which serve as the precursor of the mature HMM hA3G complex, while a minority of newly-synthesized hA3G remains in the cytoplasm as a soluble LMM form. The distribution of hA3G among the soluble LMM form, the RA LMM form and the mature forms of HMM is regulated by a mechanism involving the N-terminal part of the linker region and the C-terminus of hA3G. Mutagenesis studies reveal a direct correlation between the ability of hA3G to form the RA LMM complex and its viral incorporation.
conclusionsTogether these data suggest that the Lipid raft-associated LMM A3G complex functions as the cellular source of viral hA3G.
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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.