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 language | English |
|---|---|
| Pages (from-to) | 35511-35525 |
| Number of pages | 15 |
| Journal | Journal of Biological Chemistry |
| Volume | 288 |
| Issue number | 49 |
| DOIs | |
| State | Published - 6 Dec 2013 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
-
SDG 3 Good Health and Well-being
Fingerprint
Dive into the research topics of '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'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver