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C-Myc Indirectly Controls ATP13A2 Levels via HIF-1α Activation.

Aslı Beril Tiryakiler1, Benan Temizci2, Arzu Karabay2

  • 1Molecular Biology-Genetics and Biotechnology, Graduate School, Istanbul Technical University, Istanbul, Turkey.

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|November 26, 2025
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c-Myc overexpression initially increases ATP13A2 expression by stabilizing HIF1α, but this effect is transient. This indirect regulation impacts iron accumulation, offering insights into cellular homeostasis and disease.

Keywords:
ATP13A2HIF1αKufor‐Rakeb syndromePARK9Parkinson's diseasec‐Myc

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Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Neuroscience

Background:

  • c-Myc is a crucial transcription factor implicated in various diseases, including cancer and neurodegenerative disorders.
  • ATP13A2 (PARK9) protein is vital for lysosomal function and metal transport, with mutations linked to Kufor-Rakeb Syndrome and Parkinson's disease.

Purpose of the Study:

  • To investigate the transcriptional regulation of the ATP13A2 gene by the c-Myc transcription factor.
  • To elucidate the mechanism by which c-Myc influences ATP13A2 expression and cellular iron homeostasis.

Main Methods:

  • Identification of c-Myc binding sites on the ATP13A2 promoter.
  • Chromatin immunoprecipitation (ChIP) assay to confirm in vivo c-Myc binding.
  • Quantitative PCR (qPCR), luciferase assays, and Western blot analysis to assess gene and protein expression.
  • Prussian blue staining for intracellular iron analysis.

Main Results:

  • c-Myc binds to the ATP13A2 promoter, but its overexpression initially decreases mRNA levels while increasing protein levels.
  • ATP13A2 expression is transiently upregulated post-c-Myc overexpression, peaking at 24 hours and returning to baseline by 72 hours.
  • Hypoxia-inducible factor 1-alpha (HIF1α) stabilization by c-Myc appears to mediate the initial increase in ATP13A2 expression, correlating with altered intracellular iron levels.

Conclusions:

  • c-Myc indirectly upregulates ATP13A2 expression through HIF1α stabilization, impacting cellular iron homeostasis.
  • The findings reveal a complex, time-dependent regulatory mechanism of ATP13A2 by c-Myc.
  • This study provides novel insights into the role of c-Myc in maintaining cellular homeostasis and its potential link to neurodegenerative diseases.