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Related Experiment Video

Updated: Jun 10, 2026

Analysis of Cell Cycle Position in Mammalian Cells

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Cell cycle-dependent acetylation of Rb2/p130 in NIH3T3 cells.

F Schwarze¹, J Meraner, M Lechner

¹Division of Molecular Biology, Biocenter, Innsbruck Medical University, Innsbruck, Austria.

|August 3, 2010

Summary

Acetylation modifies the cell cycle regulator retinoblastoma protein 2 (Rb2)/p130, impacting its nuclear function. This acetylation is cell cycle-dependent and influenced by human papilloma virus 16 E7 protein.

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Area of Science:

Cell Biology
Molecular Biology
Biochemistry

Background:

Pocket proteins, including retinoblastoma protein (pRb) and its relatives p130 and p107, are key regulators of the cell cycle.
Their function is modulated by phosphorylation and, for pRb, also by acetylation.
The role of acetylation in p130 regulation remains less understood.

Purpose of the Study:

To investigate the acetylation of retinoblastoma 2 (Rb2)/p130.
To determine the cell cycle-dependency and localization of acetylated p130.
To identify the specific acetylation sites on p130 and assess the impact of HPV16 E7 protein.

Main Methods:

Western blotting to detect acetylated p130 in NIH3T3 cells.
In vitro acetylation assays using recombinant p130 and p300.
Mass spectrometry to identify acetylation sites.
Analysis of HPV16 E7 protein interaction with p130.

Main Results:

Hyperphosphorylated Rb2/p130 is acetylated in NIH3T3 cells, localized to the nucleus.
Acetylation occurs during the S to G2 phases of the cell cycle.
K1079 in the C-terminus is the major acetylation site, with minor sites in the N- and C-termini.
Human papilloma virus 16 E7 protein binds preferentially to acetylated p130 and enhances its acetylation.

Conclusions:

Acetylation is a novel regulatory mechanism for Rb2/p130 during the cell cycle.
Specific acetylation sites on p130 are identified.
HPV16 E7 interaction suggests a role for p130 acetylation in viral oncogenesis.