Evidence map›Paper›PMID 20522497›Full record

ArticleMicrobiology (Reading, England)2010

Mycobacterium tuberculosis protein kinase K confers survival advantage during early infection in mice and regulates growth in culture and during persistent infection: implications for immune modulation.

Vandana Malhotra, Lourdes T Arteaga-Cortés, Gwendolyn Clay, Josephine E Clark-Curtiss

Open access · greenAbstract read
In one paragraph

Article in Microbiology (Reading, England), 2010. 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
2.0field-weighted citation impact, top 15% 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, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Communications biology · 2019
    Article
  6. Frontiers in cellular and infection microbiology · 2018
    Article
  7. Review
  8. Article
  9. Mycobacterial Growth.Cold Spring Harbor perspectives in medicine · 2015
    Review
  10. Article
  11. Article
  12. Review
  13. Phosphorylation regulates mycobacterial proteasome.Journal of microbiology (Seoul, Korea) · 2014
    Article
  14. Review
  15. Review
  16. Article
  17. Cell death paradigms in the pathogenesis of Mycobacterium tuberculosis infection.Frontiers in cellular and infection microbiology · 2014
    Review
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Vandana MalhotraBiodesign Institute, Center for Infectious Diseases and Vaccinology, Arizona State University, Tempe, AZ 85287, USA.
Lourdes T Arteaga-CortésBiodesign Institute, Center for Infectious Diseases and Vaccinology, Arizona State University, Tempe, AZ 85287, USA.
Gwendolyn ClaySchool of Life Sciences, Arizona State University, Tempe, AZ 85287, USA.
Josephine E Clark-CurtissSchool of Life Sciences, Arizona State University, Tempe, AZ 85287, USA.
Arizona State University · US

Funding

GENE EXPRESSION IN MYCOBACTERIUM TUBERCULOSISR01AI046428 · NIAID · WASHINGTON UNIVERSITY · PI CLARK-CURTISS, JOSEPHINE E · 2000 to 2009
$2.6M
Howard Hughes Medical InstituteNIAID NIH HHS AI46428NIAID NIH HHS HHSN266200400091CNIAID NIH HHS R01 AI046428
6 · The paper itself

Abstract

Mycobacterium tuberculosis serine/threonine protein kinases (STPKs) are key regulators of growth and metabolism; however, evidence for their roles in virulence is limited. In a preliminary screen based on comparative expression between strains H37Rv and H37Ra, six STPK genes, pknD, pknG, pknH, pknJ, pknK and pknL, showed higher expression in H37Rv. In the second screen, STPK expression was analysed in H37Rv-infected human macrophages. Interestingly, significant expression of pknK was detected only at 18 h post-infection, suggesting its involvement in early infection events. We have investigated the roles of PknK in vitro and in vivo. PknK levels were induced under stationary phase and deletion of pknK resulted in increased resistance of the mutant to acidic pH, hypoxia, oxidative and stationary-phase stresses in vitro. These results, together with the increased survival of the DeltapknK strain during persistent infection in mice, reveal a role for PknK in adaptive mechanisms that slow the growth of mycobacteria. A novel finding of this study was the inhibition of growth of DeltapknK strain during acute infection in mice that correlated with the significant upregulation of tumour necrosis factor as well as the simultaneous downregulation of interleukin-12p40, interferon-gamma and induced nitric oxide synthase transcripts. Finally, we provide evidence for the localization of PknK during infection and discuss its implications in pathogenesis.

Indexed as

AnimalsBacterial ProteinsFemaleGene Expression Regulation, BacterialHumansInterferon-gammaMacrophagesMiceMice, Inbred C57BLMycobacterium tuberculosisProtein Serine-Threonine KinasesTuberculosisTumor Necrosis Factor-alphaVirulenceBacterial ProteinsInterferon-gammaPknk protein, Mycobacterium tuberculosisProtein Serine-Threonine KinasesTumor Necrosis Factor-alpha

Identifiers

PMID20522497
PMCPMC3068690
OpenAlexW2074775256

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.