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Related Experiment Video

Updated: May 2, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins SIRT2 and Specific Protein-substrates
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SIRT1 modulates miRNA processing defects in p53-mutated human keratinocytes.

Katharine J Herbert1, Anthony L Cook1, Elizabeth T Snow1

  • 1School of Health Sciences, University of Tasmania, Launceston, TAS 7250, Australia.

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|February 20, 2014
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p53 mutations impair microRNA maturation in keratinocytes. SIRT1 (NAD-dependent deacetylase) works with p53 to regulate microRNA processing and biogenesis.

Keywords:
KeratinocytesMicroRNASIRT1p53

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Area of Science:

  • Cellular biology
  • Molecular genetics
  • Biochemistry

Background:

  • The p53, SIRT1 (NAD-dependent deacetylase), and miR-34a feedback loop regulates SIRT1 expression and p53 responses.
  • p53 influences microRNA processing and maturation beyond its role in genotoxic stress responses.

Purpose of the Study:

  • To investigate the interplay between p53, SIRT1, and miR-34a.
  • To determine how p53 and SIRT1 affect microRNA biogenesis and maturation in keratinocytes.

Main Methods:

  • RNA interference (RNAi) and small molecule inhibitors modulated SIRT1 and p53.
  • Quantitative reverse transcription PCR (qRT-PCR) analyzed microRNA and mRNA levels.
  • Immunoblotting assessed protein expression.

Main Results:

  • p53 suppression reduced mature miR-34a; SIRT1 ablation decreased pri-miR-34a.
  • Inhibiting SIRT1 with p53 suppression increased pri-miR-34a but decreased mature miR-34a.
  • p53-regulated microRNAs (miR-16-1/15, miR-145, miR-107) failed to mature under these conditions.
  • p53-mutated HaCaT cells showed altered microRNA precursor and mature levels compared to primary NHEK cells.

Conclusions:

  • p53 mutations disrupt efficient microRNA biogenesis in keratinocytes.
  • SIRT1 collaborates with p53 in the microRNA biogenesis pathway.