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Small GTPases - Ras and Rho

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 Gene

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...

Negative Regulator Molecules

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.

GTPases and their Regulation

GTPases and their Regulation

Guanine nucleotide-binding proteins (G-proteins), also known as GTPases, are a superfamily of proteins that regulate many cellular processes, such as cell signaling, vesicular transport, and the regulation of cell shape and motility. Mutation or dysfunction of these proteins can lead to disease. There are around 40,000 known G-proteins that can broadly be classified into two groups ‒ small G-proteins consisting of a single domain and large multi-domain G-proteins.
Large G-proteins, also known...

GTPases and their Regulation

GTPases and their Regulation

Guanine nucleotide-binding proteins (G-proteins), also known as GTPases, are a superfamily of proteins that regulate many cellular processes, such as cell signaling, vesicular transport, and the regulation of cell shape and motility. Mutation or dysfunction of these proteins can lead to disease. There are around 40,000 known G-proteins that can broadly be classified into two groups ‒ small G-proteins consisting of a single domain and large multi-domain G-proteins.
Large G-proteins, also known...

The Retinoblastoma Gene

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,...

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Related Experiment Video

Updated: Jul 6, 2026

RhoC GTPase Activation Assay

RhoC GTPase Activation Assay

Published on: August 22, 2010

Rac GTPases as key regulators of p210-BCR-ABL-dependent leukemogenesis.

E K Thomas¹, J A Cancelas, Y Zheng

¹Division of Experimental Hematology, Cincinnati Children's Research Foundation, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

|March 21, 2008

Summary

This summary is machine-generated.

Targeting Rac GTPases alongside tyrosine kinase inhibitors may improve chronic myelogenous leukemia (CML) treatment by overcoming drug resistance and eliminating persistent cancer cells.

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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Area of Science:

Oncology
Molecular Biology
Hematology

Background:

Chronic myelogenous leukemia (CML) is driven by the p210-BCR-ABL oncoprotein.
Tyrosine kinase inhibitors (TKIs) have improved CML patient survival but do not offer a cure due to drug resistance and persistent leukemia stem cells.

Purpose of the Study:

To investigate the role of Rho GTPases Rac1 and Rac2 in p210-BCR-ABL-induced leukemogenesis.
To explore Rac GTPases as a potential therapeutic target for CML treatment.

Main Methods:

Utilized a murine model of CML.
Assessed the impact of Rac1 and Rac2 deficiency on p210-BCR-ABL-mediated proliferation and myeloproliferative disease.
Validated Rac as a target using a small molecule Rac inhibitor.

Main Results:

Deficiency in Rac1 and Rac2 significantly reduced p210-BCR-ABL-driven proliferation in vitro and myeloproliferative disease in vivo.
A first-generation Rac-specific inhibitor showed promise in targeting this pathway.

Conclusions:

Rac GTPases play a critical role in CML development.
Combinatorial therapies involving TKIs and Rac GTPase inhibitors represent a promising strategy for CML treatment.