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The Two-State Receptor Model01:29

The Two-State Receptor Model

The two-state receptor model explains a drug's interaction with receptors, such as G protein-coupled receptors and ligand-gated ion channels, to induce or inhibit a biological response. When no natural ligands are present, a receptor exists in an equilibrium of inactive (Ri) and active (Ra) conformations. The inactive form does not produce a response, while the active form generates a basal effect known as constitutive activity.
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Extracellular Recording of Neuronal Activity Combined with Microiontophoretic Application of Neuroactive Substances in Awake Mice
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SSB antagonizes RecX-RecA interaction.

Dmitry M Baitin1, Marielle C Gruenig, Michael M Cox

  • 1Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706-1544, USA.

The Journal of Biological Chemistry
|April 4, 2008
PubMed
Summary
This summary is machine-generated.

RecX protein inhibits RecA filament growth by competing with SSB proteins for DNA access. This competition suggests RecX may bind both RecA and DNA, with SSB modulating RecX activity.

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Avidity-based Extracellular Interaction Screening (AVEXIS) for the Scalable Detection of Low-affinity Extracellular Receptor-Ligand Interactions
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Avidity-based Extracellular Interaction Screening (AVEXIS) for the Scalable Detection of Low-affinity Extracellular Receptor-Ligand Interactions

Published on: March 5, 2012

Area of Science:

  • Molecular Biology
  • Biochemistry
  • Genetics

Background:

  • RecX protein from Escherichia coli inhibits RecA protein filament extension on DNA.
  • Previous studies indicated RecX's DNA binding is weak and insufficient to explain its inhibitory effects.

Purpose of the Study:

  • To investigate the mechanism by which RecX protein inhibits RecA filament formation.
  • To determine the role of single-stranded DNA binding (SSB) proteins in modulating RecX activity.

Main Methods:

  • Investigated the interaction between RecX, RecA, and SSB proteins in vitro.
  • Assessed the effect of varying concentrations of SSB and yeast RPA (replication protein A) on RecX-mediated inhibition of RecA filament extension.
  • Examined the impact of SSB C-terminal deletions on RecX-SSB interactions.

Main Results:

  • Elevated concentrations of SSB protein significantly moderated the inhibitory effects of RecX.
  • Yeast RPA protein demonstrated similar modulatory effects, indicating a non-species-specific mechanism.
  • A direct interaction between SSB and RecX is unlikely; instead, SSB appears to compete for single-stranded DNA binding sites.
  • The inhibitory effects of SSB were enhanced upon removal of the SSB C-terminus.

Conclusions:

  • RecX protein's inhibition of RecA filament extension is modulated by competition with SSB proteins for single-stranded DNA.
  • The mechanism likely involves RecX binding to both RecA and DNA, with SSB acting as a competitive inhibitor for DNA access.
  • The findings suggest a complex interplay between RecX, RecA, and SSB in regulating DNA repair pathways.