Evidence map›Paper›PMID 23335926›Full record

ArticleFrontiers in immunology2012

Protein kinase C signaling and cell cycle regulation.

Adrian R Black, Jennifer D Black

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
3.3field-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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  5. Protein Kinase C Regulates Meiosis in Mammalian Oocytes.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Calcium and Neural Stem Cell Proliferation.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

6 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.

Adrian R BlackEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center Omaha, NE, USA.
Jennifer D Black
University Medical Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
REGULATION OF CYCLIN D1 EXPRESSION IN THE INTESTINER01DK060632 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BLACK, JENNIFER D. · 2002 to 2014
$2.6M
PKC ISOZYMES AND INTESTINAL EPITHELIAL GROWTH CONTROLR01DK054909 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BLACK, JENNIFER D. · 1999 to 2009
$2.1M
Regulation of cyclin D1 expression in the intestineR56DK060632 · NIDDK · ROSWELL PARK CANCER INSTITUTE CORP · PI BLACK, JENNIFER D. · 2009 to 2009
$373k
NCI NIH HHS P30 CA036727NIDDK NIH HHS R01 DK054909NIDDK NIH HHS R01 DK060632NIDDK NIH HHS R56 DK060632
6 · The paper itself

Abstract

A link between T cell proliferation and the protein kinase C (PKC) family of serine/threonine kinases has been recognized for about 30 years. However, despite the wealth of information on PKC-mediated control of, T cell activation, understanding of the effects of PKCs on the cell cycle machinery in this cell type remains limited. Studies in other systems have revealed important cell cycle-specific effects of PKC signaling that can either positively or negatively impact proliferation. The outcome of PKC activation is highly context-dependent, with the precise cell cycle target(s) and overall effects determined by the specific isozyme involved, the timing of PKC activation, the cell type, and the signaling environment. Although PKCs can regulate all stages of the cell cycle, they appear to predominantly affect G0/G1 and G2. PKCs can modulate multiple cell cycle regulatory molecules, including cyclins, cyclin-dependent kinases (cdks), cdk inhibitors and cdc25 phosphatases; however, evidence points to Cip/Kip cdk inhibitors and D-type cyclins as key mediators of PKC-regulated cell cycle-specific effects. Several PKC isozymes can target Cip/Kip proteins to control G0/G1 → S and/or G2 → M transit, while effects on D-type cyclins regulate entry into and progression through G1. Analysis of PKC signaling in T cells has largely focused on its roles in T cell activation; thus, observed cell cycle effects are mainly positive. A prominent role is emerging for PKCθ, with non-redundant functions of other isozymes also described. Additional evidence points to PKCδ as a negative regulator of the cell cycle in these cells. As in other cell types, context-dependent effects of individual isozymes have been noted in T cells, and Cip/Kip cdk inhibitors and D-type cyclins appear to be major PKC targets. Future studies are anticipated to take advantage of the similarities between these various systems to enhance understanding of PKC-mediated cell cycle regulation in T cells.

Indexed as

cell cyclecyclincyclin-dependent kinasecyclin-dependent kinase inhibitorprotein kinase Csignal transductionT cell activation

Identifiers

PMID23335926
PMCPMC3547298
OpenAlexW2146964357

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.