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Related Concept Videos

Bacterial Phylum Chlamydiae01:29

Bacterial Phylum Chlamydiae

The phylum Chlamydiae or Chlamydiota is composed of a single order, Chlamydiales. This phylum consists entirely of obligate intracellular parasites that infect eukaryotic hosts. While human pathogens within this group have been studied extensively, the phylum encompasses many species capable of interacting with various eukaryotic organisms. Members of Chlamydiae are typically small cocci, approximately 0.5 μm in diameter, and exhibit a distinctive developmental cycle. As is characteristic of...
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GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
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Trichomoniasis01:18

Trichomoniasis

Trichomonas vaginalis is a flagellated protozoan parasite and the causative agent of trichomoniasis, one of the most prevalent non-viral sexually transmitted infections in the United States. This extracellular parasite primarily colonizes the lower genitourinary tract in women—particularly the vagina—and in men, the urethra and prostate. Its structural and functional adaptations enable its survival, motility, and pathogenicity within the host environment.Structural Features and Host EntryT.
Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

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Colonisation of Pathogens01:25

Colonisation of Pathogens

Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...
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Related Experiment Video

Updated: Jul 3, 2026

Live-Cell Forward Genetic Approach to Identify and Isolate Developmental Mutants in Chlamydia trachomatis
10:32

Live-Cell Forward Genetic Approach to Identify and Isolate Developmental Mutants in Chlamydia trachomatis

Published on: June 10, 2020

Infection-Dependent Modulation of the Host Adaptor Gab2 During Chlamydia trachomatis Intracellular Development.

Sora Kuroiwa1, Taiki Deguchi1, Torahiko Okubo1

  • 1Department of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.

Microbiology and Immunology
|July 2, 2026
PubMed
Summary
This summary is machine-generated.

Chlamydia trachomatis infection impacts host cell signaling by targeting the adaptor protein Gab2. This modulation is crucial for bacterial intracellular development and maturation.

Keywords:
Chlamydia trachomatisGab2PI3K‐AKTcellular adaptationinhibitor‐panel screening

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Last Updated: Jul 3, 2026

Live-Cell Forward Genetic Approach to Identify and Isolate Developmental Mutants in Chlamydia trachomatis
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Identification of Host Pathways Targeted by Bacterial Effector Proteins using Yeast Toxicity and Suppressor Screens
07:40

Identification of Host Pathways Targeted by Bacterial Effector Proteins using Yeast Toxicity and Suppressor Screens

Published on: October 25, 2019

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Chlamydia trachomatis (Ct) causes reproductive complications like infertility and pelvic inflammatory disease.
  • Ct pathogenicity relies on intracellular maturation, involving elementary bodies (EB) and reticulate bodies.
  • Ct modulates host PI3K-AKT signaling, but the precise mechanism is unknown.

Purpose of the Study:

  • To investigate the molecular mechanisms by which Ct modulates host PI3K-AKT signaling.
  • To identify specific host factors involved in Ct intracellular development.

Main Methods:

  • Screening of a PI3K-AKT-mTOR compound library (319 inhibitors).
  • Identification and characterization of host adaptor protein Gab2 (GRB2-associated binding protein 2) as a Ct target.
  • Assessment of Gab2 protein levels during infection and the effect of Gab2 silencing on Ct replication.

Main Results:

  • Gab2 was identified as a novel target molecule of Ct.
  • Gab2 protein levels decreased during the late stages of Ct infection.
  • Silencing Gab2 impaired Ct intracellular replication but did not affect EB formation.

Conclusions:

  • Ct infection modulates the host adaptor protein Gab2 during its intracellular development.
  • Gab2 plays a significant role in chlamydial maturation and intracellular replication.
  • These findings offer new insights into host-pathogen interactions in Ct infections.