Evidence map›Paper›PMID 23572508›Full record

ArticleJournal of cell science2013

Ubiquitylation of phosphatidylinositol 4-phosphate 5-kinase type I γ by HECTD1 regulates focal adhesion dynamics and cell migration.

Xiang Li, Qi Zhou, Manjula Sunkara, Matthew L Kutys, Zhaofei Wu, Piotr Rychahou, Andrew J Morris, Haining Zhu, B Mark Evers, Cai Huang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.6field-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

48 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Article
  8. Article
  9. Review
  10. CircRNA-miRNA interactions in atherogenesis.Molecular and cellular biochemistry · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Novel genetic variants ofAmerican journal of cancer research · 2020
    Article
  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

10 authors at 3 institutions in 1 country.

Xiang LiMarkey Cancer Center, University of Kentucky, Lexington, KY 40506, USA.
Qi Zhou
Manjula Sunkara
Matthew L Kutys
Zhaofei Wu
Piotr Rychahou
Andrew J Morris
Haining Zhu
B Mark Evers
Cai Huang
University of Kentucky · USMarkey Cancer Center · USNational Institute of Dental and Craniofacial Research · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2012 to 2017
$13.7M
Matrix Organization and DimensionalityZIADE000718 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH · 2009 to 2025
$8.9M
INTEGRIN RECEPTOR FUNCTION AND SIGNALINGZ01DE000524 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH MANAO · 1991 to 2008
$1.5M
Thermo/Finnigan TSQ AM Triple Stage Quadrupole Mass SpectrometerS10RR024598 · NCRR · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2008 to 2008
$493k
Intramural NIH HHS Z01 DE000524NCI NIH HHS P30 CA177558NCRR NIH HHS S10 RR024598NIDCR NIH HHS DE000524-21NIGMS NIH HHS GM0503888NIGMS NIH HHS P20 GM103527NIGMS NIH HHS P20 GM103527-05
6 · The paper itself

Abstract

Phosphatidylinositol 4-phosphate 5-kinase type I γ (PIPKIγ90) binds talin and localizes at focal adhesions (FAs). Phosphatidylinositol (4,5)-bisphosphate (PIP2) generated by PIPKIγ90 is essential for FA formation and cell migration. On the other hand, PIPKIγ90 and the β-integrin tail compete for overlapping binding sites on talin. Enhanced PIPKIγ90-talin interaction suppresses talin binding to the β-integrin. It is unknown how PIPKIγ90 is removed from the PIPKIγ90-talin complex after on-site PIP2 production during cell migration. Here we show that PIPKIγ90 is a substrate for HECTD1, an E3 ubiquitin ligase regulating cell migration. HECTD1 ubiquitinated PIPKIγ90 at lysine 97 and resulted in PIPKIγ90 degradation. Expression of the mutant PIPKIγ90(K97R) enhanced PIP2 and PIP3 production, inhibited FA assembly and disassembly and inhibited cancer cell migration, invasion and metastasis. Interestingly, mutation at tryptophan 647 abolished the inhibition of PIPKIγ90(K97R) on FA dynamics and partially rescued cancer cell migration and invasion. Thus, cycling PIPKIγ90 ubiquitylation by HECTD1 and consequent degradation remove PIPKIγ90 from talin after on-site PIP2 production, providing an essential regulatory mechanism for FA dynamics and cell migration.

Indexed as

AnimalsCell LineCell MovementCHO CellsCricetinaeCricetulusFocal AdhesionsHEK293 CellsHumansIntegrin beta ChainsLysineNeoplasm InvasivenessNeoplasm MetastasisPhosphatidylinositol 4,5-DiphosphatePhosphotransferases (Alcohol Group Acceptor)Talin1-phosphatidylinositol-4-phosphate 5-kinaseIntegrin beta ChainsLysinePhosphatidylinositol 4,5-DiphosphatePhosphotransferases (Alcohol Group Acceptor)TalinUbiquitin-Protein LigasesHECTD1InvasionMetastasisPIP5K1CUbiquitylation

Identifiers

PMID23572508
PMCPMC3687698
OpenAlexW2104492411

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.