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Related Experiment Video

Updated: Jun 16, 2026

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
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NF-kappaB subtypes regulate CCCTC binding factor affecting corneal epithelial cell fate.

Luo Lu1, Ling Wang1, Tie Li1

  • 1Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502.

The Journal of Biological Chemistry
|January 30, 2010
PubMed
Summary
This summary is machine-generated.

Epidermal growth factor (EGF) and UV stress differentially regulate CCCTC binding factor (CTCF) activity via NF-kappaB signaling, impacting cell proliferation and apoptosis in corneal cells.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • CCCTC binding factor (CTCF) is crucial for DNA imprinting, gene insulation, and mediating cell fate in response to growth factors and stress.
  • The intracellular regulatory mechanisms governing CTCF activity remain largely unelucidated.

Purpose of the Study:

  • To investigate how epidermal growth factor (EGF) and UV stress modulate CTCF activity.
  • To elucidate the role of NF-kappaB signaling pathways in regulating CTCF.
  • To determine the impact of altered CTCF activity on human corneal epithelial cell proliferation and apoptosis.

Main Methods:

  • Analysis of CTCF activity in human corneal epithelial cells under EGF and UV stress.
  • Investigation of NF-kappaB subunit activation (p65/p50 heterodimer and p50/p50 homodimer) in response to stimuli.
  • Chromatin immunoprecipitation assays to assess transcription factor binding to the CTCF gene promoter.

Main Results:

  • EGF stimulation increased CTCF activity, promoting human corneal epithelial cell proliferation.
  • UV stress decreased CTCF activity, leading to apoptosis in these cells.
  • EGF-induced p65/p50 heterodimer formation activated CTCF transcription by binding to a kappaB site.
  • UV stress-induced p50/p50 homodimer formation suppressed CTCF expression.

Conclusions:

  • CTCF plays a central role in mediating the opposing effects of growth factor and stress signaling on cell survival and death.
  • CTCF acts as a downstream component of the NF-kappaB pathway within the core transcriptional network governing cell fate.