Evidence map›Paper›PMID 26289115›Full record

ArticleCellular microbiology2016

Anaplasma phagocytophilum Rab10-dependent parasitism of the trans-Golgi network is critical for completion of the infection cycle.

Hilary K Truchan, Lauren VieBrock, Chelsea L Cockburn, Nore Ojogun, Brian P Griffin, Dayanjan S Wijesinghe, Charles E Chalfant, Jason A Carlyon

Open access · bronzeAbstract read
In one paragraph

Article in Cellular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 36 citations in OpenAlex.

  1. Machine Learning-Based Detection ofPathogens (Basel, Switzerland) · 2026
    Article
  2. Article
  3. Article
  4. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. Article
  7. Rab27 in tick extracellular vesicle biogenesis and infection.bioRxiv : the preprint server for biology · 2023
    Article
  8. Article
  9. Innate immunity in rickettsial infections.Frontiers in cellular and infection microbiology · 2023
    Review
  10. Establishing the intracellular niche of obligate intracellular vacuolar pathogens.Frontiers in cellular and infection microbiology · 2023
    Review
  11. Article
  12. Pathogens (Basel, Switzerland) · 2022
    Article
  13. Moonlighting in Rickettsiales: Expanding Virulence Landscape.Tropical medicine and infectious disease · 2022
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  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

8 authors at 2 institutions in 1 country.

Hilary K TruchanDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Lauren VieBrockDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Chelsea L CockburnDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Nore OjogunDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Brian P GriffinMolecular Biology and Genetics Program, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Dayanjan S WijesingheDepartment of Surgery, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Charles E ChalfantDepartment of Biochemistry and Molecular Biology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Jason A CarlyonDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Virginia Commonwealth University · USHunter Holmes McGuire VA Medical Center · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Kim Felder Rhoads · 1985 to 2026
$51.0M
Center for Clinical and Translational ResearchUL1TR000058 · NCATS · VIRGINIA COMMONWEALTH UNIVERSITY · PI MOELLER, FREDERICK GERARD · 2012 to 2015
$12.5M
The roles of Anaplasma phagocytophilum surface proteins in infectionR01AI072683 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI CARLYON, JASON A · 2007 to 2021
$5.8M
VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
The functional role of the cPLA2alpha/C1P interaction in sepsis resolutionR01HL125353 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI BROWN, RHODERICK E, CHALFANT, CHARLES E. · 2014 to 2018
$4.0M
The roles of Anaplasma phagocytophilum surface proteins in infectionR37AI072683 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI Jason A Carlyon · 2022 to 2026
$2.6M
AB SCIEX 5500 QTRAP Mass Spectrometer for Lipidomics and Metabolomics ResearchS10OD010641 · OD · VIRGINIA COMMONWEALTH UNIVERSITY · PI CHALFANT, CHARLES E. · 2012 to 2012
$578k
The role of the C1P/cPLA2alpha interaction in anaphylaxisR21AI109068 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI CHALFANT, CHARLES E. · 2014 to 2015
$419k
The roles of Anaplasma phagocytophilum surface proteins in cellular invasionR56AI072683 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI CARLYON, JASON A · 2012 to 2012
$368k
The role of RNA splicing in non-small cell lung cancerI01BX001792 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI CHALFANT, CHARLES E. · 2013 to 2024
–
BLRD VA I01 BX001792NCATS NIH HHS UL1 TR000058NCATS NIH HHS UL1TR000058NCI NIH HHS P30 CA016059NHLBI NIH HHS HL125353NHLBI NIH HHS R01 HL125353NIAID NIH HHS AI072683NIAID NIH HHS AI109068NIAID NIH HHS R01 AI072683NIAID NIH HHS R21 AI109068NIAID NIH HHS R37 AI072683NIAID NIH HHS R56 AI072683NIH HHS S10 OD010641NINDS NIH HHS 5P30NS047463NINDS NIH HHS P30 NS047463PHPPO CDC HHS R01 PH000032
6 · The paper itself

Abstract

Anaplasma phagocytophilum is an emerging human pathogen and obligate intracellular bacterium. It inhabits a host cell-derived vacuole and cycles between replicative reticulate cell (RC) and infectious dense-cored (DC) morphotypes. Host-pathogen interactions that are critical for RC-to-DC conversion are undefined. We previously reported that A. phagocytophilum recruits green fluorescent protein (GFP)-tagged Rab10, a GTPase that directs exocytic traffic from the sphingolipid-rich trans-Golgi network (TGN) to its vacuole in a guanine nucleotide-independent manner. Here, we demonstrate that endogenous Rab10-positive TGN vesicles are not only routed to but also delivered into the A. phagocytophilum-occupied vacuole (ApV). Consistent with this finding, A. phagocytophilum incorporates sphingolipids while intracellular and retains them when naturally released from host cells. TGN vesicle delivery into the ApV is Rab10 dependent, up-regulates expression of the DC-specific marker, APH1235, and is critical for the production of infectious progeny. The A. phagocytophilum surface protein, uridine monophosphate kinase, was identified as a guanine nucleotide-independent, Rab10-specific ligand. These data delineate why Rab10 is important for the A. phagocytophilum infection cycle and expand the understanding of the benefits that exploiting host cell membrane traffic affords intracellular bacterial pathogens.

Indexed as

Host-Parasite InteractionsAnaplasma phagocytophilumCell LineCytoplasmic VesiclesHumansNucleoside-Phosphate KinaseProtein Bindingrab GTP-Binding Proteinstrans-Golgi NetworkVacuolesNucleoside-Phosphate KinaseRab10 protein, humanrab GTP-Binding Proteinsuridine monophosphate kinaseAnaplasmataceaeintracellular parasitismlipidomicsnutritional virulenceobligate intracellularUMPK

Identifiers

PMID26289115
PMCPMC4891814
OpenAlexW2145649073

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.