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Related Concept Videos

Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

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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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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.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
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Functional Calcium Imaging in Developing Cortical Networks
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Calcium and activity-dependent signaling in the developing cerebral cortex.

Arpana Arjun McKinney1,2,3,4, Ralitsa Petrova2,3,4, Georgia Panagiotakos1,2,3,4

  • 1Graduate Program in Developmental and Stem Cell Biology, University of California, San Francisco, CA 94143, USA.

Development (Cambridge, England)
|September 14, 2022
PubMed
Summary
This summary is machine-generated.

Precise calcium regulation is vital for prenatal brain development. Disruptions in calcium signaling are linked to neurodevelopmental disorders, highlighting its role in neurological health.

Keywords:
Calcium signalingCortical developmentNeurodevelopmental disorders

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Molecular Signaling

Background:

  • Intracellular calcium (Ca2+) influx regulates gene expression, linking environmental signals to genetic programs.
  • Dysregulation of Ca2+ signaling is implicated in neurodevelopmental and neuropsychiatric disorders.
  • Understanding prenatal calcium dynamics is crucial for neurodevelopmental research.

Purpose of the Study:

  • To review fundamental mechanisms of spatiotemporal Ca2+ regulation in early neurodevelopment.
  • To explore the role of Ca2+ signaling in normal and abnormal prenatal brain development.
  • To identify gaps in knowledge regarding Ca2+ regulation in neurodevelopmental diseases.

Main Methods:

  • Review of existing genetic and molecular evidence.
  • Analysis of calcium signaling pathways in neurodevelopment.
  • Synthesis of data on Ca2+ homeostasis and its disruption.

Main Results:

  • Ca2+ acts as a critical nexus between external stimuli and internal genetic responses.
  • Disrupted cell-specific Ca2+ homeostasis may contribute to adult neurological disorders.
  • Developmental Ca2+ signaling mechanisms can be redeployed, potentially leading to disease.

Conclusions:

  • Cell type-specific Ca2+ signaling mechanisms are essential for understanding nervous system development.
  • Targeting Ca2+ dependent pathways offers potential therapeutic strategies for neurological diseases.
  • Further research into Ca2+ regulation is key to mitigating neurodevelopmental disorders.