Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Amplifying Signals via Enzymatic Cascade

Amplifying Signals via Enzymatic Cascade

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 the...

Antihypertensive Drugs: Action of β1 Blockers

Antihypertensive Drugs: Action of β₁ Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...

Antihypertensive Drugs: Types of β-Blockers

Antihypertensive Drugs: Types of β-Blockers

β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and vasodilation. This widens airways and...

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...

Antihypertensive Drugs: Action of Calcium Channel Blockers

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,...

Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers

Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers

β-adrenergic antagonists, or β-blockers, modulate the sympathetic nervous system by targeting β-adrenoceptors and inhibiting catecholamine-mediated sympathetic responses. β-blockers differ in their adrenoceptor subtype affinity, lipophilicity, and α-blocking capabilities. The history of β-blocker development began with the prototype, dichloroisoprenaline, which exhibited partial agonist activity. As a result, propranolol was developed as a pure antagonist but nonselective agent, paving the way...

You might also read

Related Articles

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

Sort by

Same author

Dynamic visualization of physiological CaMKII activity using sensitive FRET biosensors.

bioRxiv : the preprint server for biology·2026

Same author

GPR3 Ligands Discovered through Combined Virtual and Conformational Biosensor-Based Screening.

Journal of the American Chemical Society·2026

Same author

Ligand-specific activation trajectories dictate GPCR signalling in cells.

Nature·2026

Same author

MRAP2 modifies the signaling and oligomerization state of the melanocortin-4 receptor.

Nature communications·2025

Same author

Disruption of constitutive CXCR4 oligomers impairs oncogenic properties in lymphoid neoplasms.

Proceedings of the National Academy of Sciences of the United States of America·2025

Same author

Pharmacological characterization of a clinical candidate, TG-0054, a small molecule inverse agonist targeting CXCR4.

Molecular pharmacology·2025

Search research articles

Related Experiment Video

Updated: Jul 1, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Blocking them all: beta-arrestins inhibit cellular signaling.

Martin J Lohse¹, Christoph Klenk

¹Institute of Pharmacology and Toxicology, University of Würzburg, Versbacher Strasse 9, 97078 Würzburg, Germany. lohse@toxi.uni-wuerzburg.de

|September 9, 2008

Summary

Beta-arrestin1 acts as a crucial regulator, inhibiting STAT1 signaling to control interferon-induced antiviral responses. This finding reveals a novel mechanism for managing cellular defense against viruses.

More Related Videos

Monitoring GPCR-β-arrestin1/2 Interactions in Real Time Living Systems to Accelerate Drug Discovery

Monitoring GPCR-β-arrestin1/2 Interactions in Real Time Living Systems to Accelerate Drug Discovery

Published on: June 28, 2019

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Related Experiment Videos

Last Updated: Jul 1, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Monitoring GPCR-β-arrestin1/2 Interactions in Real Time Living Systems to Accelerate Drug Discovery

Monitoring GPCR-β-arrestin1/2 Interactions in Real Time Living Systems to Accelerate Drug Discovery

Published on: June 28, 2019

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Area of Science:

Cellular biology
Molecular signaling
Immunology

Background:

Beta-arrestins are known scaffold proteins connecting G protein-coupled receptors to nonclassical signaling pathways.
The precise roles of beta-arrestins in regulating specific transcription factors and immune responses require further elucidation.

Purpose of the Study:

To investigate the role of beta-arrestin1 in regulating STAT1 (Signal Transducer and Activator of Transcription 1) signaling.
To determine the impact of beta-arrestin1 on interferon-induced antiviral responses.

Main Methods:

The study likely involved cell-based assays to examine protein-protein interactions and signaling pathway activation.
Techniques may include Western blotting, reporter gene assays, and potentially gene silencing or overexpression studies.

Main Results:

Beta-arrestin1 was shown to inhibit signaling mediated by the STAT1 transcription factor.
This inhibition by beta-arrestin1 leads to the suppression of interferon-induced antiviral responses.

Conclusions:

Beta-arrestin1 possesses a previously unrecognized function in actively switching off STAT1 signaling.
This mechanism highlights a novel regulatory role for beta-arrestins in modulating cellular antiviral immunity.