Evidence map›Paper›PMID 20708092›Full record

ArticleThe international journal of biochemistry & cell biology2011

Inactivation of p38 MAPK during liver regeneration.

Jean S Campbell, Gretchen M Argast, Sebastian Y Yuen, Brian Hayes, Nelson Fausto

Abstract read
In one paragraph

Article in The international journal of biochemistry & cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  5. Identification of therapeutic targets in a murine model of severe exertional heat stroke.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  6. Article
  7. Article
  8. The role of stress kinases in metabolic disease.Nature reviews. Endocrinology · 2020
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. IL-1β-induced and p38The Journal of biological chemistry · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Jean S CampbellDepartment of Pathology, University of Washington, School of Medicine, Seattle, WA 98195, USA. campjs@u.washington.edu
Gretchen M Argast
Sebastian Y Yuen
Brian Hayes
Nelson Fausto
University of Washington · US

Funding

GENE EXPRESSION IN REGENERATING AND NEOPLASTIC LIVERSR37CA023226 · NCI · UNIVERSITY OF WASHINGTON · PI FAUSTO, NELSON · 2001 to 2009
$3.1M
Pathogenesis of Hepatocellular CarcinomasR01CA074131 · NCI · UNIVERSITY OF WASHINGTON · PI FAUSTO, NELSON · 1997 to 2010
$3.1M
Mechanisms of PDGF-C Induced Hepatocellular CarcinogenesisR01CA127228 · NCI · UNIVERSITY OF WASHINGTON · PI CAMPBELL, JEAN S · 2007 to 2011
$1.5M
GENE EXPRESSION IN REGENERATING AND NEOPLASTIC LIVERSR01CA023226 · NCI · UNIVERSITY OF WASHINGTON · PI FAUSTO, NELSON · 1985 to 2000
$359k
NCI NIH HHS CA-127228NCI NIH HHS CA-23226NCI NIH HHS CA-74131NCI NIH HHS R01 CA023226NCI NIH HHS R01 CA074131NCI NIH HHS R01 CA127228NCI NIH HHS R37 CA023226
6 · The paper itself

Abstract

There is increasing evidence that p38 MAPK, which is classified as a stress-activated kinase, also participates in cell cycle regulation, functioning as a suppressor of cell proliferation and tumorigenesis. We conducted a study of p38 MAPK phosphorylation during liver regeneration in mice to determine whether p38 MAPK activation or inactivation may correlate with events that lead to DNA replication after partial hepatectomy (PH), and whether p38 MAPK activation may be required for hepatocyte DNA replication in vivo and in culture. We report that active p38 (Pi-p38 MAPK) is present in normal liver, is rapidly inactivated starting 30 min after PH, and is re-activated by 12h. Although levels of Pi-MKK 3/6, the upstream kinases that activate p38 MAPK increase after PH, the expression of the dual protein phosphatase 1 is also elevated, and may be responsible for Pi-p38 MAPK dephosphorylation after PH. Inactivation and re-activation of p38 MAPK inversely correlates with the stimulation of protein synthesis and translation pathways, as indicated by activation of p70S6 kinase, increases in the phosphorylation of initiation factor elF-4E and translational repressor, 4E-BP. The activity of a p38 MAPK downstream substrate, MAPKAPK2 (MK2), did not reflect the changing levels of Pi-p38 MAPK during liver regeneration. Pi-p38 MAPK may be involved in TNF-stimulated DNA replication of murine hepatocytes in culture, but is not necessary for hepatocyte DNA replication after PH. Our results suggest that p38 MAPK inactivation plays a permissible role in DNA replication during liver regeneration and is consistent with a role for p38 MAPK in the maintenance of hepatocyte cell cycle arrest in adult liver.

Indexed as

Liver RegenerationAnimalsCell Cycle ProteinsCell LineCell ProliferationDNA ReplicationDual Specificity Phosphatase 1Dual-Specificity PhosphatasesEnzyme ActivationEnzyme AssaysImidazolesIntracellular Signaling Peptides and ProteinsLiverMaleMAP-Kinase-Activated Kinase 2MiceCell Cycle ProteinsDual Specificity Phosphatase 1Dual-Specificity PhosphatasesDusp10 protein, mouseDusp1 protein, mouseImidazolesIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsProtein Serine-Threonine KinasesPyrimidinesSB 220025Tumor Necrosis Factors

Identifiers

PMID20708092
PMCPMC3022113
OpenAlexW2068024246

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.