Evidence map›Paper›PMID 23832782›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Structural insights into the regulation of sialic acid catabolism by the Vibrio vulnificus transcriptional repressor NanR.

Jungwon Hwang, Byoung Sik Kim, Song Yee Jang, Jong Gyu Lim, Dong-Ju You, Hyun Suk Jung, Tae-Kwang Oh, Jie-Oh Lee, Sang Ho Choi, Myung Hee Kim

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  4. A bidirectionalbioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
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  11. Bacterial Sialic Acid Catabolism at the Host-Microbe Interface.Journal of microbiology (Seoul, Korea) · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. NanR RegulatesInfection and immunity · 2017
    Article
  18. Article
  19. Article
  20. 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

10 authors at 4 institutions in 1 country.

Jungwon HwangInfection and Immunity Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Korea.
Byoung Sik Kim
Song Yee Jang
Jong Gyu Lim
Dong-Ju You
Hyun Suk Jung
Tae-Kwang Oh
Jie-Oh Lee
Sang Ho Choi
Myung Hee Kim
Korea Research Institute of Bioscience and Biotechnology · KRSeoul National University · KRKorea Basic Science Institute · KRKorea Advanced Institute of Science and Technology · KR

Funding

Biotechnology and Biological Sciences Research Council
6 · The paper itself

Abstract

Pathogenic and commensal bacteria that experience limited nutrient availability in their host have evolved sophisticated systems to catabolize the mucin sugar N-acetylneuraminic acid, thereby facilitating their survival and colonization. The correct function of the associated catabolic machinery is particularly crucial for the pathogenesis of enteropathogenic bacteria during infection, although the molecular mechanisms involved with the regulation of the catabolic machinery are unknown. This study reports the complex structure of NanR, a repressor of the N-acetylneuraminate (nan) genes responsible for N-acetylneuraminic acid catabolism, and its regulatory ligand, N-acetylmannosamine 6-phosphate (ManNAc-6P), in the human pathogenic bacterium Vibrio vulnificus. Structural studies combined with electron microscopic, biochemical, and in vivo analysis demonstrated that NanR forms a dimer in which the two monomers create an arched tunnel-like DNA-binding space, which contains positively charged residues that interact with the nan promoter. The interaction between the NanR dimer and DNA is alleviated by the ManNAc-6P-mediated relocation of residues in the ligand-binding domain of NanR, which subsequently relieves the repressive effect of NanR and induces the transcription of the nan genes. Survival studies in which mice were challenged with a ManNAc-6P-binding-defective mutant strain of V. vulnificus demonstrated that this relocation of NanR residues is critical for V. vulnificus pathogenesis. In summary, this study presents a model of the mechanism that regulates sialic acid catabolism via NanR in V. vulnificus.

Indexed as

Transcription, GeneticMicroscopy, ElectronModels, MolecularN-Acetylneuraminic AcidRepressor ProteinsVibrio vulnificusN-Acetylneuraminic AcidRepressor Proteinsmucin sugar utilizationnan gene repressor

Identifiers

PMID23832782
PMCPMC3725057
OpenAlexW2010338621

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.