Evidence map›Paper›PMID 31409845›Full record

ArticleScientific reports2019

Establishment of serine protease htrA mutants in Helicobacter pylori is associated with secA mutations.

Anna Zawilak-Pawlik, Urszula Zarzecka, Dorota Żyła-Uklejewicz, Jakub Lach, Dominik Strapagiel, Nicole Tegtmeyer, Manja Böhm, Steffen Backert, Joanna Skorko-Glonek

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  19. Cells · 2020
    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

9 authors at 4 institutions in 3 countries.

Anna Zawilak-PawlikHirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Department of Microbiology, Weigla 12, 53-114, Wrocław, Poland. anna.pawlik@hirszfeld.pl.
Urszula ZarzeckaDepartment of General and Medical Biochemistry, Faculty of Biology, University of Gdańsk, Wita Stwosza 59, 80-308, Gdańsk, Poland.
Dorota Żyła-UklejewiczHirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Department of Microbiology, Weigla 12, 53-114, Wrocław, Poland.
Jakub LachBBMRI.pl Consortium, Stabłowicka 147, 54-066, Wrocław, Poland.
Dominik StrapagielBBMRI.pl Consortium, Stabłowicka 147, 54-066, Wrocław, Poland.ORCID http://orcid.org/0000-0001-9752-4270
Nicole TegtmeyerDepartment of Biology, Division of Microbiology, Friedrich-Alexander University Erlangen-Nuremberg, Staudtstr. 5, 91058, Erlangen, Germany.
Manja BöhmDepartment of Biology, Division of Microbiology, Friedrich-Alexander University Erlangen-Nuremberg, Staudtstr. 5, 91058, Erlangen, Germany.
Steffen BackertDepartment of Biology, Division of Microbiology, Friedrich-Alexander University Erlangen-Nuremberg, Staudtstr. 5, 91058, Erlangen, Germany.
Joanna Skorko-GlonekDepartment of General and Medical Biochemistry, Faculty of Biology, University of Gdańsk, Wita Stwosza 59, 80-308, Gdańsk, Poland. joanna.skorko-glonek@biol.ug.edu.pl.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DELudwik Hirszfeld Institute of Immunology and Experimental Therapy · PLUniversity of Łódź · PLUniversity of Gdańsk · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori plays an essential role in the pathogenesis of gastritis, peptic ulcer disease, and gastric cancer. The serine protease HtrA, an important secreted virulence factor, disrupts the gastric epithelium, which enables H. pylori to transmigrate across the epithelium and inject the oncogenic CagA protein into host cells. The function of periplasmic HtrA for the H. pylori cell is unknown, mainly due to unavailability of the htrA mutants. In fact, htrA has been described as an essential gene in this bacterium. We have screened 100 worldwide H. pylori isolates and show that only in the N6 strain it was possible to delete htrA or mutate the htrA gene to produce proteolytically inactive HtrA. We have sequenced the wild-type and mutant chromosomes and we found that inactivation of htrA is associated with mutations in SecA - a component of the Sec translocon apparatus used to translocate proteins from the cytoplasm into the periplasm. The cooperation of SecA and HtrA has been already suggested in Streptococcus pneumonia, in which these two proteins co-localize. Hence, our results pinpointing a potential functional relationship between HtrA and the Sec translocon in H. pylori possibly indicate for the more general mechanism responsible to maintain bacterial periplasmic homeostasis.

Indexed as

Antigens, BacterialBacterial ProteinsHelicobacter InfectionsHelicobacter pyloriHost-Pathogen InteractionsHumansMutationSecA ProteinsSerine ProteasesAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriHtrA protein, H pyloriSecA ProteinsSerine Proteases

Identifiers

PMID31409845
PMCPMC6692382
OpenAlexW2967122444

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.