ReviewCellular microbiology2015
Chlamydiae interaction with the endoplasmic reticulum: contact, function and consequences.
Review in Cellular microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 41 citations in OpenAlex.
- Transmembrane effector substrates of type IV secretion systems: mechanisms of secretion and insertion into host cell membranes.microLife · 2026Review
- Toxoplasma effector TgROP1 establishes membrane contact sites with the endoplasmic reticulum during infection.Nature microbiology · 2025Article
- Emerging Insights into Protein Post-Translational Modifications in Chlamydia-Host Interactions.The American journal of pathology · 2025Review
- Recruitment of the cellular lipid transport protein CERT to C. psittaci inclusions regulates the timing of bacterial egress.Scientific reports · 2025Article
- Chlamydia trachomatis induces disassembly of the primary cilium to promote the intracellular infection.PLoS pathogens · 2024Article
- The Endoplasmic Reticulum Is a Key Battleground between Phytoplasma Aggression and Host Plant Defense.Cells · 2023Article
- Chlamydia trachomatis Alters Mitochondrial Protein Composition and Secretes Effector Proteins That Target Mitochondria.mSphere · 2022Article
- Differential Effects of Small Molecule Inhibitors on the Intracellular Chlamydia Infection.mBio · 2022Article
- Developing Cyclic Peptomers as Broad-Spectrum Type III Secretion System Inhibitors in Gram-Negative Bacteria.Antimicrobial agents and chemotherapy · 2021Article
- The Small Molecule H89 InhibitsInfection and immunity · 2021Article
- Idiosyncratic Biogenesis of Intracellular Pathogens-Containing Vacuoles.Frontiers in cellular and infection microbiology · 2021Review
- Article
- Hostile Takeover: Hijacking of Endoplasmic Reticulum Function by T4SS and T3SS Effectors Creates a Niche for Intracellular Pathogens.Microbiology spectrum · 2019Article
- Article
- Make It a Sweet Home: Responses ofMicrobiology spectrum · 2019Review
- Phosphatidylserine decarboxylase CT699, lysophospholipid acyltransferase CT775, and acyl-ACP synthase CT776 provide membrane lipid diversity to Chlamydia trachomatis.Scientific reports · 2017Article
- Article
- The Roles of Unfolded Protein Response Pathways in Chlamydia Pathogenesis.The Journal of infectious diseases · 2017Article
- Lycopene Inhibits Propagation of Chlamydia Infection.Scientifica · 2017Article
- Simkania negevensis may produce long-lasting infections in human pneumocytes and endometrial cells.Pathogens and disease · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Chlamydiae and chlamydiae-related organisms are obligate intracellular bacterial pathogens. They reside in a membrane-bound compartment termed the inclusion and have evolved sophisticated mechanisms to interact with cellular organelles. This review focuses on the nature, the function(s) and the consequences of chlamydiae-inclusion interaction with the endoplasmic reticulum (ER). The inclusion membrane establishes very close contact with the ER at specific sites termed ER-inclusion membrane contact sites (MCSs). These MCSs are constituted of a specific set of factors, including the C. trachomatis effector protein IncD and the host cell proteins CERT and VAPA/B. Because CERT and VAPA/B have a demonstrated role in the non-vesicular trafficking of lipids between the ER and the Golgi, it was proposed that Chlamydia establish MCSs with the ER to acquire host lipids. However, the recruitment of additional factors to ER-inclusion MCSs, such as the ER calcium sensor STIM1, may suggest additional functions unrelated to lipid acquisition. Finally, chlamydiae interaction with the ER appears to induce the ER stress response, but this response is quickly dampened by chlamydiae to promote host cell survival.
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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.