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Related Concept Videos

Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

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.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
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Skeleton and Calcium Homeostasis

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Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
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Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
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Non-Canonical Wnt Signaling Pathways

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Related Experiment Video

Updated: May 12, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

Calcium influx through L-type CaV1.2 Ca2+ channels regulates mandibular development.

Kapil V Ramachandran1, Jessica A Hennessey, Adam S Barnett

  • 1Department of Medicine (Cardiology), Duke University Medical Center, Durham, North Carolina, USA.

The Journal of Clinical Investigation
|April 4, 2013
PubMed
Summary

Gain-of-function mutations in CACNA1C cause Timothy Syndrome. This study reveals the L-type voltage-gated calcium channel CaV1.2 is crucial for jaw development, impacting cellular growth in non-excitable cells.

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Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
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Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels
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Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels

Published on: December 13, 2024

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Timothy Syndrome (TS) is linked to gain-of-function mutations in CACNA1C, affecting the L-type voltage-gated calcium channel CaV1.2.
  • The role of CaV1.2 in non-excitable cells, particularly in craniofacial development, remains unclear.

Purpose of the Study:

  • To investigate the role of CaV1.2 in craniofacial development, specifically jaw formation.
  • To elucidate the mechanisms by which CaV1.2 influences cellular processes during jaw development.

Main Methods:

  • Utilized gain-of-function and loss-of-function studies in mouse models.
  • Employed knockdown/rescue and pharmacological approaches in zebrafish.
  • Examined CaV1.2 expression in pharyngeal arches and jaw primordia.

Main Results:

  • CaV1.2 is expressed in jaw primordia cells within the first and second pharyngeal arches.
  • Ca2+ influx through CaV1.2 regulates jaw development, as shown by mouse and zebrafish studies.
  • CaV1.2 knockdown did not affect cranial neural crest migration, indicating a later developmental role.
  • Cellular hypertrophy and hyperplasia in mandibular development depend on CaV1.2-mediated Ca2+ signals and calcineurin pathway activation.

Conclusions:

  • Voltage-gated calcium channel CaV1.2 plays a critical role in jaw development.
  • CaV1.2 influences cellular growth through Ca2+ signaling and the calcineurin pathway in non-excitable cells.
  • These findings expand the understanding of CaV1.2 function beyond cardiac and neuronal tissues.