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Caliban is a transcriptional target of p53 in response to DNA damage

Jiaqian Cui1, Haiyan Zhang1, Yan Cheng2

  • 1Medical School of Nantong University, Nantong, China.

Plos One
|August 28, 2025
PubMed

Insights

DNA damage activates p53, which directly increases the expression of Caliban, a key regulator of apoptosis. This study identifies Caliban as a direct transcriptional target of p53, clarifying its role in DNA damage response.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Caliban, the Drosophila ortholog of human Nuclear export mediator factor (NEMF), regulates intrinsic apoptotic signaling.
  • The precise mechanism controlling Caliban expression following DNA damage is not fully understood.

Purpose of the Study:

  • To elucidate the regulatory mechanism of Caliban expression in response to DNA damage.
  • To determine the role of p53 in controlling Caliban expression.

Main Methods:

  • Investigated Caliban expression levels after DNA damage and p53 overexpression.
  • Characterized the Caliban promoter region, including identifying and mutating a putative p53-binding site.
  • Utilized p53 knockdown experiments to assess its regulatory role.

Main Results:

  • DNA damage and p53 overexpression upregulated both mRNA and protein levels of Caliban.
  • The Caliban promoter showed increased activity upon DNA damage or p53 activation.
  • A specific p53-binding site within the Caliban promoter was identified and shown to be crucial for the DNA damage-induced upregulation.

Conclusions:

  • Caliban expression is upregulated by DNA damage through p53 activation.
  • Caliban is a direct transcriptional target of p53 in the DNA damage response pathway.

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