ReviewCellular microbiology2010
Type IV secretion in the obligatory intracellular bacterium Anaplasma phagocytophilum.
Review in Cellular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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.
Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- Obligatory intracellular bacterium Anaplasma phagocytophilum AnkA regulates actin dynamics and spatiotemporal bacterial release.PLoS pathogens · 2026Article
- Article
- Haematology, serum biochemistry, innate and adaptive immune system responses to blood pathogen infections in cattle: A review.Parasitology research · 2026Review
- Genomic characterization of an emergingEmerging microbes & infections · 2024Article
- Article
- Article
- Anaplasma phagocytophilum Ats-1 enhances exosome secretion through Syntenin-1.BMC microbiology · 2023Article
- Frankenbacteriosis targeting interactions between pathogen and symbiont to control infection in the tick vector.iScience · 2023Article
- Article
- Identification and evaluation of UL36 protein from Dermacentor silvarum salivary gland and its interaction with Anaplasma ovis VirB10.Parasites & vectors · 2020Article
- Chimeric Coupling Proteins Mediate Transfer of Heterologous Type IV Effectors through the Escherichia coli pKM101-Encoded Conjugation Machine.Journal of bacteriology · 2016Article
- The intracellular bacterium Anaplasma phagocytophilum selectively manipulates the levels of vertebrate host proteins in the tick vector Ixodes scapularis.Parasites & vectors · 2016Article
- The Rickettsia type IV secretion system: unrealized complexity mired by gene family expansion.Pathogens and disease · 2016Article
- The Prostaglandin E2-EP3 Receptor Axis Regulates Anaplasma phagocytophilum-Mediated NLRC4 Inflammasome Activation.PLoS pathogens · 2016Article
- Mechanism and Function of Type IV Secretion During Infection of the Human Host.Microbiology spectrum · 2016Review
- Article
- Discovery of putative small non-coding RNAs from the obligate intracellular bacterium Wolbachia pipientis.PloS one · 2015Article
- Secretome of obligate intracellular Rickettsia.FEMS microbiology reviews · 2015Review
- Bioinformatic and mass spectrometry identification of Anaplasma phagocytophilum proteins translocated into host cell nuclei.Frontiers in microbiology · 2015Article
- Multilocus sequence analysis of Anaplasma phagocytophilum reveals three distinct lineages with different host ranges in clinically ill French cattle.Veterinary research · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Anaplasma phagocytophilum is an obligatory intracellular bacterium that infects neutrophils, the primary host defence cells. Consequent effects of infection on host cells result in a potentially fatal systemic disease called human granulocytic anaplasmosis. Despite ongoing reductive genome evolution and deletion of most genes for intermediary metabolism and amino acid biosynthesis, Anaplasma has also experienced expansion of genes encoding several components of the type IV secretion (T4S) apparatus. Two A. phagocytophilum T4S effector molecules are currently known; Anaplasma translocated substrate 1 (Ats-1) and ankyrin repeat domain-containing protein A (AnkA) have C-terminal positively charged amino acid residues that are recognized by the T4S coupling protein, VirD4. AnkA and Ats-1 contain eukaryotic protein motifs and are uniquely evolved in the family Anaplasmataceae; Ats-1 contains a mitochondria-targeting signal. They are abundantly produced and secreted into the host cytoplasm, are not toxic to host cells, and manipulate host cell processes to aid in the infection process. At the cellular level, the two effectors have distinct subcellular localization and signalling in host cells. Thus in this obligatory intracellular pathogen, the T4S system has evolved as a host-subversive survival factor.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.