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RIC-3 expression and splicing regulate nAChR functional expression.

Yael Ben-David1, Tehila Mizrachi2, Sarah Kagan1

  • 1Department of Medical Neurobiology, Faculty of Medicine, The Hebrew University, Ein Kerem, P.O. Box 12271, Jerusalem, 91120, Israel.

Molecular Brain
|May 1, 2016
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Summary

RIC-3 protein isoforms regulate nicotinic acetylcholine receptors. Inflammation impacts RIC-3 expression and splicing in immune cells, potentially affecting neuroinflammatory diseases.

Keywords:
AcetylcholineAlternative splicingDisordered proteinInflammationNicotinic acetylcholine receptors (nAChR)Protein maturationRIC-3

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Nicotinic acetylcholine receptors are crucial ion channels in the central nervous system.
  • RIC-3 is an endoplasmic reticulum chaperone essential for nicotinic acetylcholine receptor maturation.
  • RIC-3 undergoes alternative splicing, generating multiple isoforms in mammals and Drosophila.

Purpose of the Study:

  • Investigate RIC-3 expression and splicing regulation.
  • Determine RIC-3's impact on neuronal nicotinic acetylcholine receptor expression.
  • Examine RIC-3's role in immune cells and inflammation.

Main Methods:

  • Electrophysiological analysis in Xenopus laevis oocytes.
  • In situ hybridization.
  • Quantitative real-time polymerase chain reaction (qRT-PCR).

Main Results:

  • RIC-3 expression levels and splicing significantly affect nicotinic acetylcholine receptor functional expression.
  • Two conserved RIC-3 isoforms are differentially expressed in the brain.
  • Inflammatory signals regulate RIC-3 expression and splicing in immune cells.

Conclusions:

  • RIC-3 regulation in the brain and immune cells modulates nicotinic acetylcholine receptor function.
  • RIC-3's influence on the α7 nicotinic acetylcholine receptor in immune cells may play a role in neuroinflammatory diseases.