Evidence map›Paper›PMID 27301021›Full record

ArticlePloS one2016

ALIX Regulates the Ubiquitin-Independent Lysosomal Sorting of the P2Y1 Purinergic Receptor via a YPX3L Motif.

Michael R Dores, Neil J Grimsey, Francisco Mendez, JoAnn Trejo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. The Conserved YPXViruses · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Exosomes: Methods for Isolation and Characterization in Biological Samples.Methods in molecular biology (Clifton, N.J.) · 2024
    Review
  12. Spatial Mechano-Signaling Regulation of GTPases through Non-Degradative Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  13. Vps60 initiates alternative ESCRT-III filaments.The Journal of cell biology · 2023
    Article
  14. The Machinery of Exosomes: Biogenesis, Release, and Uptake.International journal of molecular sciences · 2023
    Review
  15. Receptor Recycling by Retromer.Molecular and cellular biology · 2023
    Review
  16. Review
  17. Review
  18. Article
  19. Atypical p38 Signaling, Activation, and Implications for Disease.International journal of molecular sciences · 2021
    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

4 authors at 2 institutions in 1 country.

Michael R DoresDepartment of Pharmacology, School of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
Neil J GrimseyDepartment of Pharmacology, School of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
Francisco MendezDepartment of Pharmacology, School of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
JoAnn TrejoDepartment of Pharmacology, School of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
University of California, San Diego · USHofstra University · US

Funding

UCSD/SDSU IRACDAK12GM068524 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TREJO, JOANN · 2003 to 2025
$24.4M
Mechanisms Regulating GPCR TraffickingR01GM090689 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TREJO, JOANN · 2010 to 2018
$2.9M
NIGMS NIH HHS K12 GM068524NIGMS NIH HHS R01 GM090689
6 · The paper itself

Abstract

Endocytic sorting and lysosomal degradation are integral to the regulation of G protein-coupled receptor (GPCR) function. Upon ligand binding, classical GPCRs are activated, internalized and recycled or sorted to lysosomes for degradation, a process that requires receptor ubiquitination. However, recent studies have demonstrated that numerous GPCRs are sorted to lysosomes independent of receptor ubiquitination. Here, we describe an ubiquitin-independent lysosomal sorting pathway for the purinergic GPCR P2Y1. After activation, P2Y1 sorts to lysosomes for degradation independent of direct ubiquitination that is mediated by a YPX3L motif within the second intracellular loop that serves as a binding site for the adaptor protein ALIX. Depletion of ALIX or site-directed mutation of the YPX3L motif inhibits P2Y1 sorting into the lumen of multivesicular endosomes/lysosomes and degradation. These findings confirm the function of YPX3L motifs as lysosomal targeting sequences for GPCRs and demonstrate that ALIX mediates the ubiquitin-independent degradation of certain GPCRs.

Indexed as

Protein DenaturationAmino Acid MotifsAnimalsATPases Associated with Diverse Cellular ActivitiesCalcium-Binding ProteinsCell Cycle ProteinsEndosomal Sorting Complexes Required for TransportHeLa CellsHumansLysosomesReceptors, Purinergic P2Y1UbiquitinUbiquitinationVacuolar Proton-Translocating ATPasesATPases Associated with Diverse Cellular ActivitiesCalcium-Binding ProteinsCell Cycle ProteinsEndosomal Sorting Complexes Required for TransportPDCD6IP protein, humanReceptors, Purinergic P2Y1UbiquitinVacuolar Proton-Translocating ATPasesVPS4A protein, human

Identifiers

PMID27301021
PMCPMC4907476
OpenAlexW2429558408

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.