Evidence map›Paper›PMID 9169507›Full record

ArticleThe Journal of clinical investigation1997

EGF receptor activation stimulates endogenous gastrin gene expression in canine G cells and human gastric cell cultures.

M G Ford, J D Valle, C J Soroka, J L Merchant

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-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

17 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Clinically Defined Mutations inCancer research communications · 2023
    Article
  3. Review
  4. Article
  5. Frontiers in cellular and infection microbiology · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Somatostatin stimulates menin gene expression by inhibiting protein kinase A.American journal of physiology. Gastrointestinal and liver physiology · 2008
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

4 authors at 2 institutions in 1 country.

M G FordDepartment of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109-0650, USA.
J D Valle
C J Soroka
J L Merchant
University of Michigan · USYale University · US

Funding

ZINC GLUCONATE GLYCINE LOZENGES &VITAMIN C EFFECTS ON COMMON COLDM01RR000042 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUBENFIRE, MELVYN · 1985 to 2007
$40.8M
TRANSCRIPTIONAL CONTROL OF GASTRIN BY GROWTH FACTORSR01DK045729 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 1993 to 2021
$4.1M
GASTROINTESTINAL SIGNIFICANCE OF GASTRIN REGULATIONR01DK034306 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DELVALLE, JOHN · 1986 to 2002
$1.0M
NCRR NIH HHS M01-RR-00042NIDDK NIH HHS DK-34306NIDDK NIH HHS DK-45729
6 · The paper itself

Abstract

Gastrin release from the antral gastrin-expressing cell (G cell) is regulated by bombesin and luminal factors. Yet, these same extracellular regulators do not stimulate expression of the gene. Since the gastric mucosa expresses large quantities of EGF receptor ligands such as TGFalpha, we examined whether EGF receptor ligands stimulate gastrin gene expression in gastrin-expressing cell cultures. EGF receptor activation of primary cultures stimulated gastrin gene expression about twofold; whereas bombesin treatment of antral G cell cultures stimulated gastrin release but not gene expression. EGF and TGFalpha were weak stimulants of gastrin release. EGF receptor activation of AGS human gastric adenocarcinoma cell line stimulated gastrin gene expression nearly fourfold; and gastrin reporter constructs transfected into AGS cells were stimulated more than fourfold by EGF. EGF induction was conferred by the previously defined GC-rich gastrin EGF response element (gERE) element located at -68 to -53 bp upstream from the cap site since a mutation of the gERE element abolished both basal and EGF induction. Moreover, EGF treatment of AGS cells stimulated binding of the transcription factor Sp1 to this element. Collectively, these results demonstrate that gastrin gene expression and gastrin release are regulated by different signaling pathways: gene expression by EGF receptor activation and gastrin secretion by neuropeptides and luminal factors.

Indexed as

Gene Expression RegulationSignal TransductionAnimalsCells, CulturedDogsErbB ReceptorsGastric MucosaGastrinsHumansImmunohistochemistryLigandsErbB ReceptorsGastrinsLigands

Identifiers

PMID9169507
PMCPMC508123
OpenAlexW2001857413

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.