Evidence map›Paper›PMID 25997502›Full record

ArticleHelicobacter2016

Phosphorylation-dependent and Phosphorylation-independent Regulation of Helicobacter pylori Acid Acclimation by the ArsRS Two-component System.

Elizabeth A Marcus, George Sachs, Yi Wen, David R Scott

Abstract read
In one paragraph

Article in Helicobacter, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Single-cell Raman spectroscopy identifiesFrontiers in microbiology · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Strategies used byWorld journal of gastroenterology · 2017
    Review
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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.

Elizabeth A MarcusDepartment of Pediatrics, DGSOM at UCLA, Los Angeles, CA, 90095, USA.
George SachsVA GLAHS, Los Angeles, CA, 90073, USA.
Yi WenVA GLAHS, Los Angeles, CA, 90073, USA.
David R ScottVA GLAHS, Los Angeles, CA, 90073, USA.
VA West Los Angeles Medical Center · USUniversity of California, Los Angeles · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
The role of ArsS in gastric infection by Helicobacter pyloriR01DK105156 · NIDDK · BRENTWOOD BIOMEDICAL RESEARCH INSTITUTE · PI MARCUS, ELIZABETH A. · 2015 to 2018
$1.1M
Mechanisms of gastric mucosal response to H. pylori infection at acidic pHK08DK100661 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARCUS, ELIZABETH A. · 2014 to 2017
$561k
Acid Adaptation Targets for Eradication of Helicobacter pyloriI01BX001006 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI SACHS, GEORGE · 2011 to 2018
–
BLRD VA 2I01BX001006-05BLRD VA I01 BX001006NCATS NIH HHS UL1 TR000124NCATS NIH HHS UL1TR000124NIDDK NIH HHS K08 DK100661NIDDK NIH HHS K08DK100661-01NIDDK NIH HHS R01 DK105156
6 · The paper itself

Abstract

backgroundThe pH-sensitive Helicobacter pylori ArsRS two-component system (TCS) aids survival of this neutralophile in the gastric environment by directly sensing and responding to environmental acidity. ArsS is required for acid-induced trafficking of urease and its accessory proteins to the inner membrane, allowing rapid, urea-dependent cytoplasmic and periplasmic buffering. Expression of ArsR, but not its phosphorylation, is essential for bacterial viability. The aim of this study was to characterize the roles of ArsS and ArsR in the response of H. pylori to acid. MATERIALS AND

methodsWild-type H. pylori and an arsR(D52N) phosphorylation-deficient strain were incubated at acidic or neutral pH. Gene and protein expression, survival, membrane trafficking of urease proteins, urease activity, and internal pH were studied.

resultsPhosphorylation of ArsR is not required for acid survival. ArsS-driven trafficking of urease proteins to the membrane in acid, required for recovery of internal pH, is independent of ArsR phosphorylation. ArsR phosphorylation increases expression of the urease gene cluster, and the loss of negative feedback in a phosphorylation-deficient mutant leads to an increase in total urease activity.

conclusionsArsRS has a dual function in acid acclimation: regulation of urease trafficking to UreI at the cytoplasmic membrane, driven by ArsS, and regulation of urease gene cluster expression, driven by phosphorylation of ArsR. ArsS and ArsR work through phosphorylation-dependent and phosphorylation-independent regulatory mechanisms to impact acid acclimation and allow gastric colonization. Furthering understanding of the intricacies of acid acclimation will impact the future development of targeted, nonantibiotic treatment regimens.

Indexed as

AcidsBacterial ProteinsCell MembraneGene Expression Regulation, BacterialHelicobacter InfectionsHelicobacter pyloriHumansPhosphorylationProtein TransportUreaseAcidsBacterial ProteinsUreaseacid acclimationArsRSHelicobacter pyloritwo-component systemurease

Identifiers

PMID25997502
PMCPMC4655181
OpenAlexW2138166666

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.