The cyclin-dependent kinase inhibitor p16INK4a physically interacts with transcription factor Sp1 and cyclin-dependent kinase 4 to Transactivate MicroRNA-141 and MicroRNA-146b-5p spontaneously and in response to ultraviolet light-induced DNA Damage

  • Huda H. Al-Khalaf
  • , Peer Mohideen
  • , Shreeram C. Nallar
  • , Dhananjaya V. Kalvakolanu
  • , Abdelilah Aboussekhra

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

Background: The cyclin-dependent kinase inhibitor p16INK4a is also a modulator of gene expression through an unknown mechanism. Results: p16INK4a-CDK4 forms a heterocomplex with Sp1, which induces the expression and UV-dependent up-regulation of miR-141 and miR-146b-5p. Conclusion: p16INK4a-CDK4 complex has transcriptional activity through interaction with the transcription factor Sp1. Significance: The microRNAs are novel effectors of the p16INK4a-CDK4 complex.

Original languageEnglish
Pages (from-to)35511-35525
Number of pages15
JournalJournal of Biological Chemistry
Volume288
Issue number49
DOIs
StatePublished - 6 Dec 2013
Externally publishedYes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

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