Evidence map›Paper›PMID 26507679›Full record

ArticlePathogens and disease2016

Defective mutations within the translocation domain of Clostridium difficile toxin B impair disease pathogenesis.

Therwa Hamza, Zhifen Zhang, Roman A Melnyk, Hanping Feng

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pathogens and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
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 3 institutions in 2 countries.

Therwa HamzaDepartment of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, MD 21201, USA.
Zhifen ZhangProgram in Molecular Structure & Function, The Hospital for Sick Children, M5G 0A4, Canada.
Roman A MelnykProgram in Molecular Structure & Function, The Hospital for Sick Children, M5G 0A4, Canada Department of Biochemistry, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Hanping FengDepartment of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, MD 21201, USA hfeng@umaryland.edu.
University of Maryland, Baltimore · USHospital for Sick Children · CAUniversity of Toronto · CA

Funding

Shigella Live Vector-Based Multivalent VaccineU19AI109776 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI LEVINE, MYRON MAX · 2014 to 2018
$25.4M
Development of Vaccines against Clostridium difficile InfectionR01AI088748 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI FENG, HANPING, TZIPORI, SAUL R · 2010 to 2014
$3.1M
Epithelium, dendritic cells, and Clostridium difficile associated colitisR01DK084509 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI FENG, HANPING · 2010 to 2014
$1.7M
NIAID NIH HHS R01 AI088748NIAID NIH HHS U19 AI109776NIDDK NIH HHS R01 DK084509
6 · The paper itself

Abstract

The Clostridium difficile toxin B is one of the main virulence factors and plays an important role in the pathogenesis of C. difficile infection (CDI). We recently revealed crucial residues in the translocation domain of TcdB for the pore formation and toxin translocation. In this study, we investigated the effects of mutating a critical site involved in pore formation, Leu-1106, to residues that differ in size and polarity (Phe, Ala, Cys, Asp). We observed a broad range of effects on TcdB function in vitro consistent with the role of this site in pore formation and translocation. We show that mice challenged systemically with a lethal dose (LD100) of the most defective mutant (L1106K) showed no symptoms of disease highlighting the importance of this residue and the translocation domain in disease pathogenesis. These findings offer insights into the structure function of the toxin translocation pore, and inform novel therapeutic strategies against CDI.

Indexed as

MutationAnimalsBacterial ProteinsBacterial ToxinsClostridioides difficileClostridium InfectionsDisease Models, AnimalDNA Mutational AnalysisFemaleMicePoisoningPore Forming Cytotoxic ProteinsProtein TransportSurvival AnalysisVirulence FactorsBacterial ProteinsBacterial ToxinsPore Forming Cytotoxic ProteinstoxB protein, Clostridium difficileVirulence FactorsClostridium difficileTcdBtoxintranslocation domain

Identifiers

PMID26507679
PMCPMC4882082
OpenAlexW2208134708

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.