Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

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...
Smooth Muscle Contraction01:25

Smooth Muscle Contraction

Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
Muscle Stimulation Frequency01:22

Muscle Stimulation Frequency

The contraction strength of muscles is regulated by motor neurons, which modulate the frequency of action potentials dispatched to the motor units based on the body's requirements. This process of varying the muscle stimulation frequency allows muscles to contract with a force that is precisely tailored to the needs of the moment, whether lifting a feather or a heavy box.
Wave summation
At low firing rates, motor neurons induce individual twitch contractions in muscle fibers. These twitches...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Carcinogenicity of Dimethylarsinic Acid: Evidence From Experimental Models and Mechanistic Insights.

Pathology international·2026
Same author

A stromal platform for robust expansion of functional IL-10-producing B cells for immune regulation.

JCI insight·2026
Same author

ARAP1 fine-tunes F-actin polymerization level in lymphocytes through RhoA inhibition.

Frontiers in immunology·2026
Same author

Developing a novel in vitro toxicity assay for predicting inhalation toxicity in rats.

Toxicology letters·2025
Same author

Comparative Gene Expression Analysis of Malignant Mesothelioma and Lung Adenocarcinomas Induced by Multi-Walled Carbon Nanotube-7 and Double-Walled Carbon Nanotubes in Rats: Distinct Molecular Signatures and Canonical Pathways.

Nanomaterials (Basel, Switzerland)·2025
Same author

Construction of a Novel 3D Urinary Bladder Mucosa Model and Its Application in Toxicity Assessment of Arsenicals.

Toxics·2025

Related Experiment Video

Updated: May 22, 2026

Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels
07:17

Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels

Published on: December 13, 2024

Surf4 modulates STIM1-dependent calcium entry.

Yoko Fujii1, Masayuki Shiota, Yasuyuki Ohkawa

  • 1Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, Yokohama, Kanagawa 230-0045, Japan.

Biochemical and Biophysical Research Communications
|May 22, 2012
PubMed
Summary
This summary is machine-generated.

Surfeit locus protein 4 (Surf4) modulates store-operated calcium entry (SOCE) by interacting with STIM1. Deleting Surf4 enhances SOCE and STIM1 clustering in immune cells, revealing Surf4 as a key regulator.

More Related Videos

Isolation of Human Myoblasts, Assessment of Myogenic Differentiation, and Store-operated Calcium Entry Measurement
10:45

Isolation of Human Myoblasts, Assessment of Myogenic Differentiation, and Store-operated Calcium Entry Measurement

Published on: July 26, 2017

Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
09:07

Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis

Published on: February 18, 2020

Related Experiment Videos

Last Updated: May 22, 2026

Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels
07:17

Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels

Published on: December 13, 2024

Isolation of Human Myoblasts, Assessment of Myogenic Differentiation, and Store-operated Calcium Entry Measurement
10:45

Isolation of Human Myoblasts, Assessment of Myogenic Differentiation, and Store-operated Calcium Entry Measurement

Published on: July 26, 2017

Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
09:07

Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis

Published on: February 18, 2020

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Store-operated calcium entry (SOCE) is vital for immune cell function.
  • The precise mechanisms regulating STIM1, a key protein in SOCE, are not fully understood.

Purpose of the Study:

  • To identify proteins that modulate STIM1 function.
  • To investigate the role of identified modulators in SOCE.

Main Methods:

  • Affinity purification to identify STIM1-binding proteins.
  • Co-immunoprecipitation to confirm Surf4-STIM1 interaction.
  • CRISPR/Cas9 gene editing to delete Surf4 in DT40 B cells.
  • Calcium imaging to measure SOCE levels.

Main Results:

  • Surfeit locus protein 4 (Surf4) was identified as a STIM1-binding protein.
  • Surf4 localizes to the endoplasmic reticulum and interacts with STIM1.
  • Surf4 deletion in DT40 B cells led to significantly increased SOCE.
  • Loss of Surf4 facilitated STIM1 clustering upon calcium store depletion.

Conclusions:

  • Surf4 acts as a negative modulator of STIM1-mediated SOCE.
  • Surf4 plays a crucial role in regulating calcium signaling in immune cells.
  • Targeting Surf4 could offer therapeutic strategies for immune-related disorders.