Evidence map›Paper›PMID 20453549›Full record

ArticlePancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]2010

Dominant negative p38 mitogen-activated protein kinase expression inhibits NF-kappaB activation in AR42J cells.

Erik Twait, Deborah E Williard, Isaac Samuel

Open access · bronzeAbstract read
In one paragraph

Article in Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Involvement of the PI3K/Akt/NF-BioMed research international · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Expressions of miR-22 and miR-135a in acute pancreatitis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2014
    Article
  13. Article
  14. Article
  15. Pathogenic mechanisms of acute pancreatitis.Current opinion in gastroenterology · 2012
    Review
  16. Article
  17. Systemic inflammation with multiorgan dysfunction is the cause of death in murine ligation-induced acute pancreatitis.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2011
    Article
  18. Molecular mechanisms of pancreatic injury.Current opinion in gastroenterology · 2011
    Review
  19. A novel model of severe gallstone pancreatitis: murine pancreatic duct ligation results in systemic inflammation and substantial mortality.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2010
    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

3 authors at 1 institution in 1 country.

Erik TwaitSurgical Services, Iowa City Veterans Affairs Medical Center, and Department of Surgery, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.
Deborah E Williard
Isaac Samuel
University of Iowa · US

Funding

Gallstone Pancreatitis: Pathogenesis and TreatmentR01DK071731 · NIDDK · UNIVERSITY OF IOWA · PI SAMUEL, ISAAC · 2008 to 2012
$1.5M
NIDDK NIH HHS R01 DK-071731NIDDK NIH HHS R01 DK071731
6 · The paper itself

Abstract

backgroundThe role of the p38 mitogen-activated protein (MAP) kinase in acute pancreatitis pathogenesis is controversial. We hypothesize that p38 plays a role in regulating NF-kappaB activation in exocrine pancreatic cells.

methodsAR42J cells incorporating an NF-kappaB-responsive luciferase reporter, with and without adenoviral transduction of DNp38, were stimulated with cholecystokinin (CCK) or tumor necrosis factor-alpha (TNF-alpha) prior to measuring NF-kappaB activation.

resultsCCK- or TNF-alpha-stimulated NF-kappaB-dependent gene transcription (luciferase assay) was substantially subdued by DNp38 expression. These findings were confirmed by electrophoretic mobility shift assay. Nuclear translocation of the p65 NF-kappaB subunit following agonist stimulation was evident (supershift). Characterization studies showed excellent adenoviral infection efficiency and cell viability in our AR42J cell model. Agonist-stimulated dose- and time-dependent p38 activation, with inhibition by DNp38 expression, was also confirmed.

conclusionThe p38 MAP kinase regulates NF-kappaB pathway activation in exocrine pancreatic cells, and thus potentially plays a role in the mechanism of acute pancreatitis pathogenesis..

Indexed as

AnimalsCell LineCholecystokininEnzyme ActivationGenes, DominantNF-kappa Bp38 Mitogen-Activated Protein KinasesPancreasPancreatitisRatsTumor Necrosis Factor-alphaCholecystokininNF-kappa Bp38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alpha

Identifiers

PMID20453549
PMCPMC2899148
OpenAlexW2073089150

What OpenQuestion holds

Textmetadata
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.