Evidence map›Paper›PMID 19053526›Full record

ArticleJournal of proteome research2009

Quantitative proteomic profiling of host-pathogen interactions: the macrophage response to Mycobacterium tuberculosis lipids.

Wenqing Shui, Sarah A Gilmore, Leslie Sheu, Jun Liu, Jay D Keasling, Carolyn R Bertozzi

Open access · greenAbstract read
In one paragraph

Article in Journal of proteome research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
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

21 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Culture ofPathogens (Basel, Switzerland) · 2021
    Article
  5. Review
  6. Article
  7. Review
  8. Proteomics ofMolecular & cellular proteomics : MCP · 2018
    Article
  9. Proteomics ofFrontiers in immunology · 2018
    Review
  10. Comparative Proteomics Analysis of Human Macrophages Infected with VirulentFrontiers in cellular and infection microbiology · 2017
    Article
  11. Metabolic Perspectives on Persistence.Microbiology spectrum · 2017
    Review
  12. Article
  13. Review
  14. Article
  15. Metabolic host responses to infection by intracellular bacterial pathogens.Frontiers in cellular and infection microbiology · 2013
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Tuberculosis: global approaches to a global disease.Current opinion in biotechnology · 2010
    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

6 authors at 1 institution in 1 country.

Wenqing ShuiDepartment of Chemistry, University of California, Berkeley, California 94720, USA.
Sarah A Gilmore
Leslie Sheu
Jun Liu
Jay D Keasling
Carolyn R Bertozzi
Lawrence Berkeley National Laboratory · US

Funding

Mycobacterial Sulfation PathwaysR01AI051622 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BERTOZZI, CAROLYN · 2002 to 2015
$6.0M
Chemical MycobateriologyR37AI051622 · NIAID · STANFORD UNIVERSITY · PI BERTOZZI, CAROLYN · 2016 to 2025
$4.7M
NIAID NIH HHS AI51622NIAID NIH HHS R01 AI051622NIAID NIH HHS R37 AI051622
6 · The paper itself

Abstract

Mycobacterium tuberculosis (M. tuberculosis) is an intracellular pathogen possessing a complex mixture of cell wall lipids that are thought to modulate the activities of host macrophages. In this study, we employed two state-of-the-art quantitative proteomic approaches, metabolic labeling SILAC and chemical isobaric tagging iTRAQ, to study changes in macrophage protein expression in response to exposure to M. tuberculosis lipids. From a total of 1286 proteins identified, 463 were discovered by both isotope-labeling strategies at a high consistency, and the rest of proteins were detected by only one of the two approaches. Upon exposure to mycobacterial cell wall lipids, 166 macrophage proteins showed differential expression. These included proteins involved in the immune response, oxidation and reduction, and vesicle transport, as well as other cellular processes. The response of the macrophage proteome to M. tuberculosis lipids reflects the cell's innate defense mechanisms as well as lipid-induced processes that may benefit the pathogen.

Indexed as

Gene Expression RegulationHost-Pathogen InteractionsAnimalsBacterial ProteinsCell WallChromatography, LiquidDatabases, ProteinLipidsMacrophagesMass SpectrometryMiceModels, BiologicalMycobacterium tuberculosisProteomeProteomicsBacterial ProteinsLipidsProteome

Identifiers

PMID19053526
PMCPMC2655317
OpenAlexW2076781905

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.