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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:
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
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...
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...

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Related Experiment Video

Updated: May 23, 2026

Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells
06:44

Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells

Published on: March 1, 2024

The Rac1 splice form Rac1b promotes K-ras-induced lung tumorigenesis.

C Zhou1, S Licciulli, J L Avila

  • 1Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, PA 19104, USA.

Oncogene
|March 21, 2012
PubMed
Summary
This summary is machine-generated.

Rac1b is upregulated in lung tumors and, when combined with K-ras mutations, accelerates lung adenocarcinoma growth in mice. Rac1b is not required for K-ras-driven cell proliferation, clarifying its role in tumorigenesis.

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RhoC GTPase Activation Assay
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Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells
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RhoC GTPase Activation Assay
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RhoC GTPase Activation Assay

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Rac1b, an alternative splice form of Rac1, is upregulated in colon and breast cancers.
  • Upregulation of Rac1b in non-small cell lung cancer (NSCLC) correlates with K-ras mutational status.

Purpose of the Study:

  • To assess the in vivo oncogenic potential of Rac1b in lung adenocarcinoma.
  • To investigate the synergistic effects of Rac1b and K-ras in lung tumorigenesis.
  • To delineate the signaling pathways involved in K-ras-driven lung cancer.

Main Methods:

  • Analysis of NSCLC tumor and matched normal tissue samples.
  • Utilized a conditional mouse model of lung adenocarcinoma for in vivo Rac1b expression.
  • Assessed cellular proliferation and tumor growth kinetics.

Main Results:

  • Rac1b alone is insufficient for tumor initiation but synergizes with oncogenic K-ras.
  • Rac1b expression with oncogenic K-ras leads to increased proliferation and accelerated tumor growth.
  • Rac1b is not required for K-ras-driven cell proliferation, unlike Rac1.

Conclusions:

  • Rac1b plays a synergistic role in K-ras-driven lung tumorigenesis.
  • Findings clarify the distinct roles of Rac1 and Rac1b in K-ras signaling pathways.
  • Rac1b contributes to lung adenocarcinoma progression through mechanisms independent of direct requirement in K-ras-driven proliferation.