Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A functional conserved intronic G run in HIV-1 intron 3 is critical to counteract APOBEC3G-mediated host restriction.

Retrovirology - 29 Aug 2014

Widera Marek, Hillebrand Frank, Erkelenz Steffen, Vasudevan Ananda Ayyappan Jaguva, Münk Carsten, Schaal Heiner

Abstract excerpt

BACKGROUND: The HIV-1 accessory proteins, Viral Infectivity Factor (Vif) and the pleiotropic Viral Protein R (Vpr) are important for efficient virus replication. While in non-permissive cells an appropriate amount of Vif is critical to counteract APOBEC3G-mediated host restriction, the Vpr-induced G2 arrest sets the stage for highest transcriptional activity of the HIV-1 long terminal repeat. RESULTS: We...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to APOBEC-3G Deaminase
Share to Cytidine Deaminase

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Products, vpr

Share to Host Specificity

Share to RNA Splicing

Share to vif Gene Products, Human Immunodeficiency Virus

Share to Virus Replication

Share to vpr Gene Products, Human Immunodeficiency Virus

Source

Open in PubMed Open full text

Identifiers

PMID: 25169827
DOI: 10.1186/s12977-014-0072-1
PMCID: PMC4163160

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A functional conserved intronic G run in HIV-1 intron 3 is critical to counteract APOBEC3G-mediated host restriction.PMID 25169827Read ↗

An intronic G run within HIV-1 intron 2 is critical for splicing regulation of vif mRNA.Semantic proximity Read ↗

Regulation of Vif mRNA splicing by human immunodeficiency virus type 1 requires 5' splice site D2 and an exonic splicing enhancer to counteract cellular restriction factor APOBEC3G.Semantic proximity Read ↗

Translational regulation of APOBEC3G mRNA by Vif requires its 5'UTR and contributes to restoring HIV-1 infectivity.Semantic proximity Read ↗

Functional domains of APOBEC3G required for antiviral activity.Semantic proximity Read ↗

Multifaceted counter-APOBEC3G mechanisms employed by HIV-1 Vif.Semantic proximity Read ↗

HIV-1 subtype variability in Vif derived from molecular clones affects APOBEC3G-mediated host restriction.Semantic proximity Read ↗

Vpr14-88-Apobec3G fusion protein is efficiently incorporated into Vif-positive HIV-1 particles and inhibits viral infection.Semantic proximity Read ↗

Natural APOBEC3C variants can elicit differential HIV-1 restriction activitySemantic proximity Read ↗

GANP interacts with APOBEC3G and facilitates its encapsidation into the virions to reduce HIV-1 infectivity.Semantic proximity Read ↗

Suppression of HIV-1 Infection by APOBEC3 Proteins in Primary Human CD4 <sup>+</sup> T Cells Is Associated with Inhibition of Processive Reverse Transcription as Well as Excessive Cytidine DeaminationSemantic proximity Read ↗

APOBEC3F can inhibit the accumulation of HIV-1 reverse transcription products in the absence of hypermutation. Comparisons with APOBEC3G.Semantic proximity Read ↗

APOBEC3G induces a hypermutation gradient: purifying selection at multiple steps during HIV-1 replication results in levels of G-to-A mutations that are high in DNA, intermediate in cellular viral RNA, and low in virion RNA.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.