Evidence map›Paper›PMID 21468218›Full record

ReviewGut microbes

Helicobacter pylori activation of PARP-1: usurping a versatile regulator of host cellular health.

Carlos W Nossa, Steven R Blanke

Open access · hybridAbstract readReview
In one paragraph

Review in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact, top 89% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular Mechanisms ofInternational journal of molecular sciences · 2018
    Review
  4. Article
  5. Article
  6. 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

2 authors at 2 institutions in 1 country.

Carlos W NossaDepartment of Microbiology and the Institute for Genomic Biology, University of Illinois, Urbana, IL, USA.
Steven R Blanke
University of Illinois Urbana-Champaign · USUrbana University · US

Funding

MOLECULAR MECHANISMS OF THE H. PYLORI VACUOLATING TOXINR01AI045928 · NIAID · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI BLANKE, STEVEN R. · 2000 to 2010
$1.9M
NIAID NIH HHS R01 AI045928
6 · The paper itself

Abstract

Chronic infection of the human stomach by Helicobacter pylori is an important risk factor for gastric cancer. H. pylori produces a cache of virulence factors that promote colonization and persistence, which, in turn, contributes to a robust inflammatory response at the host-pathogen interface. Recently, we reported that H. pylori activates the abundant nuclear regulator poly(ADP-ribose) polymerase (PARP)-1, resulting in the production of the catabolite poly(ADP-ribose) (PAR). PARP-1 is emerging as a key player in establishing homeostasis at the host-pathogen interface. In this article, we summarize the discovery of H. pylori-dependent PARP-1 activation, and discuss potential roles for PARP-1 in H. pylori-mediated gastric disease. In light of the remarkable successes that have reported for treating inflammatory disorders and cancers with PARP-1 inhibitors, we discuss the prospects of targeting PARP-1 for treatment of H. pylori-associated gastric disease.

Indexed as

Host-Pathogen InteractionsAnimalsHelicobacter InfectionsHelicobacter pyloriHumansPoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesPARP1 protein, humanPoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesactivationapoptosiscancerHelicobacter pyloriinflammationPARP-1

Identifiers

PMID21468218
PMCPMC3056101
OpenAlexW2039453469

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.