Evidence map›Paper›PMID 21083750›Full record

ArticleHelicobacter2010

Helicobacter pylori induction of the gastrin promoter through GC-rich DNA elements.

Tamara P Tucker, Brian M Gray, Kathyrn A Eaton, Juanita L Merchant

Open access · greenAbstract read
In one paragraph

Article in Helicobacter, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Frontiers in cellular and infection microbiology · 2017
    Article
  4. Article
  5. 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

4 authors at 1 institution in 1 country.

Tamara P TuckerDepartments of Internal Medicine, Microbiology and Immunology and Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-2200, USA.
Brian M Gray
Kathyrn A Eaton
Juanita L Merchant
University of Michigan–Ann Arbor · US

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OWYANG, CHUNG · 1986 to 2021
$22.5M
TRANSCRIPTIONAL CONTROL OF GASTRIN BY GROWTH FACTORSR01DK045729 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 1993 to 2021
$4.1M
Transcriptional Control of GastrinR37DK045729 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 2007 to 2016
$3.4M
NIDDK NIH HHS P30 DK034933NIDDK NIH HHS P30 DK34933NIDDK NIH HHS R01 DK045729NIDDK NIH HHS R01-DK45729NIDDK NIH HHS R37 DK045729
6 · The paper itself

Abstract

backgroundHelicobacter pylori (H. pylori) infection has been linked to the development of chronic gastritis, duodenal ulcer disease, and gastric cancer. Helicobacter pylori- infected patients and animal models develop hypergastrinemia, chronic gastritis, and gastric atrophy. Since gastrin is an important regulator of gastric acid secretion and cell growth, H. pylori regulation of this hormone has been implicated in its pathogenesis.

objectivesTo investigate the effect of H. pylori on gastrin gene expression in mice and of human bacterial isolates on gastrin mRNA expressed in a human cell line.

methodsGastrin mRNA was measured by qRT-PCR in H. pylori-infected mice. H. pylori were co-cultured with AGS cells to study regulation of human gastrin gene expression. Various MAP kinases were implicated in signal transduction from the bacteria using specific inhibitors. Gastrin reporter constructs and gel shift assays were used to map DNA responsive elements.

resultsIn addition to an increase in gastrin mRNA in H. pylori-infected mice, H. pylori induced the endogenous human gastrin gene through MAP kinase-dependent signaling but not NFκB-dependent signaling. Activation of gastrin through MAPK signaling did not require CagA or VacA virulence factors. Transfection studies demonstrated that a GC-rich motif mediated H. pylori-induction of the gastrin promoter and that the motif inducibly binds Sp1 and Sp3 transcription factors.

conclusionsDirect contact of live H. pylori bacteria with human cells is sufficient to induce gastrin gene expression.

Indexed as

Gene ExpressionPromoter Regions, GeneticAnimalsArtificial Gene FusionCell Line, TumorDisease Models, AnimalElectrophoretic Mobility Shift AssayGastrinsGene Expression ProfilingGenes, ReporterHelicobacter InfectionsHelicobacter pyloriHumansMiceMice, Inbred C57BLReverse Transcriptase Polymerase Chain ReactionGastrinsRNA, Messenger

Identifiers

PMID21083750
PMCPMC3306726
OpenAlexW1495964018

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.