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Related Concept Videos

GTPases and their Regulation02:14

GTPases and their Regulation

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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.
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Small GTPases - Ras and Rho01:24

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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.
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Regulation of Expression Occurs at Multiple Steps02:24

Regulation of Expression Occurs at Multiple Steps

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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
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The Ras Gene02:38

The Ras Gene

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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.
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Related Experiment Video

Updated: Feb 6, 2026

Detection of Small GTPase Prenylation and GTP Binding Using Membrane Fractionation and GTPase-linked Immunosorbent Assay
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Detection of Small GTPase Prenylation and GTP Binding Using Membrane Fractionation and GTPase-linked Immunosorbent Assay

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Systems level expression correlation of Ras GTPase regulators.

E Besray Unal1,2, Christina Kiel3,4, Hannah Benisty5

  • 1Institute of Pathology, Charité - Universitätsmedizin Berlin, 10117, Berlin, Germany.

Cell Communication and Signaling : CCS
|August 17, 2018
PubMed
Summary

Protein levels for essential cellular functions remain constant across species. This balance, crucial for Ras GTPase regulation, is disrupted in cancer and cell lines, impacting gene knockout study interpretations.

Keywords:
GTPase activating proteinsGene expression networkGuanine nucleotide exchange factorsRas small GTPasesTissue expression

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Area of Science:

  • Molecular Biology
  • Genomics
  • Proteomics

Background:

  • Core proteome proteins show quantitative correlation across eukaryotic species.
  • Anticorrelation in protein paralogue expression suggests functional constancy.
  • This implies a regulatory mechanism maintaining total protein levels for specific functions.

Purpose of the Study:

  • To investigate expression patterns of RAS GTPase subfamily and their regulators (GEFs and GAPs).
  • To determine if total protein levels for specific functions are maintained across tissues and individuals.
  • To assess the impact of cellular context (normal tissue, cancer, cell line) on this balance.

Main Methods:

  • Spearman's rank correlation analysis of gene expression data.
  • Analysis across diverse datasets: normal tissues (multiple species), human cancer tissues, and human cell lines.
  • Focus on the RAS GTPase subfamily and their Guanine nucleotide Exchange Factor (GEF) and GTPase Activating Protein (GAP) regulators.

Main Results:

  • Despite significant variability in individual gene expression, total levels of Ras GTPase regulators (GEFs and GAPs) are balanced in normal tissues.
  • This balance is maintained across different tissues and individuals within those tissues.
  • Impairment of this GEF/GAP balance is observed in cancer tissues and cell lines.

Conclusions:

  • The study highlights a conserved mechanism for maintaining functional protein homeostasis.
  • The observed imbalance in cancer and cell lines has implications for understanding disease mechanisms.
  • Findings are critical for interpreting results from gene knockout experiments, where compensatory mechanisms may exist.