Evidence map›Paper›PMID 28264927›Full record

ArticleJournal of cell science2017

Missing-in-metastasis protein downregulates CXCR4 by promoting ubiquitylation and interaction with small Rab GTPases.

Lushen Li, Shaneen S Baxter, Ning Gu, Min Ji, Xi Zhan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Trial
  2. Article
  3. MTSS1: beyond the integration of actin and membrane dynamics.Cellular and molecular life sciences : CMLS · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
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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 2 institutions in 2 countries.

Lushen LiSchool of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, China.
Shaneen S BaxterCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Ning GuSchool of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, China.ORCID 0000-0003-0047-337X
Min JiSchool of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, China.
Xi ZhanCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, USA xzhan@som.umaryland.edu.ORCID 0000-0003-3291-3050
University of Maryland, Baltimore · USSoutheast University · CN

Funding

EXPAND PARTICIPATION BY MINORITIES IN BIOMEDICAL SCIENCER25GM055036 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE COUNTY · PI SUMMERS, MICHAEL FINLEY · 1996 to 2021
$16.9M
Vascular Biology Training ProgramT32HL007698 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI Rosemary A Kozar, Dudley K. Strickland · 1991 to 2026
$8.7M
The Role of MIM in growth factor signaling and cell motilityR01CA113809 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI ZHAN, STEVEN · 2006 to 2016
$2.7M
NCI NIH HHS R01 CA113809NHLBI NIH HHS T32 HL007698NIGMS NIH HHS R25 GM055036
6 · The paper itself

Abstract

Surface expression of chemokine receptor CXCR4 is downregulated by missing-in-metastasis protein (MIM; also known as MTSS1), a member of the inverse BAR (I-BAR)-domain protein family that recognizes and generates membranes with negative curvature. Yet, the mechanism for the regulation is unknown. Here, we show that MIM forms a complex with CXCR4 by binding to E3 ubiquitin ligase AIP4 (also known as ITCH) in response to stromal cell-derived factor 1 (SDF-1; also known as CXCL12). Overexpression of MIM promoted CXCR4 ubiquitylation, inhibited cellular response to SDF-1, caused accumulation and aggregation of multivesicular bodies (MVBs) in the cytoplasm, and promoted CXCR4 sorting into MVBs in a manner depending on binding to AIP4. In response to SDF-1, MIM also bound transiently to the small GTPase Rab5 at 5 min and to Rab7 at 30 min. Binding to Rab7 requires an N-terminal coiled-coil motif, deletion of which abolished MIM-mediated MVB formation and CXCR4 internalization. Our results unveil a previously unknown property of MIM that establishes the linkage of protein ubiquitylation with Rab-guided trafficking of CXCR4 in endocytic vesicles.

Indexed as

Down-RegulationAnimalsChemokine CXCL12EndocytosisEndosomesHeLa CellsHumansMiceMice, KnockoutMicrofilament ProteinsNeoplasm ProteinsProtein BindingProtein Transportrab GTP-Binding ProteinsReceptors, CXCR4Transport VesiclesChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanCXCR4 protein, mouseMicrofilament ProteinsMtss1 protein, mouseNeoplasm Proteinsrab GTP-Binding ProteinsReceptors, CXCR4AIP4CXCR4MIMMVBsRab7Ubiquitylation

Identifiers

PMID28264927
PMCPMC5399787
OpenAlexW2594394947

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.