Evidence map›Paper›PMID 25362646›Full record

ArticleOncotarget2014

A novel DAG-dependent mechanism links PKCɑ and Cyclin B1 regulating cell cycle progression.

Alessandro Poli, Giulia Ramazzotti, Alessandro Matteucci, Lucia Manzoli, Annalisa Lonetti, Pann-Ghill Suh, James A McCubrey, Lucio Cocco

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. 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
1.4field-weighted citation impact, top 20% 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, 22 citations in OpenAlex.

  1. Secondary Metabolites fromMetabolites · 2025
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  7. Nuclear Phosphoinositides: Their Regulation and Roles in Nuclear Functions.International journal of molecular sciences · 2019
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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 4 institutions in 3 countries.

Alessandro PoliCell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy.
Giulia RamazzottiCell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy.
Alessandro MatteucciCNR-National Research Council of Italy, Institute of Molecular Genetics, Bologna, Italy.
Lucia ManzoliCell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy.
Annalisa LonettiCell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy.
Pann-Ghill SuhSchool of Nano-Biotechnology and Chemical Engineering, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea.
James A McCubreyDepartment of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Lucio CoccoCell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy.
University of Bologna · ITEast Carolina University · USNational Research Council · ITUlsan National Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Through the years, different studies showed the involvement of Protein Kinase C (PKC) in cell cycle control, in particular during G1/S transition. Little is known about their role at G2/M checkpoint. In this study, using K562 human erythroleukemia cell line, we found a novel and specific mechanism through which the conventional isoform PKCα positively affects Cyclin B1 modulating G2/M progression of cell cycle. Since the kinase activity of this PKC isoform was not necessary in this process, we demonstrated that PKCα, physically interacting with Cyclin B1, avoided its degradation and stimulated its nuclear import at mitosis. Moreover, the process resulted to be strictly connected with the increase in nuclear diacylglycerol levels (DAG) at G2/M checkpoint, due to the activity of nuclear Phospholipase C β1 (PLCβ1), the only PLC isoform mainly localized in the nucleus of K562 cells. Taken together, our findings indicated a novel DAG dependent mechanism able to regulate the G2/M progression of the cell cycle.

Indexed as

Active Transport, Cell NucleusCell CycleCell Line, TumorCell NucleusCell SeparationCyclin B1DiglyceridesFlow CytometryHumansIsoenzymesK562 CellsMicroscopy, FluorescenceMitosisPhospholipase C betaProtein Kinase C-alphaCCNB1 protein, humanCyclin B1DiglyceridesIsoenzymesPhospholipase C betaPLCB1 protein, humanPRKCA protein, humanProtein Kinase C-alpha

Identifiers

PMID25362646
PMCPMC4294327
OpenAlexW1543497389

What OpenQuestion holds

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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.