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Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Nuclear factor Y (NF-Y) and cellular senescence.

K Matuoka1, K Yu Chen

  • 1Graduate Program in Molecular Biosciences, and, Rutgers-The State University of New Jersey, Piscataway, New Jersey 08854-8087, USA.

Experimental Cell Research
|December 10, 1999
PubMed
Summary

NF-Y (Nuclear Factor Y) is a crucial transcription factor regulating eukaryotic gene expression. Its trimeric form binds DNA, influencing genes involved in cell cycle and senescence, like TK and DHFR.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • NF-Y (Nuclear Factor Y) is a CCAAT-binding transcription factor essential for regulating eukaryotic gene expression.
  • It recognizes specific DNA sequences in the promoter regions of various genes.
  • The functional form of NF-Y is a heterotrimer composed of A, B, and C subunits.

Purpose of the Study:

  • To elucidate the structure and function of the NF-Y transcription factor.
  • To understand the regulatory mechanisms governing NF-Y activity.
  • To explore the role of NF-Y in cellular processes like replicative senescence.

Main Methods:

  • Analysis of NF-Y subunit composition and DNA-binding activity.
  • Investigation of regulatory mechanisms including differential expression and protein interactions.
  • Examination of NF-Y's role in regulating specific genes (e.g., TK, DHFR) in human diploid fibroblasts.

Main Results:

  • Only the trimeric form of NF-Y exhibits DNA-binding activity.
  • NF-Y transcriptional activity is modulated by expression levels, splicing, protein interactions, and redox potential.
  • NF-Y regulates age-dependent G1/S genes, exemplified by thymidine kinase and dihydrofolate reductase.

Conclusions:

  • NF-Y is a vital transcription factor with a complex regulatory network.
  • Its function is dependent on its trimeric structure and interactions.
  • NF-Y plays a significant role in replicative senescence by controlling cell cycle gene expression.