Evidence map›Paper›PMID 25590520›Full record

ArticleCell cycle (Georgetown, Tex.)2015

Evolutionarily conserved pressure for the existence of distinct G2/M cell cycle arrest and A3H inactivation functions in HIV-1 Vif.

Ke Zhao, Juan Du, Yajuan Rui, Wenwen Zheng, Jian Kang, Jingwei Hou, Kang Wang, Wenyan Zhang, Viviana A Simon, Xiao-Fang Yu

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 33% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Structural insights into PPP2R5A degradation by HIV-1 Vif.Nature structural & molecular biology · 2024
    Article
  5. Article
  6. Article
  7. Demystifying Cell Cycle Arrest by HIV-1 Vif.Trends in microbiology · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Ke Zhaoa Institute of Virology and AIDS Research ; First Hospital of Jilin University ; Changchun , Jilin , China.
Juan Du
Yajuan Rui
Wenwen Zheng
Jian Kang
Jingwei Hou
Kang Wang
Wenyan Zhang
Viviana A Simon
Xiao-Fang Yu
First Hospital of Jilin University · CNJilin University · CNOffice of Infectious Diseases · USUniversity of Baltimore · US

Funding

HIV Evolution Driven by Intracellular DefensesR01AI064001 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SIMON, VIVIANA A · 2005 to 2015
$3.8M
Genomic Determinants of Intrinsic Antiviral Host DefensesR01AI089246 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SIMON, VIVIANA A · 2010 to 2014
$2.1M
Role of Cul5 E3 Ubiquitin ligasae in HIV Vif function: A novel regulatorR56AI062644 · NIAID · JOHNS HOPKINS UNIVERSITY · PI YU, XIAO-FANG · 2010 to 2010
$369k
NIAID NIH HHS 2R56AI62644-6NIAID NIH HHS R01 AI064001NIAID NIH HHS R01 AI089246
6 · The paper itself

Abstract

HIV-1 Vif assembles the Cul5-EloB/C E3 ubiquitin ligase to induce proteasomal degradation of the cellular antiviral APOBEC3 proteins. Detailed structural studies have confirmed critical functional domains in Vif that we have previously identified as important for the interaction of EloB/C, Cul5, and CBFβ. However, the mechanism by which Vif recognizes substrates remains poorly understood. Specific regions of Vif have been identified as being responsible for binding and depleting APOBEC3G and APOBEC3F. Interestingly, we have now identified distinct yet overlapping domains that are required for HIV-1 Vif-mediated G2/M-phase cell cycle arrest and APOBEC3H degradation, but not for the inactivation of APOBEC3G or APOBEC3F. Surprisingly, Vif molecules from primary HIV-1 variants that caused G2/M arrest were unable to inactivate APOBEC3H; on the other hand, HIV-1 Vif variants that could inactivate APOBEC3H were unable to induce G2/M arrest. All of these Vif variants still maintained the ability to inactivate APOBEC3G/F. Thus, primary HIV-1 variants have evolved to possess distinct functional activities that allow them to suppress APOBEC3H or cause G2 cell cycle arrest, using mutually exclusive interface domains. APOBEC3H depletion and G2 arrest are apparently evolutionary selected features that cannot co-exist on a single Vif molecule. The existence and persistence of both types of HIV-1 Vif variant suggests the importance of APOBEC3H suppression and cell cycle regulation for HIV-1's survival in vivo.

Indexed as

Biological EvolutionG2 Phase Cell Cycle CheckpointsM Phase Cell Cycle CheckpointsAmino AcidsAmino Acid SequenceAminohydrolasesHEK293 CellsHIV-1HumansModels, MolecularMolecular Sequence DataProteolysisSequence Deletionvif Gene Products, Human Immunodeficiency VirusAmino AcidsAminohydrolasesAPOBEC3H protein, humanvif Gene Products, Human Immunodeficiency Virusvif protein, Human immunodeficiency virus 1APOBEC3Hcell cycle regulationevolutionary selectionproteasomal degradationVif

Identifiers

PMID25590520
PMCPMC4612454
OpenAlexW1549244925

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.