Evidence map›Paper›PMID 22194455›Full record

ArticleJournal of bacteriology2012

Helicobacter pylori relies primarily on the purine salvage pathway for purine nucleotide biosynthesis.

George Liechti, Joanna B Goldberg

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

47 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Challenges and Prospects for Eradication ofPathogens (Basel, Switzerland) · 2025
    Review
  6. Article
  7. Article
  8. Crystal structure of dihydroorotate dehydrogenase from Helicobacter pylori with bound flavin mononucleotide.Acta crystallographica. Section F, Structural biology communications · 2025
    Article
  9. Article
  10. Vitamin B6 inhibits activity ofJournal of enzyme inhibition and medicinal chemistry · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Interactions of 2,6-substituted purines with purine nucleoside phosphorylase fromJournal of enzyme inhibition and medicinal chemistry · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

George LiechtiDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia Health System, Charlottesville, Virginia, USA.
Joanna B Goldberg
University of Virginia Health System · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
Cancer Research Training Program: From Molecular Mechanisms to Therapeutic StrategiesT32CA009109 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Andrew Carl Dudley, Melanie R Rutkowski · 1985 to 2026
$13.9M
NCI NIH HHS 5T32 CA 009109NCI NIH HHS P30 CA044579NCI NIH HHS P30 CA44579NCI NIH HHS T32 CA009109
6 · The paper itself

Abstract

Helicobacter pylori is a chronic colonizer of the gastric epithelium and plays a major role in the development of gastritis, peptic ulcer disease, and gastric cancer. In its coevolution with humans, the streamlining of the H. pylori genome has resulted in a significant reduction in metabolic pathways, one being purine nucleotide biosynthesis. Bioinformatic analysis has revealed that H. pylori lacks the enzymatic machinery for de novo production of IMP, the first purine nucleotide formed during GTP and ATP biosynthesis. This suggests that H. pylori must rely heavily on salvage of purines from the environment. In this study, we deleted several genes putatively involved in purine salvage and processing. The growth and survival of these mutants were analyzed in both nutrient-rich and minimal media, and the results confirmed the presence of a robust purine salvage pathway in H. pylori. Of the two phosphoribosyltransferase genes found in the H. pylori genome, only gpt appears to be essential, and an Δapt mutant strain was still capable of growth on adenine, suggesting that adenine processing via Apt is not essential. Deletion of the putative nucleoside phosphorylase gene deoD resulted in an inability of H. pylori to grow on purine nucleosides or the purine base adenine. Our results suggest a purine requirement for growth of H. pylori in standard media, indicating that H. pylori possesses the ability to utilize purines and nucleosides from the environment in the absence of a de novo purine nucleotide biosynthesis pathway.

Indexed as

Adenine PhosphoribosyltransferaseHelicobacter pyloriHypoxanthine PhosphoribosyltransferasePentosyltransferasesPurine NucleosidesPurine NucleotidesPurinesAdenine PhosphoribosyltransferaseHypoxanthine Phosphoribosyltransferasenucleoside phosphorylasePentosyltransferasesPurine NucleosidesPurine NucleotidesPurines

Identifiers

PMID22194455
PMCPMC3272961
OpenAlexW2127781435

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.