Evidence map›Paper›PMID 27456933›Full record

ReviewJournal of molecular biology2016

Avoidance and Subversion of Eukaryotic Homeostatic Autophagy Mechanisms by Bacterial Pathogens.

Cheryl Miller, Jean Celli

Abstract readReview
In one paragraph

Review in Journal of molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. Cells · 2025
    Article
  3. Review
  4. Article
  5. International journal of molecular sciences · 2022
    Article
  6. Identification ofFrontiers in cellular and infection microbiology · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Do cells use passwords in cell-state transitions? Is cell signaling sometimes encrypted?Theory in biosciences = Theorie in den Biowissenschaften · 2020
    Article
  12. Article
  13. Diverse Facets of Sphingolipid Involvement in Bacterial Infections.Frontiers in cell and developmental biology · 2019
    Review
  14. Article
  15. [Role of p38MAPK signaling pathway in autophagy of Henle-407 cells induced by spvB of Salmonella typhimurium].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Importance of Metabolic Adaptations inFrontiers in cellular and infection microbiology · 2017
    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

2 authors.

Cheryl MillerPaul G. Allen School for Global Animal Health, College of Veterinary Medicine, Washington State University, Pullman, 99164-7090 WA, USA. Electronic address: cherylmiller@vetmed.wsu.edu.
Jean CelliPaul G. Allen School for Global Animal Health, College of Veterinary Medicine, Washington State University, Pullman, 99164-7090 WA, USA. Electronic address: jcelli@vetmed.wsu.edu.

Funding

Infectious Diseases and Microbial Immunology Training ProgramT32AI007025 · NIAID · WASHINGTON STATE UNIVERSITY · PI Thomas H KAWULA, M KARIUKI NJENGA · 1985 to 2026
$7.4M
Brucella mechanisms of autophagy mediated egressR21AI112649 · NIAID · WASHINGTON STATE UNIVERSITY · PI CELLI, JEAN A · 2014 to 2015
$378k
NIAID NIH HHS R21 AI112649NIAID NIH HHS T32 AI007025
6 · The paper itself

Abstract

Autophagy is a conserved lysosomal recycling process, which maintains cellular homeostasis during stress and starvation conditions by degrading and recycling proteins, lipids, and carbohydrates, ultimately increasing nutrient availability in eukaryotes. An additional function of autophagy, termed xenophagy, is to detect, capture, and destroy invading microorganisms, such as viruses, bacteria, and protozoa, providing autophagy with a role in innate immunity. Many intracellular pathogens have, however, developed mechanisms to avoid xenophagy and have evolved strategies to take advantage of select autophagic processes to undergo their intracellular life cycle. This review article will discuss the molecular mechanisms used by the intracellular bacterial pathogens Francisella spp. and Brucella spp. to manipulate components of the autophagic pathway, promoting cytosolic growth in the case of Francisella spp. and facilitating cellular egress and cell-to-cell spread in the case of Brucella spp. These examples highlight how successful, highly infectious bacterial pathogens avoid or subvert host autophagy mechanisms normally employed to maintain eukaryotic homeostasis.

Indexed as

AutophagyHost-Pathogen InteractionsImmune EvasionAnimalsBrucellaFrancisellaHumansbacterial secretion systemcellular egressinfectionnutrient acquisitionO-antigen

Identifiers

PMID27456933
PMCPMC5010449

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.