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Related Concept Videos

G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Cell Polarization by Rho Proteins01:21

Cell Polarization by Rho Proteins

Cell polarity is the asymmetric distribution of cellular and membrane components, making one side of the cell different from the other. This polarity is essential to many processes such as embryogenesis, axon migration, glucose transport across epithelial cells, and directional cell migration. A migrating cell responds to intracellular or extracellular signals via molecular cascades that reorganize the actin cytoskeleton to establish this polarity. In these cells, the Rho family proteins Cdc42,...
GPCRs Regulate Adenylyl Cylase Activity01:09

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.
Two...
Esophageal Achalasia01:27

Esophageal Achalasia

Esophageal achalasia is a chronic neurogenic disorder characterized by impaired relaxation of the lower esophageal sphincter (LES) and absent or ineffective peristalsis in the distal esophagus. This leads to a functional obstruction without a physical blockage, despite significant disruption of esophageal motility.EtiologyAchalasia is caused by degeneration of the myenteric (Auerbach's) plexus, specifically the loss of inhibitory ganglion cells that produce vasoactive intestinal peptide (VIP)...

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Updated: Jun 6, 2026

Electrophysiological Assessment of Murine Atria with High-Resolution Optical Mapping
08:19

Electrophysiological Assessment of Murine Atria with High-Resolution Optical Mapping

Published on: February 22, 2018

Pg-Induced ATR Activation Promotes ESCC Progression via M2 TAM Polarization.

Yanhua Sun1,2, Lin Yang1,3, Xiaodong Wei1,3

  • 1Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Diseases, Hubei Minzu University, Enshi, Hubei, China.

Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
|June 5, 2026
PubMed
Summary
This summary is machine-generated.

Porphyromonas gingivalis (Pg) promotes esophageal cancer growth by activating the ATR pathway, leading to M2 macrophage polarization. Inhibiting ATR reduces tumor progression, offering a new therapeutic target for ESCC.

Keywords:
Porphyromonas gingivalisATRM2 tumor‐associated macrophagesesophageal squamous cell carcinomapolarization

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Last Updated: Jun 6, 2026

Electrophysiological Assessment of Murine Atria with High-Resolution Optical Mapping
08:19

Electrophysiological Assessment of Murine Atria with High-Resolution Optical Mapping

Published on: February 22, 2018

Area of Science:

  • Oncology
  • Microbiology
  • Immunology

Background:

  • Periodontal pathogens like Porphyromonas gingivalis (Pg) are increasingly linked to systemic malignancies.
  • Pg has been specifically implicated in esophageal squamous cell carcinoma (ESCC), but the underlying molecular mechanisms require elucidation.

Purpose of the Study:

  • To investigate the impact of Pg on ESCC growth.
  • To explore the molecular mechanisms, particularly the role of the ATR signaling pathway and macrophage polarization, in Pg-mediated ESCC progression.

Main Methods:

  • In vitro studies involved differentiating THP-1 cells into macrophages and treating them with Pg, with or without ATR inhibition (siATR).
  • Macrophage polarization and co-culture with ESCC cells (KYSE150) were analyzed.
  • In vivo studies utilized a mouse model where Pg was administered, and ESCC cells (with or without ATR inhibition) were implanted to assess tumor growth and macrophage polarization in tumor tissues.

Main Results:

  • Pg promoted M2 macrophage polarization and enhanced the proliferation and invasion of ESCC cells.
  • Inhibition of ATR (siATR) reduced M2 macrophage polarization and suppressed ESCC cell progression.
  • Pg-induced ATR activation in vivo promoted tumor growth by recruiting M2 tumor-associated macrophages (TAMs).

Conclusions:

  • Pg activates the ATR signaling pathway, inducing M2 TAM polarization, which promotes ESCC growth.
  • Targeting the ATR pathway presents a novel therapeutic strategy for ESCC prevention and treatment.