Evidence map›Paper›PMID 20929444›Full record

ArticleThe Biochemical journal2010

Decoding the intrinsic mechanism that prohibits ALIX interaction with ESCRT and viral proteins.

Xi Zhou, Jiali Si, Joe Corvera, Gary E Gallick, Jian Kuang

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. The Roles of Exosomal Proteins: Classification, Function, and Applications.International journal of molecular sciences · 2023
    Review
  4. The Role of Exosome and the ESCRT Pathway on Enveloped Virus Infection.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Article
  7. Review
  8. Syntenin mediates SRC function in exosomal cell-to-cell communication.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
  10. Multifaceted Roles of ALG-2 in Ca(2+)-Regulated Membrane Trafficking.International journal of molecular sciences · 2016
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Virus budding and the ESCRT pathway.Cell host & microbe · 2013
    Review
  17. Article
  18. Review
  19. Review
  20. Article
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

5 authors at 3 institutions in 1 country.

Xi ZhouDepartment of Experimental Therapeutics, The University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, USA.
Jiali Si
Joe Corvera
Gary E Gallick
Jian Kuang
The University of Texas MD Anderson Cancer Center · USA&G Pharmaceutical (United States) · USUniversity of Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Effects of DNA Damaging Agents on G2 Phase CheckpointR01CA093941 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI KUANG, JIAN · 2002 to 2005
$998k
NCI NIH HHS 1 R01 CA93941NCI NIH HHS CA-16672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA093941
6 · The paper itself

Abstract

The adaptor protein ALIX [ALG-2 (apoptosis-linked-gene-2 product)-interacting protein X] links retroviruses to ESCRT (endosomal sorting complex required for transport) machinery during retroviral budding. This function of ALIX requires its interaction with the ESCRT-III component CHMP4 (charged multivesicular body protein 4) at the N-terminal Bro1 domain and retroviral Gag proteins at the middle V domain. Since cytoplasmic or recombinant ALIX is unable to interact with CHMP4 or retroviral Gag proteins under non-denaturing conditions, we constructed ALIX truncations and mutations to define the intrinsic mechanism through which ALIX interactions with these partner proteins are prohibited. Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins. Relieving the intramolecular interaction of ALIX, by ectopically expressing a binding partner for one of the intramolecular interaction sites or by deleting one of these sites, promotes ALIX interaction with these partner proteins and facilitates ALIX association with the membrane. Ectopic expression of a GFP (green fluorescent protein)-ALIX mutant with a constitutively open conformation, but not the wild-type protein, increases EIAV (equine infectious anaemia virus) budding from HEK (human embryonic kidney)-293 cells. These findings predict that relieving the autoinhibitory intramolecular interaction of ALIX is a critical step for ALIX to participate in retroviral budding.

Indexed as

Calcium-Binding ProteinsCell Cycle ProteinsCell MembraneDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportGene Products, gagHEK293 CellsHumansHydrophobic and Hydrophilic InteractionsInfectious Anemia Virus, EquineMutant ProteinsOncogene Protein pp60(v-src)Proline-Rich Protein DomainsProtein Interaction Domains and MotifsRecombinant Fusion ProteinsRecombinant ProteinsCalcium-Binding ProteinsCell Cycle ProteinsCHMP4B protein, humanDNA-Binding Proteinsearly endosome antigen 1Endosomal Sorting Complexes Required for TransportGene Products, gagMutant ProteinsOncogene Protein pp60(v-src)PDCD6IP protein, humanRecombinant Fusion ProteinsRecombinant ProteinsRetroviridae ProteinsTranscription FactorsTsg101 ProteinVesicular Transport Proteins

Identifiers

PMID20929444
PMCPMC4391464
OpenAlexW2082670593

What OpenQuestion holds

Textmetadata
LicenceTDM
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.