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Updated: May 23, 2026

Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy
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Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy

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Gs cascade regulates canonical transient receptor potential 5 (TRPC5) through cAMP mediated intracellular Ca2+

Chansik Hong1, Jinsung Kim, Jae-Pyo Jeon

  • 1Department of Physiology and Institute of Dermatological Science, Seoul National University College of Medicine, Seoul, Republic of Korea.

Biochemical and Biophysical Research Communications
|April 12, 2012
PubMed

Insights

The Gα(s)-cAMP pathway enhances Canonical Transient Receptor Potential (TRPC5) channel activity. This involves increased intracellular calcium dynamics and TRPC5 channel trafficking to the plasma membrane.

Area of Science:

  • Molecular Biology
  • Cell Physiology
  • Ion Channel Function

Background:

  • Canonical Transient Receptor Potential (TRPC) channels are Ca(2+)-permeable cation channels found in mammalian cells.
  • The precise mechanisms by which heterotrimeric G proteins regulate TRPC5 activity remain incompletely understood.

Purpose of the Study:

  • To investigate the role of the Gα(s) regulatory pathway in modulating TRPC5 channel activity.
  • To elucidate the downstream signaling events linking Gα(s) activation to TRPC5 potentiation.

Main Methods:

  • Whole-cell patch-clamp electrophysiology to measure TRPC5 currents.
  • Calcium imaging techniques to assess intracellular Ca(2+) transients.
  • Intracellular infusion of signaling molecules (e.g., IP3) and buffering of intracellular calcium.
  • Confocal microscopy to quantify membrane localization of TRPC5.

Main Results:

  • Activation of the Gα(s) pathway using isoproterenol, forskolin, or 8-Br-cAMP significantly potentiated TRPC5 currents.
  • Isoproterenol induced robust intracellular Ca(2+) transients, which were attenuated by buffering intracellular calcium.
  • Calcium release mediated by inositol trisphosphate (IP3) was implicated in the potentiation.
  • Gα(s) pathway activation led to increased TRPC5 channel trafficking to the plasma membrane.

Conclusions:

  • The Gα(s)-cAMP signaling pathway potentiates TRPC5 channel activity.
  • This potentiation is mediated by alterations in intracellular calcium dynamics and enhanced channel insertion into the plasma membrane.

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