Evidence map›Paper›PMID 24082073›Full record

ArticleInfection and immunity2013

Differential roles of ASK1 and TAK1 in Helicobacter pylori-induced cellular responses.

Yoku Hayakawa, Yoshihiro Hirata, Hiroto Kinoshita, Kosuke Sakitani, Hayato Nakagawa, Wachiko Nakata, Ryota Takahashi, Kei Sakamoto, Shin Maeda, Kazuhiko Koike

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023
    Review
  5. Heliyon · 2023
    Review
  6. Review
  7. Review
  8. Non-Gastro hep advances · 2023
    Article
  9. Article
  10. Article
  11. Mature gastric chief cells are not required for the development of metaplasia.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Article
  12. Article
  13. Article
  14. Metaplasia in the Stomach-Precursor of Gastric Cancer?International journal of molecular sciences · 2017
    Review
  15. Review
  16. Review
  17. Article
  18. Review
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

10 authors at 3 institutions in 1 country.

Yoku HayakawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Yoshihiro Hirata
Hiroto Kinoshita
Kosuke Sakitani
Hayato Nakagawa
Wachiko Nakata
Ryota Takahashi
Kei Sakamoto
Shin Maeda
Kazuhiko Koike
The University of Tokyo · JPInstitute for Adult Diseases Asahi Life Foundation · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitogen-activated protein kinase (MAPK) signaling pathway regulates various cellular functions, including those induced by Helicobacter pylori. TAK1 is an upstream MAPK kinase kinase (MAP3K) required for H. pylori-induced MAPK and NF-κB activation, but it remains unclear whether other MAP3Ks are involved in H. pylori-induced cellular responses. In this study, we focused on the MAP3K ASK1, which plays a critical role in gastric tumorigenesis. In gastric epithelial cells, H. pylori activates ASK1 in a reactive oxygen species (ROS)- and cag pathogenicity island-dependent manner, and ASK1 regulates sustained JNK activation and apoptosis induced by H. pylori. In contrast, TAK1 regulates H. pylori-mediated early JNK activation and cytokine production. We also found reciprocal regulation between ASK1 and TAK1 in H. pylori-related responses, whereby inhibition of TAK1 or downstream p38 MAPK activates ASK1 through ROS production, and ASK1 suppresses TAK1 and downstream NF-κB activation. We identified ROS/ASK1/JNK as a new signaling pathway induced by H. pylori, which regulates apoptotic cell death. The balance of ASK1-induced apoptosis and TAK1-induced antiapoptotic or inflammatory responses may determine the fate of epithelial cells infected with H. pylori and thus be involved in the pathogenesis of gastritis and gastric cancer.

Indexed as

ApoptosisCarcinogenesisCell LineEnzyme ActivationEpithelial CellsGastric MucosaHelicobacter InfectionsHelicobacter pyloriHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5MAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMAP Kinase Signaling SystemNF-kappa Bp38 Mitogen-Activated Protein KinasesJNK Mitogen-Activated Protein KinasesMAP3K5 protein, humanMAP Kinase Kinase Kinase 5MAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesRNA, Small Interfering

Identifiers

PMID24082073
PMCPMC3837986
OpenAlexW2118094338

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.