Evidence map›Paper›PMID 18755809›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008

Somatostatin stimulates menin gene expression by inhibiting protein kinase A.

Edith Mensah-Osman, Yana Zavros, Juanita L Merchant

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Epigenetic regulation by the menin pathway.Endocrine-related cancer · 2017
    Review
  6. Deletion ofGut · 2017
    Article
  7. Article
  8. Review
  9. Article
  10. Conditional deletion of menin results in antral G cell hyperplasia and hypergastrinemia.American journal of physiology. Gastrointestinal and liver physiology · 2012
    Article
  11. A high-fat diet regulates gastrin and acid secretion through primary cilia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    Article
  12. Article
  13. Menin and JunD regulate gastrin gene expression through proximal DNA elements.American journal of physiology. Gastrointestinal and liver physiology · 2011
    Article
  14. Article
  15. Menin immunoreactivity in secretory granules of human pancreatic islet cells.Applied immunohistochemistry & molecular morphology : AIMM
    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.

Edith Mensah-OsmanDepartment of Internal Medicine, Division of Gastroenterology, University of Michigan, Ann Arbor, Michigan, USA.
Yana Zavros
Juanita L Merchant
University of Michigan–Ann Arbor · US

Funding

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 R01-DK45729NIDDK NIH HHS R37 DK045729
6 · The paper itself

Abstract

Somatostatin is a potent inhibitor of gastrin secretion and gene expression. Menin is a 67-kDa protein product of the multiple endocrine neoplasia type 1 (MEN1) gene that when mutated leads to duodenal gastrinomas, a tumor that overproduces the hormone gastrin. These observations suggest that menin might normally inhibit gastrin gene expression in its role as a tumor suppressor. Since somatostatin and ostensibly menin are both inhibitors of gastrin, we hypothesized that somatostatin signaling directly induces menin. Menin protein expression was significantly lower in somatostatin-null mice, which are hypergastrinemic. We found by immunohistochemistry that somatostatin receptor-positive cells (SSTR2A) express menin. Mice were treated with the somatostatin analog octreotide to determine whether activation of somatostatin signaling induced menin. We found that octreotide increased the number of menin-expressing cells, menin mRNA, and menin protein expression. Moreover, the induction by octreotide was greater in the duodenum than in the antrum. The increase in menin observed in vivo was recapitulated by treating AGS and STC cell lines with octreotide, demonstrating that the regulation was direct. The induction required suppression of protein kinase A (PKA) since forskolin treatment suppressed menin protein levels and octreotide inhibited PKA enzyme activity. Small-interfering RNA-mediated suppression of PKA levels raised basal levels of menin protein and prevented further induction by octreotide. Using AGS cells, we also showed for the first time that menin directly inhibits endogenous gastrin gene expression. In conclusion, somatostatin receptor activation induces menin expression by suppressing PKA activation.

Indexed as

AnimalsCyclic AMP-Dependent Protein KinasesDuodenumGastrinsGene ExpressionMiceMice, Inbred C57BLOctreotideProto-Oncogene ProteinsPyloric AntrumReceptors, SomatostatinSomatostatinCyclic AMP-Dependent Protein KinasesGastrinsMen1 protein, mouseOctreotideProto-Oncogene ProteinsReceptors, SomatostatinSomatostatinsomatostatin receptor 2

Identifiers

PMID18755809
PMCPMC2575917
OpenAlexW2111916543

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.