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Related Concept Videos

Membrane Domains01:18

Membrane Domains

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The membrane domains concentrate specific lipids and proteins at one place within the membrane, which helps in cell signaling, adhesion, and other critical cellular processes. These domains can differ in size, composition, function, and lifespan.
Protein Domains
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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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Mechanisms of Membrane Domain Formation00:59

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Different physical properties of lipids and proteins allow them to localize and form distinct islands or domains in the membrane. Some membrane domains are formed due to protein-protein interactions, whereas others are formed due to the presence of specific lipids such as sphingolipids and sterols—for example, large proteins, such as bacteriorhodopsin, aggregate and create distinct domains.
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The cadherins were one of the first cell adhesion molecules discovered; the term “cadherins”   is based on their calcium-dependent adhering properties. The first cadherins discovered on the epithelial, neuronal, and placental cells were named E-cadherin, P-cadherin, and N-cadherin, respectively. These classical cadherins share sequence and structural similarities. Other cadherins, including those involved in cell signaling, are grouped into non-classical cadherins. This...
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Tight Junctions

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Tight junctions are molecular seals between cells that prevent the leaking of fluids, ions, and other small solutes across cavities and compartments in multicellular organisms. They are mainly composed of claudin and occludin transmembrane proteins, and other proteins such as tricellulin and JAM (junctional adhesion molecule). All these proteins are 4-pass transmembrane proteins, except JAM, which is a single-pass transmembrane protein belonging to the immunoglobulin superfamily. The...
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Secretory vesicles, also known as dense core vesicles (DCVs), are membrane-bound vesicles that transport secretory proteins, such as hormones or neurotransmitters. Regulated secretory vesicles transport proteins from the trans-Golgi network to the exterior of the cell. Proteins present in regulated secretory vesicles are required to be rapidly exocytosed in large amounts upon a specific stimulus.
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Related Experiment Video

Updated: Apr 17, 2026

Membrane Remodeling of Giant Vesicles in Response to Localized Calcium Ion Gradients
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Ca²⁺ microdomains organized by junctophilins.

Hiroshi Takeshima1, Masahiko Hoshijima2, Long-Sheng Song3

  • 1Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto 606-8501, Japan.

Cell Calcium
|February 10, 2015
PubMed
Summary

Junctophilins are crucial proteins that build and maintain junctional membrane complexes in excitable cells. Their deficiency or mutations can lead to muscle and neurodegenerative diseases.

Keywords:
Calcium channelExcitation–contraction couplingMuscle

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Physiology

Background:

  • Excitable cells utilize junctional membrane complexes (JMCs) for communication between the plasma membrane and the endo/sarcoplasmic reticulum (ER/SR).
  • JMCs, including triads, dyads, peripheral couplings, and subsurface cisterns, are vital for cellular function.
  • Junctophilins (JPs) are key proteins involved in the formation and maintenance of these JMCs.

Purpose of the Study:

  • To investigate the role of junctophilin subtypes in the formation and maintenance of junctional membrane complexes.
  • To understand the functional consequences of junctophilin deficiency on channel crosstalk in muscle cells.
  • To explore the link between junctophilin mutations and human diseases.

Main Methods:

  • The study likely involves molecular biology techniques to study junctophilin expression and function.
  • Genetic analysis of junctophilin mutations in patients with related diseases.
  • Cellular imaging and electrophysiology to assess JMC formation and function.

Main Results:

  • Junctophilin deficiency impairs JMC formation and the functional crosstalk between plasma membrane Ca(2+) channels and ER/SR Ca(2+) release channels.
  • Human genetic mutations in junctophilin subtypes are associated with congenital hypertrophic cardiomyopathy and neurodegenerative diseases.
  • Dysregulation of junctophilins is implicated in pathological changes in skeletal and cardiac muscle.

Conclusions:

  • Junctophilins are essential for the structural integrity and function of JMCs across various cell types.
  • Defects in junctophilins have significant implications for muscle and neuronal health.
  • Further research into junctophilins may reveal therapeutic targets for related diseases.