Evidence map›Paper›PMID 16525020›Full record

ArticleMolecular biology of the cell2006

Protein kinase Czeta mediates insulin-induced glucose transport through actin remodeling in L6 muscle cells.

Li-Zhong Liu, Hai-Lu Zhao, Jin Zuo, Stanley K S Ho, Juliana C N Chan, Yan Meng, Fu-De Fang, Peter C Y Tong

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.4field-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

27 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
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  7. The Effect of SIN1 and Microtubules on Insulin Induced PKC ζ Activation.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  8. Review
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  10. Cracking the O-GlcNAc code in metabolism.Trends in endocrinology and metabolism: TEM · 2013
    Review
  11. Article
  12. Article
  13. Article
  14. Article
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  16. Metabolic functions of atypical protein kinase C: "good" and "bad" as defined by nutritional status.American journal of physiology. Endocrinology and metabolism · 2010
    Review
  17. Article
  18. 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 2 countries.

Li-Zhong LiuDepartment of Biochemistry, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, 100005 Beijing, China.
Hai-Lu Zhao
Jin Zuo
Stanley K S Ho
Juliana C N Chan
Yan Meng
Fu-De Fang
Peter C Y Tong
Chinese University of Hong Kong · HKChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase C (PKC) zeta has been implicated in insulin-induced glucose uptake in skeletal muscle cell, although the underlying mechanism remains unknown. In this study, we investigated the effect of PKCzeta on actin remodeling and glucose transport in differentiated rat L6 muscle cells expressing myc-tagged glucose transporter 4 (GLUT4). On insulin stimulation, PKCzeta translocated from low-density microsomes to plasma membrane accompanied by increase in GLUT4 translocation and glucose uptake. Z-scan confocal microscopy revealed a spatial colocalization of relocated PKCzeta with the small GTPase Rac-1, actin, and GLUT4 after insulin stimulation. The insulin-mediated colocalization, PKCzeta distribution, GLUT4 translocation, and glucose uptake were inhibited by wortmannin and cell-permeable PKCzeta pseudosubstrate peptide. In stable transfected cells, overexpression of PKCzeta caused an insulin-like effect on actin remodeling accompanied by a 2.1-fold increase in GLUT4 translocation and 1.7-fold increase in glucose uptake in the absence of insulin. The effects of PKCzeta overexpression were abolished by cell-permeable PKCzeta pseudosubstrate peptide, but not wortmannin. Transient transfection of constitutively active Rac-1 recruited PKCzeta to new structures resembling actin remodeling, whereas dominant negative Rac-1 prevented the insulin-mediated PKCzeta translocation. Together, these results suggest that PKCzeta mediates insulin effect on glucose transport through actin remodeling in muscle cells.

Indexed as

ActinsAnimalsBiological Transport, ActiveCell MembraneCells, CulturedGlucoseGlucose Transporter Type 4InsulinMonomeric GTP-Binding ProteinsMuscle CellsPhosphorylationProtein Kinase CProtein Kinase C zetaProtein Transportrac1 GTP-Binding ProteinRatsActinsGlucoseGlucose Transporter Type 4InsulinMonomeric GTP-Binding ProteinsProtein Kinase CProtein Kinase C zetarac1 GTP-Binding ProteinSlc2a4 protein, rat

Identifiers

PMID16525020
PMCPMC1446104
OpenAlexW2107615542

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.