Evidence map›Paper›PMID 25824232›Full record

ArticleAntimicrobial agents and chemotherapy2015

Candida albicans Cek1 mitogen-activated protein kinase signaling enhances fungicidal activity of salivary histatin 5.

Rui Li, Sumant Puri, Swetha Tati, Paul J Cullen, Mira Edgerton

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. MIG1, TUP1 and NRG1 mediated yeast to hyphal morphogenesis inhibition in Candida albicans by ganciclovir.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2024
    Article
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  7. 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

5 authors at 1 institution in 1 country.

Rui LiDepartment of Oral Biology, University at Buffalo, Buffalo, New York, USA.
Sumant PuriDepartment of Oral Biology, University at Buffalo, Buffalo, New York, USA.
Swetha TatiDepartment of Oral Biology, University at Buffalo, Buffalo, New York, USA.
Paul J CullenDepartment of Biological Sciences, University at Buffalo, Buffalo, New York, USA.
Mira EdgertonDepartment of Oral Biology, University at Buffalo, Buffalo, New York, USA edgerto@buffalo.edu.
University at Buffalo, State University of New York · US

Funding

Supplements to Support Candida DNA Microarray FacilitiesR01DE010641 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI EDGERTON, MIRA · 2000 to 2019
$6.7M
Advanced Training in Oral BiologyT32DE023526 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI Stefan Hans-Klaus Ruhl · 2013 to 2026
$3.7M
Regulation of Candida albicans Pathogenesis by the Signaling Mucin Msb2R01DE022720 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CULLEN, PAUL JAMES, EDGERTON, MIRA · 2013 to 2017
$1.9M
NIDCR NIH HHS R01 DE010641NIDCR NIH HHS R01DE010641NIDCR NIH HHS R01 DE022720NIDCR NIH HHS R01DE022720NIDCR NIH HHS T32 DE023526
6 · The paper itself

Abstract

Candida albicans is a major etiological organism for oropharyngeal candidiasis (OPC), while salivary histatin 5 (Hst 5) is a human fungicidal protein that protects the oral cavity from OPC. C. albicans senses its environment by mitogen-activated protein kinase (MAPK) activation that can also modulate the activity of some antifungal drugs, including Hst 5. We found that phosphorylation of the MAPK Cek1, induced either by N-acetylglucosamine (GlcNAc) or serum, or its constitutive activation by deletion of its phosphatase Cpp1 elevated the susceptibility of C. albicans cells to Hst 5. Cek1 phosphorylation but not hyphal formation was needed for increased Hst 5 sensitivity. Interference with the Cek1 pathway by deletion of its head sensor proteins, Msb2 and Sho1, or by addition of secreted aspartyl protease (SAP) cleavage inhibitors, such as pepstatin A, reduced Hst 5 susceptibility under Cek1-inducing conditions. Changes in fungal cell surface glycostructures also modulated Hst 5 sensitivity, and Cek1-inducing conditions resulted in a higher uptake rate of Hst 5. These results show that there is a consistent relationship between activation of Cek1 MAPK and increased Hst 5 susceptibility in C. albicans.

Indexed as

Antifungal AgentsCandida albicansFungal ProteinsHistatinsMitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesPhosphorylationSalivaSignal TransductionAntifungal AgentsCEK1 protein, Candida albicansFungal ProteinsHistatinsMitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinases

Identifiers

PMID25824232
PMCPMC4432120
OpenAlexW2138221359

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.