Related Experiment Video

Updated: Mar 28, 2026

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

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The protein kinase DYRK1B is a p53 target gene and functions as a negative feedback regulator of the transcription

Gerrit Wilms1, Katharina Schwandt1, Stefan Düsterhöft2

  • 1Institute of Pharmacology and Toxicology, RWTH Aachen University, Aachen, Germany.

Cell Death & Disease
|March 27, 2026
PubMed

Insights

The tumor suppressor protein p53 activates RFX7, but DYRK1B protein kinase inhibits this activation, forming a negative feedback loop. Inhibiting DYRK1B may enhance RFX7 tumor suppressor function.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • The tumor suppressor protein p53 regulates cellular stress responses, including DNA repair and apoptosis.
  • DYRK1B kinase promotes cancer cell survival and DNA repair, and is overexpressed in tumors.

Purpose of the Study:

  • To investigate the relationship between p53, DYRK1B, and RFX7 in cancer cells.
  • To elucidate the role of DYRK1B in p53-mediated gene regulation.

Main Methods:

  • Utilized cancer cell lines treated with cytostatic drugs (Actinomycin D, Doxorubicin).
  • Assessed DYRK1B and DYRK1A expression levels.
  • Investigated p53-dependent activation of RFX7 and DYRK1B interaction with RFX7.
  • Examined the effect of DYRK1B catalytic activity and inhibitors on RFX7 activation.

Main Results:

  • DYRK1B, but not DYRK1A, expression is upregulated by cytostatic drugs in a p53-dependent manner via RFX7.
  • DYRK1B physically interacts with RFX7 and inhibits its activation by p53, creating a negative feedback loop.
  • DYRK1B's inhibitory effect is catalytic and can be blocked by DYRK1 inhibitors.

Conclusions:

  • DYRK1B is an indirect p53 target that suppresses p53-mediated RFX7 activation.
  • Pharmacological inhibition of DYRK1B could enhance RFX7 tumor suppressor function and represents a potential therapeutic strategy.

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