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Related Experiment Video

Updated: Jan 3, 2026

Functional Assessment of Intestinal Tight Junction Barrier and Ion Permeability in Native Tissue by Ussing Chamber Technique

Functional Assessment of Intestinal Tight Junction Barrier and Ion Permeability in Native Tissue by Ussing Chamber Technique

Published on: May 26, 2021

Claudin-2: Roles beyond Permeability Functions.

Shruthi Venugopal¹, Shaista Anwer¹, Katalin Szászi¹

¹Keenan Research Centre for Biomedical Science of the St. Michael's Hospital and Department of Surgery, University of Toronto, Toronto, ON M5B 1W8, Canada.

International Journal of Molecular Sciences

|November 16, 2019

Summary

Claudin-2 protein forms channels in leaky epithelia, crucial for ion and water transport. Its dysregulation is linked to diseases like cancer, impacting cell functions through signaling pathways.

Keywords:

cancer claudin-2 epithelium fibrosis inflammation migration paracellular permeability proliferation tight junctions

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Last Updated: Jan 3, 2026

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Published on: May 26, 2021

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A Proteoliposome-Based Efflux Assay to Determine Single-molecule Properties of Cl- Channels and Transporters

A Proteoliposome-Based Efflux Assay to Determine Single-molecule Properties of Cl- Channels and Transporters

Published on: April 20, 2015

Area of Science:

Cell Biology
Molecular Biology
Pathophysiology

Background:

Claudin-2 forms cation-selective, water-permeable channels in leaky epithelia.
Its expression is tightly regulated by signaling networks and altered in diseases like cancer, inflammation, and fibrosis.

Purpose of the Study:

To review claudin-2 properties, regulation, and functions.
To emphasize claudin-2's role in signal modulation and disease pathogenesis.

Main Methods:

Literature review of claudin-2 properties and functions.
Analysis of claudin-2's role in cellular events and disease mechanisms.

Main Results:

Claudin-2 is vital for kidney and gut transport.
Altered claudin-2 expression affects cell proliferation, migration, and fate.
Dysregulation contributes to disease via permeability-dependent and -independent mechanisms.

Conclusions:

Claudin-2 dysregulation is implicated in disease generation and progression.
Intracellular adapters may mediate claudin-2's signaling effects.
Further research is needed to elucidate specific mechanisms.