Evidence map›Paper›PMID 27780861›Full record

ArticleThe Journal of biological chemistry2016

p70S6K1 (S6K1)-mediated Phosphorylation Regulates Phosphatidylinositol 4-Phosphate 5-Kinase Type I γ Degradation and Cell Invasion.

Naser Jafari, Qiaodan Zheng, Liqing Li, Wei Li, Lei Qi, Jianyong Xiao, Tianyan Gao, Cai Huang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. S6 kinase 1 at the central node of cell size and ageing.Frontiers in cell and developmental biology · 2022
    Review
  9. Article
  10. Novel genetic variants ofAmerican journal of cancer research · 2020
    Article
  11. Article
  12. Cdk5-mediated phosphorylation regulates phosphatidylinositol 4-phosphate 5-kinase type I γ 90 activity and cell invasion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. 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

8 authors at 2 institutions in 1 country.

Naser JafariFrom the Markey Cancer Center and.
Qiaodan ZhengFrom the Markey Cancer Center and.
Liqing LiFrom the Markey Cancer Center and.
Wei LiFrom the Markey Cancer Center and.
Lei QiFrom the Markey Cancer Center and.
Jianyong XiaoFrom the Markey Cancer Center and.
Tianyan GaoFrom the Markey Cancer Center and.
Cai HuangFrom the Markey Cancer Center and cai-huang@uky.edu.ORCID http://orcid.org/0000-0003-4258-3841
Markey Cancer Center · USUniversity of Kentucky · 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 PHLPP in Colon CancerR01CA133429 · NCI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GAO, TIANYAN · 2009 to 2024
$5.6M
NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA133429
6 · The paper itself

Abstract

Phosphatidylinositol 4-phosphate 5-kinase type I γ (PIPKIγ90) ubiquitination and subsequent degradation regulate focal adhesion assembly, cell migration, and invasion. However, it is unknown how upstream signals control PIPKIγ90 ubiquitination or degradation. Here we show that p70S6K1 (S6K1), a downstream target of mechanistic target of rapamycin (mTOR), phosphorylates PIPKIγ90 at Thr-553 and Ser-555 and that S6K1-mediated PIPKIγ90 phosphorylation is essential for cell migration and invasion. Moreover, PIPKIγ90 phosphorylation is required for the development of focal adhesions and invadopodia, key machineries for cell migration and invasion. Surprisingly, substitution of Thr-553 and Ser-555 with Ala promoted PIPKIγ90 ubiquitination but enhanced the stability of PIPKIγ90, and depletion of S6K1 also enhanced the stability of PIPKIγ90, indicating that PIPKIγ90 ubiquitination alone is insufficient for its degradation. These data suggest that S6K1-mediated PIPKIγ90 phosphorylation regulates cell migration and invasion by controlling PIPKIγ90 degradation.

Indexed as

ProteolysisAnimalsCell MovementCHO CellsCricetinaeCricetulusFocal AdhesionsHumansPhosphorylationPhosphotransferases (Alcohol Group Acceptor)Ribosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine KinasesUbiquitination1-phosphatidylinositol-4-phosphate 5-kinaseMTOR protein, humanPhosphotransferases (Alcohol Group Acceptor)ribosomal protein S6 kinase, 70kD, polypeptide 1Ribosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine Kinasescell invasioncell migrationphosphatidylinositol kinasePIP5K1Cprotein degradationS6 kinase

Identifiers

PMID27780861
PMCPMC5207268
OpenAlexW2533675856

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.