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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
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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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Second Messenger-Operated Calcium Entry Through TRPC6.

Alexandre Bouron1,2, Sylvain Chauvet3,4, Stuart Dryer5,6

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Advances in Experimental Medicine and Biology
|May 11, 2016
PubMed
Summary

Canonical transient receptor potential 6 (TRPC6) channels are key cation channels involved in various cellular functions. This review highlights TRPC6

Keywords:
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Area of Science:

  • Molecular Biology
  • Cell Physiology
  • Biochemistry

Background:

  • Canonical transient receptor potential 6 (TRPC6) proteins form heteromultimeric non-selective cation channels.
  • TRPC6 interacts with diverse proteins, forming macromolecular complexes involved in cellular signaling.
  • TRPC6 activity is modulated by various factors, including diacylglycerol, store depletion, hyperforin, and H2O2.

Purpose of the Study:

  • To review the key features of TRPC6 channels.
  • To emphasize the biological significance of TRPC6 in kidney and blood cells.
  • To discuss the diverse regulatory mechanisms and consequences of TRPC6 activation.

Main Methods:

  • Literature review of TRPC6 channel function.
  • Analysis of TRPC6 protein interactions and signaling pathways.
  • Examination of TRPC6 roles in cellular calcium homeostasis.

Main Results:

  • TRPC6 activation leads to elevated cytosolic Ca(2+) concentrations.
  • Ca(2+) influx can occur via TRPC6 channels, reverse mode Na(+)/Ca(2+) exchanger, or voltage-gated Ca(2+) channels.
  • TRPC6 plays a role in various biological functions across different tissues.

Conclusions:

  • TRPC6 channels are crucial regulators of cellular ion transport and signaling.
  • Understanding TRPC6 function is vital for elucidating its pathophysiological roles.
  • Further research is needed to fully comprehend TRPC6's involvement in disease processes, particularly in renal and hematopoietic systems.