Related Experiment Video

Updated: Jun 14, 2026

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
10:27

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

Published on: March 9, 2012

The Ras effector RASSF2 controls the PAR-4 tumor suppressor

Howard Donninger1, Luke Hesson, Michele Vos

  • 1Department of Medicine, James Graham Brown Cancer Center, Molecular Targets Program, University of Louisville, 505 S. Hancock St., Louisville, KY 40202, USA.

Molecular and Cellular Biology
|April 7, 2010
PubMed

Insights

The Ras association domain family protein 2 (RASSF2) acts as a tumor suppressor by interacting with prostate apoptosis response protein 4 (PAR-4). This interaction is crucial for RASSF2

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Ras association domain family protein 2 (RASSF2) is a proapoptotic protein implicated as a tumor suppressor.
  • Inhibition of RASSF2 expression promotes K-Ras-driven cell transformation.
  • Epigenetic inactivation of RASSF2 is common in primary tumors with mutant Ras.

Purpose of the Study:

  • To elucidate the mechanism of action of the RASSF2 tumor suppressor.
  • To identify novel signaling pathways regulated by RASSF2.
  • To explain the frequent inactivation of RASSF2 in prostate tumors.

Main Methods:

  • Co-immunoprecipitation assays to detect protein-protein interactions.
  • Western blotting to analyze protein expression and localization.
  • Cellular fractionation and immunofluorescence microscopy to study protein translocation.

Main Results:

  • RASSF2 directly complexes with the prostate apoptosis response protein 4 (PAR-4) tumor suppressor.
  • K-Ras regulates the RASSF2-PAR-4 interaction, which is essential for PAR-4's apoptotic activity.
  • RASSF2 modulates the nuclear translocation of PAR-4 in prostate cancer cells.

Conclusions:

  • RASSF2 functions as a tumor suppressor by regulating PAR-4 nuclear localization and apoptotic signaling.
  • This study identifies a novel mechanism of action for RASSF proteins.
  • The findings provide a molecular explanation for RASSF2 inactivation in prostate tumorigenesis.

More Related Videos

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein07:08

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein

Published on: January 16, 2020

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans08:12

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Published on: October 5, 2020

Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...