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Updated: Nov 8, 2025

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
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SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry

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The claudin-transcription factor signaling pathway

Kotaro Sugimoto1, Hideki Chiba1

  • 1Department of Basic Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan.

Tissue Barriers
|April 28, 2021
PubMed

Insights

Claudins (CLDNs) are key tight junction proteins involved in cell signaling. This review details CLDNs

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Claudins (CLDNs) are essential transmembrane proteins forming tight junctions, crucial for cellular barrier function.
  • While CLDNs anchor signaling proteins, the molecular mechanisms remain incompletely understood.
  • CLDNs play roles in both physiological processes and various diseases.

Purpose of the Study:

  • To review recent advancements in understanding Claudin (CLDN) signaling pathways in health and disease.
  • To elucidate the functional significance of phosphotyrosine motifs in CLDNs and their interaction with Src-family kinases (SFKs).
  • To explore the crosstalk between CLDNs and transcription factor signaling in physiological and pathological contexts, particularly cancer.

Main Methods:

  • Literature review of recent research on CLDN signaling.
  • Analysis of functional relevance of phosphotyrosine motifs in CLDN C-terminal domains.
  • Investigation of mutual regulation between CLDNs and SFKs.
  • Examination of CLDN crosstalk with transcription factor signaling pathways.

Main Results:

  • Phosphotyrosine motifs in CLDNs are functionally relevant for signaling.
  • A mutual regulatory relationship exists between CLDNs and Src-family kinases (SFKs).
  • Aberrant CLDN-transcription factor signaling significantly impacts cancer progression, either promoting or inhibiting it.

Conclusions:

  • CLDNs are central to cell signaling, with phosphotyrosine motifs mediating interactions with kinases like SFKs.
  • The interplay between CLDNs and transcription factors is critical for coordinating physiological and pathological events.
  • Dysregulated CLDN-transcription factor signaling represents a potential therapeutic target in cancer.
Keywords:
AKTCLDNPI3KSrc-family kinaseTight junctioncell adhesion signalnuclear receptorsignal transductiontranscription factors

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