Evidence map›Paper›PMID 22435553›Full record

ReviewImmunological reviews2012

The atypical PKCs in inflammation: NF-κB and beyond.

Maria T Diaz-Meco, Jorge Moscat

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

74 citing papers in PubMed, 126 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. High Expression ofCancer genomics & proteomics · 2025
    Article
  9. Article
  10. Lung Transcriptomics Link Emphysema to Barrier Dysfunction and Macrophage Subpopulations.American journal of respiratory and critical care medicine · 2025
    Article
  11. Article
  12. Anti-Neuroinflammatory Effects ofInternational journal of molecular sciences · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

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.

Maria T Diaz-MecoSanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA.
Jorge Moscat
Sanford Burnham Prebys Medical Discovery Institute · US

Funding

The p62/atypical PKC signaling complex in Th2 differentiation and asthmaR01AI072581 · NIAID · UNIVERSITY OF CINCINNATI · PI MOSCAT, JORGE · 2008 to 2012
$2.1M
Role and mechanism of action of p62/Sqstm1 in Ras-induced tumorigenesis in lungR01CA132847 · NCI · UNIVERSITY OF CINCINNATI · PI MOSCAT, JORGE · 2009 to 2013
$2.0M
The Par-4/PKCz complex in prostate cancerR01CA134530 · NCI · UNIVERSITY OF CINCINNATI · PI DIAZ MECO CONDE, MARIA TERESA · 2009 to 2013
$1.8M
Obesity-Induced Inflammation and Insulin Resistance by the p62/PKCzeta SignalingR01DK088107 · NIDDK · UNIVERSITY OF CINCINNATI · PI MOSCAT, JORGE · 2010 to 2012
$1.1M
NCI NIH HHS R01 CA132847NCI NIH HHS R01CA132847NCI NIH HHS R01 CA134530NCI NIH HHS R01CA134530NIAID NIH HHS R01 AI072581NIAID NIH HHS R01AI072581NIDDK NIH HHS R01 DK088107NIDDK NIH HHS R01DK088107
6 · The paper itself

Abstract

From the very early days of nuclear factor-κB (NF-κB) research, it was recognized that different protein kinase C (PKC) isoforms might be involved in the activation of NF-κB. Pharmacological tools and pseudosubstrate inhibitors suggested that these kinases play a role in this important inflammatory and survival pathway; however, it was the analysis of several genetic mouse knockout models that revealed the complexity and interrelations between the different components of the PB1 network in several cellular functions, including T-cell biology, bone homeostasis, inflammation associated with the metabolic syndrome, and cancer. These studies unveiled, for example, the critical role of PKCζ as a positive regulator of NF-κB through the regulation of RelA but also its inflammatory suppressor activities through the regulation of the interleukin-4 signaling cascade. This observation is of relevance in T cells, where p62, PKCζ, PKCλ/ι, and NBR1 establish a mesh of interactions that culminate in the regulation of T-cell effector responses through the modulation of T-cell polarity. Many questions remain to be answered, not just from the point of view of the implication for NF-κB activation but also with regard to the in vivo interplay between these pathways in pathophysiological processes like obesity and cancer.

Indexed as

AdipocytesAnimalsHumansInflammationIsoenzymesLymphocyte ActivationNF-kappa BProtein Kinase CProtein Kinase C-lambdaReceptors, Proteinase-ActivatedSignal TransductionT-LymphocytesIsoenzymesNF-kappa BProtein Kinase CProtein Kinase C-lambdaReceptors, Proteinase-Activated

Identifiers

PMID22435553
PMCPMC3531713
OpenAlexW1879241542

What OpenQuestion holds

Textmetadata
LicenceTDM
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.