Related Experiment Video

Updated: May 17, 2026

In Vitro SUMOylation Assay to Study SUMO E3 Ligase Activity
09:45

In Vitro SUMOylation Assay to Study SUMO E3 Ligase Activity

Published on: January 29, 2018

SUMOylation negatively regulates the stability of CHFR tumor suppressor

Young Eun Kwon1, Sung Jun Bae, Myungjin Kim

  • 1School of Biological Sciences, Research Center for Functional Cellulomics, Seoul National University, Seoul 151-742, Republic of Korea.

Biochemical and Biophysical Research Communications
|November 8, 2012
PubMed

Insights

The CHFR (Checkpoint Forter) protein

Area of Science:

  • Cellular biology
  • Molecular oncology
  • Protein regulation

Background:

  • CHFR (Checkpoint Forter) is a ubiquitin ligase crucial for DNA damage response and cell cycle control.
  • Inactivation of CHFR is linked to cancer development and metastasis.
  • Mechanisms regulating CHFR protein stability remain largely unknown.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling CHFR protein stability.
  • To elucidate the role of post-translational modifications in CHFR regulation.

Main Methods:

  • SUMOylation assays to detect CHFR modification.
  • Site-directed mutagenesis (CHFR K663R) to assess SUMOylation-defective mutants.
  • Western blotting to analyze protein levels and stability.
  • Cellular growth assays to evaluate functional consequences.

Main Results:

  • CHFR undergoes covalent modification by SUMO-1 at lysine 663.
  • SUMOylation of CHFR targets it for degradation via the ubiquitin-proteasome system.
  • A SUMOylation-defective mutant (CHFR K663R) exhibits increased stability and suppresses cell growth.
  • SENP2 deSUMOylating enzyme reverses CHFR SUMOylation.

Conclusions:

  • CHFR stability is regulated by SUMOylation-dependent proteasomal degradation.
  • CHFR SUMOylation represents a novel regulatory mechanism impacting its stability and function.
  • This study highlights the role of SUMOylation in modulating protein stability, with implications for cancer research.

More Related Videos

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model09:00

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model

Published on: April 17, 2026

In Vivo Detection and Analysis of Rb Protein SUMOylation in Human Cells09:40

In Vivo Detection and Analysis of Rb Protein SUMOylation in Human Cells

Published on: November 2, 2017

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...