Evidence map›Paper›PMID 8739230›Full record

ReviewMolecular and cellular biochemistry

Signalling by protein kinase C isoforms in the heart.

M Pucéat, G Vassort

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular and cellular biochemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Molecular and cellular mechanisms of cardiotoxicity.Environmental health perspectives · 2001
    Review
  9. Article
  10. Activation of epsilon protein kinase C correlates with a cardioprotective effect of regular ethanol consumption.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  11. 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

2 authors at 1 institution in 1 country.

M PucéatLaboratoire de Physiopathologie Cardiovasculaire, INSERM U390, Montpellier, France.
G Vassort
Hôpital Arnaud de Villeneuve · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding transmembrane signalling process is one of the major challenge of the decade. In most tissues, since Fisher and Krebs's discovery in the 1950's, protein phosphorylation has been widely recognized as a key event of this cellular function. Indeed, binding of hormones or neurotransmitters to specific membrane receptors leads to the generation of cytosoluble second messengers which in turn activate a specific protein kinase. Numerous protein kinases have been so far identified and roughly classified into two groups, namely serine/threonine and tyrosine kinases on the basis of the target acid although some more recently discovered kinases like MEK (or MAP kinase kinase) phosphorylate both serine and tyrosine residues. Protein kinase C is a serine/threonine kinase that was first described by Takai et al. [1] as a Ca- and phospholipid-dependent protein kinase. Later on, Kuo et al. [2] found that PKC was expressed in most tissues including the heart. The field of investigation became more complicated when it was found that the kinase is not a single molecular entity and that several isoforms exist. At present, 12 PKC isoforms and other PKC-related kinases [3] were identified in mammalian tissues. These are classified into three groups. (1) the Ca-activated alpha-, beta-, and gamma-PKCs which display a Ca-binding site (C2); (2) the Ca-insensitive delta-, epsilon-, theta-, eta-, and mu-PKCs. The kinases that belong to both of these groups display two cysteine-rich domains (C1) which bind phorbol esters (for recent review on PKC structure, see [4]). (3) The third group was named atypical PKCs and include zeta, lambda, and tau-PKCs that lack both the C2 and one cysteine-rich domain. Consequently, these isoforms are Ca-insensitive and cannot be activated by phorbol esters [5]. In the heart, evidence that multiple PKC isoforms exist was first provided by Kosaka et at. [6] who identified by chromatography at least two PKC-related isoenzymes. Numerous studies were thus devoted to the biochemical characterization of these isoenzymes (see [7] for review on cardiac PKCs) as well as to the identification of their substrates. This overview aims at updating the present knowledge on the expression, activation and functions of PKC isoforms in cardiac cells.

Indexed as

Signal TransductionAnimalsBinding SitesCalciumCardiomegalyCell MembraneContractile ProteinsHeartHeart DiseasesHumansIsoenzymesMitogen-Activated Protein Kinase KinasesMyocardiumProtein Kinase CProtein KinasesProtein Serine-Threonine KinasesCalciumContractile ProteinsIsoenzymesMitogen-Activated Protein Kinase KinasesProtein Kinase CProtein KinasesProtein Serine-Threonine KinasesProtein-Tyrosine Kinases

Identifiers

PMID8739230
OpenAlexW2091093895

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.