Evidence map›Paper›PMID 19170105›Full record

ArticleJournal of cellular physiology2009

CDK inhibitors selectively diminish cell cycle controlled activation of the histone H4 gene promoter by p220NPAT and HiNF-P.

Partha Mitra, Prachi N Ghule, Margaretha van der Deen, Ricardo Medina, Rong-Lin Xie, William F Holmes, Xin Ye, Keiichi I Nakayama, J Wade Harper, Janet L Stein and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2009. 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
1.2field-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, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
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  10. Article
  11. The histone gene activator HINFP is a nonredundant cyclin E/CDK2 effector during early embryonic cell cycles.Proceedings of the National Academy of Sciences of the United States of America · 2009
    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

12 authors at 4 institutions in 2 countries.

Partha MitraDepartment of Cell Biology and Cancer Center, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
Prachi N Ghule
Margaretha van der Deen
Ricardo Medina
Rong-Lin Xie
William F Holmes
Xin Ye
Keiichi I Nakayama
J Wade Harper
Janet L Stein
Gary S Stein
Andre J van Wijnen
University of Massachusetts Chan Medical School · USHarvard University · USHarvard University Press · USKyushu University · JP

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
SYSTEMATIC ANALYSIS OF THE DUB PROTEOMER01GM054137 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI HARPER, JEFFREY W · 1996 to 2012
$4.1M
IDENTIFICATION OF HUMAN HISTONE GENE REGULATORY SEQUENCER01GM032010 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STEIN, GARY S. · 1985 to 2006
$3.4M
NIDDK NIH HHS P30 DK032520NIDDK NIH HHS P30 DK32520NIGMS NIH HHS GM32010NIGMS NIH HHS GM54137NIGMS NIH HHS R01 GM032010NIGMS NIH HHS R01 GM054137
6 · The paper itself

Abstract

Cell cycle progression into S phase requires the induction of histone gene expression to package newly synthesized DNA as chromatin. Cyclin E stimulation of CDK2 at the Restriction point late in G1 controls both histone gene expression by the p220(NPAT)/HiNF-P pathway and initiation of DNA replication through the pRB/E2F pathway. The three CDK inhibitors (CKIs) p21(CIP1/WAF1), p27(KIP1), and p57(KIP2) attenuate CDK2 activity. Here we find that gamma-irradiation induces p21(CIP1/WAF1) but not the other two CKIs, while reducing histone H4 mRNA levels but not histone H4 gene promoter activation by the p220(NPAT)/HiNF-P complex. We also show that p21(CIP1/WAF1) is less effective than p27(KIP1) and p57(KIP2) in inhibiting the CDK2 dependent phosphorylation of p220(NPAT) at subnuclear foci and transcriptional activation of histone H4 genes. The greater effectiveness of p57(KIP2) in blocking the p220(NPAT)/HiNF-P pathway is attributable in part to its ability to form a specific complex with p220(NPAT) that may suppress CDK2/cyclin E phosphorylation through direct substrate inhibition. We conclude that CKIs selectively control stimulation of the histone H4 gene promoter by the p220(NPAT)/HiNF-P complex.

Indexed as

Gene Expression RegulationPromoter Regions, GeneticAnimalsCell CycleCell Cycle ProteinsCell LineCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p57Cyclin-Dependent KinasesCyclin EGamma RaysGenes, ReporterHistonesHumansMiceNuclear ProteinsCDKN1A protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p57Cyclin-Dependent KinasesCyclin EHINFP protein, humanHistonesNPAT protein, humanNuclear ProteinsRecombinant Fusion ProteinsRepressor Proteins

Identifiers

PMID19170105
PMCPMC2981436
OpenAlexW2118322545

What OpenQuestion holds

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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.