Evidence map›Paper›PMID 14734537›Full record

ArticleThe Journal of cell biology2004

Atypical protein kinase C (PKCzeta/lambda) is a convergent downstream target of the insulin-stimulated phosphatidylinositol 3-kinase and TC10 signaling pathways.

Makoto Kanzaki, Silvia Mora, Joseph B Hwang, Alan R Saltiel, Jeffrey E Pessin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.Cellular and molecular life sciences : CMLS · 2018
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Epidermal polarity genes in health and disease.Cold Spring Harbor perspectives in medicine · 2014
    Review
  9. Review
  10. Article
  11. 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 1 country.

Makoto KanzakiDept. of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, NY 11794-8651, USA.
Silvia Mora
Joseph B Hwang
Alan R Saltiel
Jeffrey E Pessin
Stony Brook University · USUniversity of Michigan–Ann Arbor · US

Funding

REGULATION OF THE INSULIN RECEPTOR KINASER01DK033823 · NIDDK · UNIVERSITY OF IOWA · PI KURLAND, IRWIN JACK, PESSIN, JEFFREY E. · 1986 to 2022
$6.7M
The Role of G Proteins in Insulin ActionR01DK061618 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SALTIEL, ALAN R. · 2002 to 2016
$5.1M
Signaling Pathways in Insulin ActionR01DK060591 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SALTIEL, ALAN R. · 2002 to 2016
$4.9M
Intracellular signaling by the insulin receptor kinaseR37DK033823 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI PESSIN, JEFFREY E. · 2005 to 2014
$4.2M
Novel Insulin Signals Regulating GLUT4 TranslocationR01DK059291 · NIDDK · UNIVERSITY OF IOWA · PI PESSIN, JEFFREY E · 2001 to 2005
$1.9M
The Regulation of Glucose Transport by InsulinF32DK061188 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HWANG, JOSEPH B · 2002 to 2004
$143k
NIDDK NIH HHS DK33823NIDDK NIH HHS DK59291NIDDK NIH HHS DK60591NIDDK NIH HHS DK61188NIDDK NIH HHS DK61618NIDDK NIH HHS F32 DK061188NIDDK NIH HHS R01 DK033823NIDDK NIH HHS R01 DK059291NIDDK NIH HHS R01 DK060591NIDDK NIH HHS R01 DK061618NIDDK NIH HHS R37 DK033823
6 · The paper itself

Abstract

Insulin stimulation of adipocytes resulted in the recruitment of atypical PKC (PKCzeta/lambda) to plasma membrane lipid raft microdomains. This redistribution of PKCzeta/lambda was prevented by Clostridium difficile toxin B and by cholesterol depletion, but was unaffected by inhibition of phosphatidylinositol (PI) 3-kinase activity. Expression of the constitutively active GTP-bound form of TC10 (TC10Q/75L), but not the inactive GDP-bound mutant (TC10/T31N), targeted PKCzeta/lambda to the plasma membrane through an indirect association with the Par6-Par3 protein complex. In parallel, insulin stimulation as well as TC10/Q75L resulted in the activation loop phosphorylation of PKCzeta. Although PI 3-kinase activation also resulted in PKCzeta/lambda phosphorylation, it was not recruited to the plasma membrane. Furthermore, insulin-induced GSK-3beta phosphorylation was mediated by both PI 3-kinase-PKB and the TC10-Par6-atypical PKC signaling pathways. Together, these data demonstrate that PKCzeta/lambda can serve as a convergent downstream target for both the PI 3-kinase and TC10 signaling pathways, but only the TC10 pathway induces a spatially restricted targeting to the plasma membrane.

Indexed as

3T3 CellsAdipocytesAnimalsCell FractionationCell MembraneInsulinIsoenzymesMicePhosphatidylinositol 3-KinasesProtein Kinase CProtein Kinase C-lambdaProtein Kinase C zetaProtein Transportrho GTP-Binding ProteinsSubstrate SpecificityInsulinIsoenzymesPhosphatidylinositol 3-KinasesProtein Kinase CProtein Kinase C-lambdaProtein Kinase C zetarho GTP-Binding ProteinsRhoq protein, mouse

Identifiers

PMID14734537
PMCPMC2172328
OpenAlexW2110816024

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.