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

Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

2.2K
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,...
2.2K
Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

4.2K
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...
4.2K
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

7.0K
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,...
7.0K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

13.8K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
13.8K
Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

2.7K
Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
2.7K
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

19.2K
When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
19.2K

You might also read

Related Articles

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

Sort by
Same author

Antifibrotic Effects of Yi-Qi-Jian-Pi-Xiao-Yu Formula in Kidney via HIF1A-Driven M1 Macrophage Polarization.

Phytochemical analysis : PCA·2026
Same author

Hydrogen-Bond-Directed Assembly of Polyanionic Cluster [Mo<sub>2</sub>O<sub>5</sub>(IO<sub>3</sub>)<sub>4</sub>]<sup>2-</sup> for Nonlinear Optical Crystal Design.

Inorganic chemistry·2026
Same author

Effectiveness and safety of probiotics in treating knee osteoarthritis: an updated systematic review and meta-analysis of randomized controlled trials.

Frontiers in medicine·2026
Same author

Cerebrovascular thrombosis during pediatric ALL therapy: a case series highlighting temporal association with PEG-asparaginase exposure.

Frontiers in pediatrics·2026
Same author

Diversity of stem endophytes communities from wild asparagus resources and the biocontrol potential on Phomopsis asparagi.

BMC microbiology·2026
Same author

Disruption of BnPHT5;1b gene enhances arsenate tolerance through increased arsenate retention in shoot cell walls of Brassica napus.

Journal of hazardous materials·2026

Related Experiment Video

Updated: Mar 26, 2026

Fluorescence-based Measurement of Store-operated Calcium Entry in Live Cells: from Cultured Cancer Cell to Skeletal Muscle Fiber
14:18

Fluorescence-based Measurement of Store-operated Calcium Entry in Live Cells: from Cultured Cancer Cell to Skeletal Muscle Fiber

Published on: February 13, 2012

21.9K

Decrease of Store-Operated Ca2+ Entry and Increase of Na+/Ca2+ Exchange by Pharmacological JAK2 Inhibition.

Jing Yan1, Zohreh Hosseinzadeh, Bingbing Zhang

  • 1Departments of Cardiology & Cardiovascular Medicine, University of Tx00FC;bingen, Tx00FC;bingen, Germany.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|February 10, 2016
PubMed
Summary

Pharmacological JAK2 inhibition impacts cellular calcium handling and migration. Inhibiting JAK2 reduces store-operated calcium entry (SOCE) and calcium release while increasing calcium extrusion, ultimately decreasing cell migration.

More Related Videos

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium
08:46

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium

Published on: September 1, 2015

10.3K
Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting
10:08

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting

Published on: December 9, 2022

2.7K

Related Experiment Videos

Last Updated: Mar 26, 2026

Fluorescence-based Measurement of Store-operated Calcium Entry in Live Cells: from Cultured Cancer Cell to Skeletal Muscle Fiber
14:18

Fluorescence-based Measurement of Store-operated Calcium Entry in Live Cells: from Cultured Cancer Cell to Skeletal Muscle Fiber

Published on: February 13, 2012

21.9K
Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium
08:46

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium

Published on: September 1, 2015

10.3K
Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting
10:08

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting

Published on: December 9, 2022

2.7K

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cell proliferation and migration are critically regulated by intracellular calcium levels ([Ca2+]i).
  • Key mechanisms controlling [Ca2+]i include store-operated calcium entry (SOCE) via Orai1 and STIM1, and calcium extrusion by the Na+/Ca2+ exchanger (NCX1).
  • Janus activated kinase 2 (JAK2) is implicated in cell proliferation signaling pathways.

Purpose of the Study:

  • To investigate the effect of pharmacological JAK2 inhibition on SOCE and Na+/Ca2+ exchange.
  • To explore the influence of JAK2 inhibition on cellular calcium homeostasis and migration in breast carcinoma cells.

Main Methods:

  • MCF-7 breast carcinoma cells were treated with JAK2 inhibitors (TG101348 or AG490).
  • Gene and protein expression, intracellular calcium levels, SOCE, Na+/Ca2+ exchanger activity, and cell migration were assessed.
  • Techniques included RT-PCR, immunoblotting, Fura-2 fluorescence, and whole-cell patch clamp electrophysiology.

Main Results:

  • JAK2 inhibition decreased Orai1 and STIM1 protein levels, reduced intracellular calcium release, and inhibited SOCE.
  • Conversely, JAK2 inhibition increased NCX1 transcript levels and enhanced calcium entry/current upon extracellular sodium removal.
  • Cell migration was significantly decreased following JAK2 inhibition.

Conclusions:

  • Pharmacological JAK2 inhibition modulates key components of cellular calcium regulation, including SOCE and NCX1 activity.
  • This modulation of calcium handling by JAK2 inhibition affects cell migration, revealing a novel regulatory mechanism.